Bronchopulmonary dysplasia
Bronchopulmonary dysplasia (BPD)
is a form of chronic lung disease that affects infants who have been born
preterm. Over the last decade advances in neonatal care, including the
increasing use of antenatal steroids, and early surfactant therapy, have
modified a change in the underlying pathology in many cases. ‘Old’ BPD was
described as a disease of scarring, and repair. This condition was associated
with long periods of mechanical ventilation, often with high PIP, and high FiO2.
‘New’ BPD is a condition of impaired alveolar development, with less
destruction and scarring. Mechanical, oxidative and inflammatory factors all contrib-ute
to lung injury. The radiographic appearances of more recent cases are less
dramatic (see Fig. 6.6), however, the impairment in lung function continues
through childhood, and is associated with a number of other impairments.
The definition of BPD has evolved
with time. The most commonly used definition is ‘Oxygen requirement at 36/40
corrected gestational age (CGA)’. This definition does not have any grading of
severity, and encom-passes a wide spectrum of disease.
•
Mild: need for supplemental O2 at age 28 days, but not at 36/40 CGA
•
Moderate: need for supplemental O2 <30% at age 28 days and at 36/40 CGA
•
Severe: mechanical ventilation or
requiring >30% O2 at 36/40 CGA
‘Walsh’ test (2003)
•
Test
at 36±1/40 CGA. Aim to maintain SpO2 > 88%
•
BPD if
need 30% O2 to maintain SpO2
>88% (or ventilated)
•
If
<30% O2, then FiO2 is gradually decreased
to air. BPD is defined as inability to maintain SpO2 >88% for 1hr
Incidence is dependent on
definition used. Wide variations between cen-tres with a range of 4–58% (mean
23%) of at-risk babies. BPD more likely with:
· Gestational immaturity.
• Low birth weight.
• Males.
• Caucasian heritage.
• IUGR.
• Family history of asthma.
•
History
of chorioamnionitis.
•
Surfactant
and ANC steroids (effect may be off-set by increased survival?)
•
Closure
of PDA
•
Diuretics
•
Inhaled
steroids
•
Inhaled
nitric oxide
•
HFOV
compared to conventional ventilation
•
Treating
Ureaplasma urealyticum (more research
needed)
•
Systemic
corticosteroids (clinical trials needed as increased risk of CP)
•
nCPAP
vs. intubation(need for surfactant, risk of pneumothorax)
•
Caffeine
citrate for apnoea of prematurity in infants <1250g
•
Vitamin
A supplementation for infants <1000g
No specific treatment has been
demonstrated to show an improve-ment in outcome of BPD. Oxygen is the most
commonly used therapeutic agent, although the ‘correct’ dose and what SpO2
is acceptable has not been established. A number of large trials are ongoing
and their results are awaited (Ref: NeOPrOM Collaboration).
Other treatments include;
diuretics, corticosteroids, sildenafil, optimiz-ing nutrition.
Immunization for at-risk infants
with monoclonal respiratory syncytial virus (RSV) antibody has recently been
recommended by the UK depart-ment of health. This involves monthly injections
during the RSV season.
Increased survival of preterm
infants has led to an increase in the number surviving with BPD. Mortality has
improved (previously 10–20% would die from cor-pulmonale or respiratory
infection). Other problems include:
•
Increased
risk of CP.
•
Poorer
cognitive functioning and academic performance.
•
High
risk of re-hospitalization with respiratory illness.
•
Poorer
lung function.
Respiratory problems seem to
lessen as children get older, perhaps reflecting the lung’s continued growth
and development.
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