Prematurity Flashcards
Main abnormality in “new” BPD
more uniform and milder regions of injury but impaired alveolar and vascular growth = prominent (persistent abnormality of lung architecture)
Features of “old” BPD (6)
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
Features of “new” BPD (6)
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
Mild BPD criteria
<32 wks = RA at 36 weeks or discharge (whichever first)
>32 wks = RA by 56 days of discharge
Moderate BPD criteria
<32 wks = need for <30% O2 at 36 weeks or at discharge
>32 wks = need for <30% O2 to 56 days or at discharge
Severe BPD criteria
<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
Stages of Lung Development
“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
Endogenous risk factors for BPD
gestational immaturity lower birth weight male sex white/non-black race family history of asthma SGA
Prenatal risk factors for BPD
maternal smoking pre-eclampsia placental abnormalities chorioamnionitis IUGR no maternal steroids perinatal asphyxia
Post natal risk factors for BPD
lower Apgars RDS PDA higher weight -adjusted fluid intake earlier use of IV lipid light exposed TPN duration of O2 therapy
Risk factors for BPD in at-risk infants
Duration and approach of mechanical ventilation (increased O2, PIP, rate, decreased PEEP) hypocarbia colonization with ureaplasma urealyticum post-natal CMV post-natal sepsis
How can increased O2 lead to BPD?
Increased production of reactive O2 species -> overwhelm host antioxidant defenses in immature lung
Prems have lungs deficient in antioxidant enzymes systems
Method of ventilator-induced lung injury and BPD
“volutrauma” = plastic stretch/over-distension of lung can induce inflammation, permeability edema and structural changes
also: aggressive ventilation with hypocarbia, avoid high tidal volumes
Mechanism of inflammation in BPD
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
2 Chest x ray features in neonatal RDS
Low volume lung
Bilateral diffuse air space opacification
3 criteria for periodic breathing
** Think of 3’s!
3 episodes of apnea
>3 seconds each
separated by continued breathing for ≤ 20 seconds
Mechanism of periodic breathing
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.
Hypoxia as per ATS home oxygen statement
<90% for more than 5% of oximetry (<1 year of age)
<93% for more than 5% of oximetry (>1 year of age)
Structural changes in BPD that contribute to increased pulmonary vascular resistance
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
Other CV abnormalities that can be seen with BPD
LVH
Systemic HTN
Collateral development
PFT findings in BPD grads
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)
Prevention strategies for BPD
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)
BPD treatment
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)
