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Neonatal Pathophysiology > Chronic Lung Disease > Flashcards

Chronic Lung Disease Flashcards

1
Q

What is the NIH consensus of time point for assessment for BPD in infants born < 32 wk GA at birth?

A

36 wk PMA or at dc to home, which ever comes first

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2
Q

What is the NIH consensus of time point for assessment for BPD in infants born > 32 wk GA at birth?

A

> 28 dol, but < 56 postnatal age or at dc to home, which ever comes first

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3
Q

What is the NIH consensus of mild classification of BPD in infants born < 32 wk GA at birth?

A
  • h/o treatment with O2 > 21% for at least 28 days
    &
  • breathing RA at 36 wk PMA or discharge, which ever comes first
    (infants who have been weaned from any supplemental oxygen)
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4
Q

How is BPD classified?

A

at a later postnatal age according to type of respiratory support required to maintain a normal arterial oxygen saturation (89%)

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5
Q

What is the NIH consensus of mild classification of BPD in infants born > 32 wk GA at birth?

A

breathing RA by 56 days postnatal age, or dc home which ever comes first

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6
Q

What is the NIH consensus of moderate classification of BPD in infants born < 32 wk GA at birth?

A

need for < 30% oxygen at 36 weeks PMA or dc, which ever comes first

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7
Q

What is the NIH consensus of moderate classification of BPD in infants born > 32 wk GA at birth?

A

need for < 30% oxygen 56 days PNA or dc to home, which ever comes first

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8
Q

What is the NIH consensus of severe classification of BPD in infants born < 32 wk GA at birth?

A

need for > 30% oxygen and/or positive pressure at 56 days PMA or dc, which ever comes first

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9
Q

What is the NIH consensus of severe classification of BPD in infants born > 32 wk GA at birth?

A

need for oxygen and/or positive pressure at 56 days PMA or dc, which ever comes first

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10
Q

What are typical etiologies for severe BPD in infants born >32 wk GA?

A

MAS, CDH, GBS

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11
Q

Why is 36 weeks PMA significant?

A

by that time, an infant should have recovered from hyaline membrane dz; standardizing PMA helps to assess process instead of 28 dol- very different for an x 24 wk v x 30 wk

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12
Q

What is the classic definition of BPD?

A

a neonatal form of chronic pulmonary disorder that follows a primary course of respiratory failure (ex: RDS or MAS) in the first few days of life; characterized by:

1) persistent respiratory failure with hypoxia/hypercapnea
2) frequent cor pulmonale
3) CXR findings of hyperinflation and increased densities

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13
Q

What is the incidence of CLD in infants born at < 1500g?

A

35%; there are more babies in the US with BPD than CF

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14
Q

In what population are long-term complications of BPD the most common?

A

< 1000g at birth

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15
Q

What is the trend of BPD incidence?

A

the overall rates of CLD are not declining; however, mortality and rates of severe BPD are down with significant preventative measures

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16
Q

What is included in the cost of BPD?

A

prolonged ICU stays, frequent hospital readmissions, home health care charges and parent time off

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17
Q

Why is BPD not considered only a childhood problem?

A

1) persistent small airway damage
2) persistent airway obstruction
3) pulmonary dysfunction (increased risk for asthma)
4) neurdevelopmental outcomes

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18
Q

What is the etiology for infants who have BPD without a previous h/o hyaline membrane dz?

A
  • smoke inhalation

- alpha 1 antitripsin deficiency

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19
Q

What was the result of introducing mechanical ventilation for PT infants in the 1960s?

A

changed the natural course of RDS disease progression resulting in increased survival of smaller and sicker infants

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20
Q

What is characteristic of BPD presentation of CXR?

A

1) streaky interstitial markings
2) patchy atelectasis intermingled with cystic areas
3) severe overall lung hyperinflation

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21
Q

What is the rationale for permissive hypercapnea?

A

to provide a more gentle ventilation, we avoid O2 toxicity and tolerate higher CO2s

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22
Q

What is the rationale for NEW BPD?

A

it is seen as a developmental problem, where we catch the lung before its ready, and the baby is forced to breathe before it should; alveoli are disrupted from development and pulmonary capillaries are not finished developing (now we are seeing more vascular problems and PPHN than asthma like issues (old BPD) when the biggest concern was airway trauma

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23
Q

What is the incidence of BPD in an infant that has never been intubated?

A

1/30th; intubation is one of the biggest problems causing BPD

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24
Q

What are recent practices changes geared toward reducing the incidence of BPD?

A

1) trying to keep from intubating
2) non invasive ventilation
3) eliminate prematurity
4) antenatal steroids
5) exogenous surfactant therapy

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25
Q

Why has surfactant not been shown to decrease the incidence of BPD?

A

r/t increased number of ELBW survivors

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26
Q

How does the ETT contribute to the development of BPD?

A

1) route for “rain out”
2) dysplastic airway ∆ (tracheomalacia, etc)
3) distrupt ciliary bodies and cells are replaced with less effective functioning, hyperplasia cells
4) portal of entry for infection

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27
Q

Why is the incidence of new BPD increasing?

A

occurring with increasing frequency as smaller and more immature infants are surviving; occurs even after gentle ventilation techniques
- affects subsequent alveolarization and pulmonary vascular development

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28
Q

What is the “second week dwindle”?

A

around day 10-12, the ductus is open, pneumonia, fluid overloaded may be apart of the natural course of a lung thats not supposed to be exposed to O2 or functioning&raquo_space;> there is a progressive decline in respiratory fx

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29
Q

What are the clinical features of new BPD?

A
  • smaller infants affected ( 400 g +)
  • early mechanical ventilation followed by a “honeymoon”
  • second week dwindles
  • often require ventilation and supplemental O2 for months
  • clinical progression is accompanied by a slow improvement and gradual weaning of support
    (small # of affected babes demonstrate a more severe course)
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30
Q

What is apart of the sequelae of severe BPD?

A
  • progressive respiratory failure
  • pulmonary HTN (some arteries become so hypertrophied that it induces RVH)
  • cor pulmonale
  • death
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31
Q

What is cor pulmonale?

A

heart failure secondary to lung dz

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32
Q

What factors typically contribute an infant’s failure to reverse the BPD dz process and improve?

A

1) fluid overload
2) infection
3) aspiration
4) L > R shunts (VSD, PDA, ASD)

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33
Q

What embryonic processes are disrupted when an infant is born at 22 or 23 weeks GA?

A
  • last generations of the lung periphery are formed
  • epithelial differentiation
  • air blood barrier formed
    essentially you are using airways for gas exchange, which will work for a little while
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34
Q

What is barotrauma?

A

trauma attributed to pressure; some studies say that it is volutrauma that is more damaging

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35
Q

How many breaths can irreversibly ruin your alveoli?

A

as few as 6 too big breaths (tV); this damage can lead to protein leaks from capillaries into alveolar space; that protein sucks in O2 and sets the stage for pulmonary edema

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36
Q

What is the pathophysiology of BPD?

A

a primary lung injury is not always evident at birth; the secondary development of a persistent lung injury is a/w an abnormal repair process and leads to structural changes such as arrested alveolarization and pulmonary vascular dysgensis.

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37
Q

Why is oxygen a risk factor for the development of BPD?

A

hyperoxia can have major effects on lung tissue, including:

1) proliferation of alveolar type II cells and fibroblast
2) alterations in surf system
3) increases in inflammatory cells and cytokines
4) increased collagen deposition
5) decreased alveolarization and microvascular density
6) pulmonary edema

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38
Q

How significant a risk factor is O2 toxicity to new BPD?

A

the association for persistent need for mechanical ventilation and supplemental oxygen in the first 2 weeks of life is not as dominant as in the past
- O2, independent of mechanical ventilatory support can cause lethal damage to previously normal lungs

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39
Q

What are the ideal SpO2 goals?

A

85-93%; has lead to a decrease in the need for supplemental O2 at 36 weeks PMA in this post surf era

40
Q

How does lung immaturity contribute to BPD?

A

this is the new key and the one element we don’t have control over
- the lung is developing ex utero > it shouldn’t be opening and closing yet or getting blood flow through it

41
Q

Why is the pulmonary vasculature at such great risk?

A

in utero receives < 7% of CO; after birth receives 100%

- vessels are not developed enough to handle that volume or to be perfused at that time

42
Q

How does inflammation contribute to BPD?

A

an exaggerated inflammatory response (alveolar influx of numerous proinflammatory cytokines as well as macrophages and leukocytes) occurs in the first few days of life; neutrophils “eat” the bacteria and then continue onto the alveoli themselves

43
Q

How do infections contribute to BPD?

A

there are some bacteria that are seen in increased incidnce in tinier babes; Ureaplasma; unfortunately, tx of these organisms has not decreased incidence of BPD and secondary infx exacerbate it (E coli, Klebsiella, Pseudomonas)

44
Q

What percentage of very PT infants has ureaplasma?

A

~ 50%

45
Q

How does fluid overload and pulmonary edema contribute to BPD?

A

essentially an effect from leak; “a dry lung is a happy lung”

46
Q

How does a PDA contribute to BPD?

A

big problem as blood shunts L > R as pulmonary vascular resistance decreases and ends up flooding their lungs
- one reason they tried PDA prophylaxis

47
Q

How does increased airway resistance contribute to BPD?

A

caused from injury by ETT ruining cilia and the body responds by increasing layers of cells

48
Q

How does nutrition contribute to BPD?

A

necessary to keep the baby growing and facilitate healing; fatty acid isotiol has been a/w healing

49
Q

Why is vitamin A a promising practice in decreasing the course of BPD?

A

one of the few tx that has decreased rate of BPD by 6%

50
Q

What medication should vitamin A not be given with?

A

steroids; can cause vitamin A toxicity

51
Q

What are known risk factors for the development of BPD?

A

1) PREMATURITY
2) race (white)
3) sex (male)
4) chorioamnionitis
5) tracheal colonization with ureaplasma
6) ELBW
7) RDS
8) vitamin A deficiency
9) excessive IVF administration
10) sepsis
11) PDA
12) oxygen therapy
13) family h/o atopic disease

52
Q

How is prematurity a risk factor for BPD?

A
  • not necessarily wholey d/t lung immaturity
  • increased risk of ventilatory support (sometimes prolonged)
  • infx, sepsis, maternal chorio
  • younger GA: increased risk of BPD (uncommon after 32 weeks)
53
Q

How does mechanical ventilation induce lung injury?

A
  • high airway pressure (barotrauma)
  • high tV (volutrauma)
  • lack of adequate recruitment (atelectotrauma)
  • ventilation induced lung injury increases cytokine production
  • HFOV has not proven to prevent of decrease severity of BPD
54
Q

What is atelectotrauma?

A

if you are too gentle, then alveoli collapse and you have to open it back up again, much more likely to cause trauma if you let it collapse > need high pressure to reopen

55
Q

Why is early rescue surfactant therapy best?

A
  • avoid prophyactic intubation
  • make them declare HMD and CPAP failure, CXR c/w RDS, increased WOB and FiO2 > 40%
  • trend toward in/out surf with early CPAP maintenance
56
Q

What is the effect of CO2 < 35, even one time?

A

a/w BPD

57
Q

What is considered a high risk infant for BPD?

A

< 1000g with CO2 > 70 (set up increases risk for IVH), but if you intubate, you increase risk for BPD, but you don’t want to wait for total collapse and atelectotrauma

58
Q

What are the known effects of oxidative stress?

A
  • alveolar edema
  • neutrophil infiltration
  • alveolar cell proliferation
  • fibrosis
59
Q

How do the pathologic changes a/w new BPD differ from classic BPD?

A

classic: (pre surf) normal appearing airways, less fibrosis and more uniform inflation
new: deficient septation, leading to fewer and larger alveoli with possible reduced pulmonary capillarization that may lead to PPHN

60
Q

What were the clinical take aways from the BOOST trial concerning SpO2 range?

A

no evidence that higher ranges improved growth or development but it did increase days of oxygen threapy and use of health care resources

61
Q

What is the effect of maternal chorio on fetal lungs?

A

inflammatory cascade simulates surf production (less HMD) but then results in neutrophil infiltration and later parenchyma inflammation (more CLD)

62
Q

Besides infection, what other factors can trigger inflammation in the lung?

A

1) oxygen
2) high pressures
3) increased pulmonic blood flow

63
Q

What is the correlation between increased inflammatory stimuli and BPD?

A

increased inflammatory stimulus in the first 5 days of life correlate with developing BPD (IL-6, IL-1Bb, IL-8, TNF-a)

64
Q

What is the typical antenatal infectious agent that increases the risk of BPD?

A

ureaplasma urealyticum

65
Q

What are the typical postnatal infectious agents that increase the risk of BPD?

A

1) coag neg staph
2) CMV
3) RSV
most common are gram neg (pseudomonas and klebsiella)

66
Q

What factors favor pulmonary edema following PTB?

A

1) excess fetal lung fluid per unit lung mass
2) fewer Na channels and less Na, K, ATPase activity in epithelium
3) increased lung vascular filtration pressure
4) increased lung epithelial protein leak with postnatal ventilation
5) increased lung vascular protein permeability
- if infant doesn’t lose wt within first week of life, more likely to have BPD

67
Q

What is the correlation between BPD and increased airway resistance?

A

infants that later develop BPD have been shown to have increased pulmonary resistance in the first week of life- possibly from obstruction

68
Q

What are possible causes of obstruction that can cause a subsequent increase in airway resistance?

A
  • epithelial hyperplasia
  • edema
  • inflammation
69
Q

What genetic predispositions can translate into increased airway resistance?

A
  • family h/o reactive airway dz
  • glutathione S- transferase P1 gene
  • if you have a twin with BPD, you are more likely to have BPD
70
Q

What are the effects of under nutrition on the neonatal lung?

A

general under nutrition, particularly an insufficiency in dietary protein may increase the vulnerability of the PTB to oxidant lung injury and the development of BPD

71
Q

How is vitamin A vital to lung functioning and health?

A
  • similarities b/w epithelial ∆ seen with vit a deficiency and BPD
  • lower levels of vit a in the first week show increased risk of BPD
  • administration of vit a in the first week of life shown to be protective against BPD
72
Q

How is magnesium vital to lung functioning and health?

A

magnesium deficiencies increase the susceptibility of cells to perioxidation and worsens inflammatory reactions
(weak evidence)

73
Q

How is selenium vital to lung functioning and health?

A

is essential compoent for the antioxidant glutathione peroxidase; investigations into this trace metal have not borne out just yet

74
Q

How is inositol vital to lung functioning and health?

A

inositol serves as a precursor to surfactant and has been reported to be deficient in PTB. one study improved survival without BPD with supps (not confirmed)

75
Q

What is the effect of low cortisol levels in LBW infant in the first week of life?

A

increased incidence of PDA
increased lung inflammation
increased risk of BPD

76
Q

Why might an infant be given low dose hydrocort?

A

to treat adrenal insufficiency; larger trial showed benefit only to infants exposed to chorio

77
Q

What are some of the side effects of steroid therapy?

A
  • spontaneous bowel perforations

- some evidence suggests that steroids is damaging to the developing lung and can stop its branching

78
Q

What is the theoretical link between early PRBC tx and BPD?

A
  • free Fe increases oxidative stress
  • malondialdehyde, a biochemical marker of lipid perioxidation, measured in BAL specimens from ventilated patient was found to be elevated s/p tx
79
Q

What should be considered when addressing the management of BPD?

A

you look at 3 stages:

1) antenatal drugs and management aiming to prevent BPD
2) postnatal drugs and management strategies aimed at preventing BPD
3) strategies aimed at improving clinical outcomes of infants with established BPD

80
Q

What are the benefits of prenatally administered glucocorticoids?

A

1) promote maturation of surf
2) increase antioxidant capacity
3) increased activity of lung endothelial nitric oxide synthase
(net result is a decrease in RDS; no clear evidence that this decreases BPD)
- also protective against IVH

81
Q

What are the risks a/w prenatally administered steroids?

A

1) increased expression of VEGF (dex) leading to decreased alveolarization
2) multiple courses of prenatal steroids are a/w risk for BPD
3) a decrease in lung to body weight ratio
4) prenatal steroids given in presence of inflammation have short term anti-inflammatory effects with later rebound of inflammation to higher levels

82
Q

What is the tradeoff with lung function with prenatal steroids?

A

the benefit of lung maturation may lead to increased survival but be somewhat off set by an increased susceptibility to lung injury and rebound inflammation

83
Q

What is the role of thyroid hormones in fetal lung growth?

A

involved in fetal lung growth and maturation and act with glucorticoids for surfactant synthesis; the basis for prenatal thyrotropin- releasing hormone

84
Q

What are the results of clinical trials with prenatal thyrotropin- releasing hormone?

A
  • early, small trials were promising
  • larger trials showed TRH and steroids no more effective in preventing RDS than steroids alone. Furthermore, those in the Australian study had an increased risk of developmental delay after TRH
85
Q

How should volume targeted ventilation therapy work?

A
  • set tV 5-7cc/kg
  • pressure varies with compliance of lung
  • set pressure limit to avoid accidental overdistension of single lobe
  • will not work if leak is large
  • select mode based on infant’s ventilatory drive and rate
    (not significant in helping reduce the risk of BPD)
86
Q

Why is volume targeted ventilation a promising practice?

A
  • injury that sets up BPD is volutrauma, not barotrauma
  • inadvertent hyperventilation is common
  • hypocarbia is bad for the brain and lungs
  • adult type volume controlled ventilation doesnt work well in babes
87
Q

How does VG compare to PC?

A
  • same or lower PIP
  • more stable tV
  • less hypocapnia
  • less overexpansion
  • faster recovery from forced exhalation episodes
  • works better with AC than SIMV
  • faster recovery from suctioning
  • pro inflammatory cytokines decreased at 5mL/kg
  • faster weaning from mechanical vent
  • higher tV needed with advanced post natal age
88
Q

What is the premise of VG ventilation?

A

the ventilator servo controls PIP within preset limits to achieve the target tV. In this fashion, the ventilator automatically compensates for changes in lung mechanics and fluctuations in spontaneous respiratory effort to maintain the set tV

89
Q

What is the rationale for postnatal steroid early physiologic replacement?

A

low levels of endogenous glucocorticoids in infants that progress to BPD

90
Q

What is the rationale for postnatal steroid for inflammation?

A

inflammation begins early in RDS and early glucocorticoids alter this so that progression to BPD is reduced

91
Q

What is the evidence for the use of inhaled steroids?

A

suggests a trend for improved mortality, decreased vent courses and lower BPD; but none were significantly significant

92
Q

What is the theoretical indication for iNO?

A

selective pulmonary vasodilator that reduces VQ mismatch thus reducing ventilator and oxygen requirements
- animal models suggest a reduction in pulmonary inflammatory markers and decreased artery remodeling

93
Q

What are the effects of inositol tx?

A
  • showed a trend in favoring reduction of BPD at 28d
  • decreased mortality
  • decreased grade III/IV IVH
  • decreased stage IV ROP
94
Q

How should ventilation strategy change when treating BPD v RDS?

A

1) need very long itime (to distribute gas to areas of atelectatic alveoli and even longer for the gas to get out- think air trapping) in airways with increased resistance
2) instead of a RR of 60 ∆ to RR of 20 with very large peeps; BIG tV (10-15cc/kg)
3) need exhalation to be very long to empty remote, obstructed alveoli

95
Q

What are the effects of sildeneafil on BPD?

A

cGMP- specific phosphodiesterase inhibitor

  • improves alveolar growth
  • improves lung angeogensis
  • reduces PPHN
96
Q

What is the indication for pentoxifylline?

A

methytxanthine with anti inflammatory and anti-cytokine effects

97
Q

What is the indication for citrulline?

A

preserves tissue architecture following PTB and respiratory support

Neonatal Pathophysiology (17 decks)

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