Discussion.
In this study population, the incidence of BPD was 25.7%. Our incidence
of BPD is higher than rates reported in developed countries but similar
to cities with higher altitudes in Colombia such as Bogota(12,13). A
previous case-control study found variations in the prevalence of BPD
according to altitude in Colombia. In cities located a higher altitude
(more than 2600 meters above sea level), the prevalence of BPD were
higher than other cities with lower altitude as Bucaramanga and Cali
(10). Highest altitude city (Bogotá) was associated with a higher risk
of dysplasia (OR 1.82 95% CI 1.31-2.53) (12). Infants who are born in
cities with higher altitudes (> 2000 meters above sea
level) have twice the risk of developing BPD than infants born in cities
with lower altitudes, independently of differences in maternal, infant,
and therapeutic risk factors(12,14). Altitude play an important role in
the pathogenesis of BPD. The decreased partial pressure of oxygen in the
environment, in cities with higher altitudes, has also been associated
with higher pulmonary artery pressures, delayed in the functional
closure of the ductus arteriosus in the newborn, tortuous transition
from oxygenation via placenta to oxygenation across the lungs resulting
in postnatal persistence of fetal circulation(15). As a result of these
events, it is possible that premature infants born at high altitudes
have an early dependency on high concentrations of oxygen and
ventilatory support compared to patients born at lower altitudes. In our
study, sepsis was a risk factor associated with BPD severity. Multiple
studies indicate that postnatal sepsis independently increases the
incidence of BPD
Preterm infants are more susceptible to infections since their immune
defenses are not fully developed, have vulnerable skin barrier, and
require multiple invasive procedures. Late-onset sepsis induces a
pro-inflammatory and pro-fibrotic response in the preterm lung
predisposing it to BPD . Neonatal mice injected with intraperitoneal LPS
demonstrated reduced lung inflammation and apoptosis after 24 h as
compared to adults, and this was associated with activation of the
transcription factor, nuclear factor kappa B. Inhibition of NF-κB
resulted in increased cell death and alveolar simplification and
disruption of angiogenesis via vascular growth factor (VEGF)-R2 (9-11)
We found that pulmonary arterial hypertension (PH) was an independent
predictor of BPD severity. PH is a common complication of neonatal
respiratory diseases including BPD. Up to 18% of all extremely low
birth weight infants will develop some degree of PH, and the incidence
rises to 25–40% of infants with established BPD (12). PH worsens the
clinical course, morbidity, and mortality of BPD(12). PH also is a
common disease in individuals living at high altitudes, yet this is a
understudied disorder especially in patients with BPD (13). A better
understanding of the pathogenesis is necessary to optimize current drugs
and newer therapeutic targets.
A number of important limitations need to be considered. As occurs in
longitudinal studies, information bias cannot be excluded. However we
include all patients registered in the hospital and the reported
incidence cannot be attributed to the bias of selection; nor can it be
attributed to overdiagnosis of oxygen dependence, since the
neonatologist in all patient verified with physiological tests (dynamic
oximetry standardized) that children truly require supplemental oxygen.
Second, hospitalizations due to other medical conditions sometimes can
prolong the hospital stay and the withdrawal of oxygen (inefficiencies
within the healthcare system, placement difficulties, operational
delays, and payer-related issues). However, the plausibility of the
identified clinical factors suggests that the above-mentioned
non-medical factors account for a minimal part of the causality in the
studied population. Third , in our study used the echocardiography for
PH diagnosis. However in infants with BPD can be especially challenging
due to the presence of lung hyperinflation and heart rotation, both of
which impact the sensitivity of imaging and identification of the
tricuspid regurgitant jet. The echocardiography correctly diagnosed the
presence or absence of PH 79% of the time, but correctly determined the
severity PH only 47% of the time. These results imply that in the
absence of a quantifiable TR jet, the currently available indirect
measurements are insufficient for the assessment of the degree of PH in
infants with BPD(13).
In conclusion, the incidence of BPD was higher than the average rates
reported in populations with similar gestational ages in developed
countries but similar to cities with higher altitudes. In our
population, the variables associated with BPD severity levels were:
duration of oxygen therapy and pulmonary hypertension. It is necessary
to increase the awareness of risk factors, the effect of clinical
practices, and early recognition of bronchopulmonary dysplasia to reduce
morbidity in patients with this pathology.
Acknowledgements: None