Paediatrics: Bronchopulmonary dysplasia

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 F_iO₂. ‘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.

Definition

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.

NICHD/NHLBI Definitions (2001)

•   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 S_pO₂ > 88%

•   BPD if need   30% O₂ to maintain SpO₂ >88% (or ventilated)

•   If <30% O₂, then F_iO₂ is gradually decreased to air. BPD is defined as inability to maintain SpO₂ >88% for 1hr

Incidence and risk-factors

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.

Prevention of BPD

No evidence of effect

•   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)

May be of benefit in certain infants

•   Systemic corticosteroids (clinical trials needed as increased risk of CP)

•   nCPAP vs. intubation(need for surfactant, risk of pneumothorax)

Evidence of effect

•   Caffeine citrate for apnoea of prematurity in infants <1250g

•   Vitamin A supplementation for infants <1000g

Treatment of established BPD

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.

Outcome

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.