Prematurity

Question 1

Main abnormality in “new” BPD

Answer 1

more uniform and milder regions of injury but impaired alveolar and vascular growth = prominent (persistent abnormality of lung architecture)

Question 2

Features of “old” BPD (6)

Answer 2

1) alternating atelectasis with hyperinflation
2) severe airway epithelial lesions
3) marked airway smooth muscle hyperplasia
4) extensive diffuse fibroproliferation
5) hypertensive remodeling of pulmonary arteries
6) decreased alveolarization and overall surface area

Question 3

Features of “new” BPD (6)

Answer 3

1) less regional heterogeneity
2) rare airway epithelial lesions
3) mild airway smooth muscle thickening
4) rare fibroproliferative changes
5) fewer arteries but “dysmorphic”
6) fewer, larger, and simplified alveoli

Question 4

Mild BPD criteria

Answer 4

<32 wks = RA at 36 weeks or discharge (whichever first)

>32 wks = RA by 56 days of discharge

Question 5

Moderate BPD criteria

Answer 5

<32 wks = need for <30% O2 at 36 weeks or at discharge

>32 wks = need for <30% O2 to 56 days or at discharge

Question 6

Severe BPD criteria

Answer 6

<32 wks = need >30% O2 +/- PPV/CPAP at 36 weeks or at discharge
>32 wks = need for >30% O2 +/- PPV/CPAP at 56 days or at discharge

Question 7

Stages of Lung Development

Answer 7

“Every Pulmonologist Can See Alveoli”

1) Embryonic 4-7 wks
2) Pseudoglandular 5-17 wks
3) Canalicular 16-26 wks
4) Saccular 24 wks- term
5) Alveolarization 36 wks to 21 years

Question 8

Endogenous risk factors for BPD

Answer 8

gestational immaturity
lower birth weight
male sex
white/non-black race
family history of asthma
SGA

Question 9

Prenatal risk factors for BPD

Answer 9

maternal smoking
pre-eclampsia
placental abnormalities
chorioamnionitis
IUGR
no maternal steroids
perinatal asphyxia

Question 10

Post natal risk factors for BPD

Answer 10

lower Apgars
RDS
PDA
higher weight -adjusted fluid intake
earlier use of IV lipid
light exposed TPN
duration of O2 therapy

Question 11

Risk factors for BPD in at-risk infants

Answer 11

Duration and approach of mechanical ventilation (increased O2, PIP, rate, decreased PEEP)
hypocarbia
colonization with ureaplasma urealyticum
post-natal CMV
post-natal sepsis

Question 12

How can increased O2 lead to BPD?

Answer 12

Increased production of reactive O2 species -> overwhelm host antioxidant defenses in immature lung
Prems have lungs deficient in antioxidant enzymes systems

Question 13

Method of ventilator-induced lung injury and BPD

Answer 13

“volutrauma” = plastic stretch/over-distension of lung can induce inflammation, permeability edema and structural changes
also: aggressive ventilation with hypocarbia, avoid high tidal volumes

Question 14

Mechanism of inflammation in BPD

Answer 14

1) O2 toxicity, volutrauma, infection
2) IL-1B = release inflammatory mediators
3) ICAM-1 = cell-cell contact
4) Il-8 = neutrophil chemotaxis, inhibits surfactant
5) Inactivation of alpha-1 antiprotease
6) TNF and IL-6 = fibroblast and collagen production
7) chorioamnionitis = endotoxin exposure in utero

Question 15

2 Chest x ray features in neonatal RDS

Answer 15

Low volume lung

Bilateral diffuse air space opacification

Question 16

3 criteria for periodic breathing

Answer 16

** Think of 3’s!
3 episodes of apnea
>3 seconds each
separated by continued breathing for ≤ 20 seconds

Question 17

Mechanism of periodic breathing

Answer 17

CO2 censor working well (central)
O2 censor not working as efficiently (peripheral)
Central censor is driving breathing, peripheral censor lags in giving feedback
If kid is not hypoventilating, then there shouldn’t be any danger in sending home with oxygen. In that scenario with no hypoventilation, we wouldn’t expect oxygen to significantly depress respiratory drive.

Question 18

Hypoxia as per ATS home oxygen statement

Answer 18

<90% for more than 5% of oximetry (<1 year of age)

<93% for more than 5% of oximetry (>1 year of age)

Question 19

Structural changes in BPD that contribute to increased pulmonary vascular resistance

Answer 19

Histologically:
o Smooth muscle cell proliferation
o Early maturation of pericytes into smooth muscle cells o Fibroblast incorporation into vessel wall and adventitia

Structural
o Narrowed vascular diameter
o Decreased vascular compliance
o Decreased angiogenesis and reduced vascular surface area
o Abnormal vasoreactivity

Question 20

Other CV abnormalities that can be seen with BPD

Answer 20

LVH
Systemic HTN
Collateral development

Question 21

PFT findings in BPD grads

Answer 21

Usually low normal range by 2 or 3 years and improve over time
o Flow abnormalities remain
▪ Reduced absolute and size corrected flow rates
o Abnormalities often persist through adolescence (increased resistance and
reactivity)

Question 22

Prevention strategies for BPD

Answer 22

Antenatal steroids (reduce death but not BPD incidence)
Surfactant
Avoid volutrauma
Ventilation - avoid hypocarbia, volutrauma, oxygen toxicity
Avoidance of I&V with nCPAP
Avoidance of fluid overload
Aggressive treatment of symptomatic PDA
Nutritional support
Caffeine (may reduce BPD risk)
iNO (lower PVR, improves oxygenation, may be lung protective but controversial)

Question 23

BPD treatment

Answer 23

Supplemental O2 (keep sats >92-94)
nCPAP
Trach (for chronic vent requirement)
Diuretics (improves compliance and AW resistance by reducing edema)
Bronchodilators (?may help)
Steroids (only role in pre-exubation)
RSV prophylaxis (for those on O2)
PH (treat underlying lung disease first)