Flashcards in Chronic Lung Disease Deck (97)
What is the NIH consensus of time point for assessment for BPD in infants born < 32 wk GA at birth?
36 wk PMA or at dc to home, which ever comes first
What is the NIH consensus of time point for assessment for BPD in infants born > 32 wk GA at birth?
> 28 dol, but < 56 postnatal age or at dc to home, which ever comes first
What is the NIH consensus of mild classification of BPD in infants born < 32 wk GA at birth?
- 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)
How is BPD classified?
at a later postnatal age according to type of respiratory support required to maintain a normal arterial oxygen saturation (89%)
What is the NIH consensus of mild classification of BPD in infants born > 32 wk GA at birth?
breathing RA by 56 days postnatal age, or dc home which ever comes first
What is the NIH consensus of moderate classification of BPD in infants born < 32 wk GA at birth?
need for < 30% oxygen at 36 weeks PMA or dc, which ever comes first
What is the NIH consensus of moderate classification of BPD in infants born > 32 wk GA at birth?
need for < 30% oxygen 56 days PNA or dc to home, which ever comes first
What is the NIH consensus of severe classification of BPD in infants born < 32 wk GA at birth?
need for > 30% oxygen and/or positive pressure at 56 days PMA or dc, which ever comes first
What is the NIH consensus of severe classification of BPD in infants born > 32 wk GA at birth?
need for oxygen and/or positive pressure at 56 days PMA or dc, which ever comes first
What are typical etiologies for severe BPD in infants born >32 wk GA?
MAS, CDH, GBS
Why is 36 weeks PMA significant?
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
What is the classic definition of BPD?
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
What is the incidence of CLD in infants born at < 1500g?
35%; there are more babies in the US with BPD than CF
In what population are long-term complications of BPD the most common?
< 1000g at birth
What is the trend of BPD incidence?
the overall rates of CLD are not declining; however, mortality and rates of severe BPD are down with significant preventative measures
What is included in the cost of BPD?
prolonged ICU stays, frequent hospital readmissions, home health care charges and parent time off
Why is BPD not considered only a childhood problem?
1) persistent small airway damage
2) persistent airway obstruction
3) pulmonary dysfunction (increased risk for asthma)
4) neurdevelopmental outcomes
What is the etiology for infants who have BPD without a previous h/o hyaline membrane dz?
- smoke inhalation
- alpha 1 antitripsin deficiency
What was the result of introducing mechanical ventilation for PT infants in the 1960s?
changed the natural course of RDS disease progression resulting in increased survival of smaller and sicker infants
What is characteristic of BPD presentation of CXR?
1) streaky interstitial markings
2) patchy atelectasis intermingled with cystic areas
3) severe overall lung hyperinflation
What is the rationale for permissive hypercapnea?
to provide a more gentle ventilation, we avoid O2 toxicity and tolerate higher CO2s
What is the rationale for NEW BPD?
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
What is the incidence of BPD in an infant that has never been intubated?
1/30th; intubation is one of the biggest problems causing BPD
What are recent practices changes geared toward reducing the incidence of BPD?
1) trying to keep from intubating
2) non invasive ventilation
3) eliminate prematurity
4) antenatal steroids
5) exogenous surfactant therapy
Why has surfactant not been shown to decrease the incidence of BPD?
r/t increased number of ELBW survivors
How does the ETT contribute to the development of BPD?
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
Why is the incidence of new BPD increasing?
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
What is the "second week dwindle"?
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 >>> there is a progressive decline in respiratory fx
What are the clinical features of new BPD?
- 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)