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Babies born very early have lungs that have not finished developing. If they need help with breathing in their first weeks, the delicate process of building air sacs and blood vessels can be interrupted, and the lungs end up with fewer, larger air sacs than they should have. That is bronchopulmonary dysplasia, or chronic lung disease of prematurity. It is a growth problem, not a mucus problem — which is why chest physiotherapy and percussion are not part of routine treatment. Most babies improve steadily as they grow, come off oxygen within the first year or two, and go on to run around like other children. They may catch chest infections more easily and tire a little sooner, and as adults they benefit greatly from staying active and never smoking.
Definition
Bronchopulmonary dysplasia (BPD), increasingly called chronic lung disease of prematurity, is lung injury that develops in babies born very preterm whose lungs were still forming when they were born. It is defined not by an appearance on imaging but by how much respiratory support the baby still needs at 36 weeks postmenstrual age — that is, at around the time they would otherwise have been born.
| Grade | Support required at 36 weeks postmenstrual age |
|---|---|
| Grade 1 (mild) | Nasal cannula at ≤2 L/min |
| Grade 2 (moderate) | Nasal cannula >2 L/min, or non-invasive positive pressure (CPAP, NIPPV) |
| Grade 3 (severe) | Invasive mechanical ventilation |
The 2019 definition above replaced earlier versions that relied on supplemental oxygen alone, because modern neonatal care uses high-flow and non-invasive support that an oxygen-only definition failed to capture.1 The grading matters clinically: it tracks with later respiratory readmission, neurodevelopmental outcome and death better than the older definitions did.
Pathophysiology
Old BPD and new BPD
The disease Northway described in 1967 was a fibrotic, heterogeneous, heavily scarred lung produced by high-pressure ventilation and high oxygen concentrations in relatively mature preterm infants.2 That disease is now rare. Antenatal corticosteroids, surfactant, gentler ventilation and the survival of much smaller babies have produced a different condition, usually called “new” BPD.
Arrested development, not destruction
New BPD is a disease of arrested development rather than destruction. A baby born at 24–28 weeks is in the canalicular or early saccular stage of lung development; alveolarisation and pulmonary microvascular growth have barely begun. Injury at this point — from mechanical stretch, oxygen, inflammation or infection — does not primarily scar the lung, it stops it growing. The result is fewer, larger, simplified alveoli with a reduced total gas-exchange surface, and a dysmorphic pulmonary capillary bed that is both smaller and abnormally distributed. Airway smooth muscle may be increased, producing variable airflow obstruction, and some infants develop tracheobronchomalacia from prolonged positive pressure.
The two consequences that matter
Two consequences follow that shape everything downstream: gas exchange is limited by surface area, not by secretions; and the abnormal vasculature predisposes to pulmonary hypertension.
Co-morbidities
- Pulmonary hypertension — present in 15–25% of infants with moderate-to-severe BPD and a major driver of mortality. Screening echocardiography is recommended in severe disease.
- Gastro-oesophageal reflux and aspiration — common, and a cause of apparently unexplained respiratory deterioration.
- Feeding difficulty and poor growth — increased work of breathing raises energy expenditure at exactly the time when oral feeding is hardest to establish.
- Neurodevelopmental impairment — BPD is independently associated with cerebral palsy, cognitive delay and later attention difficulty, over and above the effect of prematurity itself.
- Retinopathy of prematurity, intraventricular haemorrhage, necrotising enterocolitis — the shared consequences of extreme prematurity.
- Recurrent viral respiratory infection — particularly RSV, the leading cause of readmission in the first two years.
Prevalence
BPD affects roughly a quarter to a half of infants born below 29 weeks' gestation, with incidence rising steeply as gestational age falls: uncommon above 30 weeks, and affecting the majority of survivors born at 23–24 weeks. In absolute terms the number of affected children has not fallen over three decades, because improved survival of the smallest infants offsets improvements in care. In Australia and New Zealand, several thousand infants are affected each year, and BPD is the most common chronic complication of extreme prematurity.
Causes and risk factors
| Factor | Mechanism |
|---|---|
| Extreme prematurity and low birthweight | The dominant risk factor — the more immature the lung, the more vulnerable the alveolarisation process |
| Fetal growth restriction | Impaired antenatal lung and vascular growth before any postnatal insult |
| Mechanical ventilation | Volutrauma from over-distension, not simply pressure; even brief large tidal volumes injure the immature lung |
| Supplemental oxygen | Free radical injury in a lung with immature antioxidant defences |
| Chorioamnionitis and postnatal sepsis | Inflammatory cytokines disrupt alveolar and vascular development |
| Patent ductus arteriosus | Pulmonary overcirculation and oedema; the benefit of closing it remains contested |
| Absent antenatal corticosteroids | Less mature surfactant system and greater need for ventilation |
| Male sex, family history of asthma or atopy | Consistent but incompletely explained associations |
Symptoms
In the neonatal unit
In the neonatal unit: persistent oxygen requirement, tachypnoea, subcostal and intercostal recession, poor weight gain, desaturation with handling and feeding, and apnoeic or desaturation episodes.
After discharge
After discharge, parents typically describe fast breathing, a chest that pulls in when the baby is unsettled, tiring or desaturating during feeds, noisy breathing or wheeze, and frequent chest infections that are more severe and last longer than in other babies. Some infants go home on oxygen, and a smaller number on non-invasive support or via a tracheostomy.
In older children
In older children a history of BPD often presents as exercise limitation, exercise-induced wheeze, or a diagnosis of “asthma” that responds only partially to inhaled therapy.
Diagnosis
Importance of a diagnosis
The grade of BPD determines discharge planning, home oxygen, RSV immunoprophylaxis eligibility, respiratory follow-up and the threshold for escalation during future infections. It also gives families an accurate framework: this is a growth problem that improves as the lung grows, not a permanent scarring disease.
How is it diagnosed?
By assessment at 36 weeks postmenstrual age of the mode and amount of respiratory support required, applied prospectively using the graded definition above. There is no confirmatory test.
Imaging
Chest radiographs show hyperinflation, coarse interstitial markings and areas of cystic change or atelectasis, but appearances correlate poorly with severity and imaging is not required for diagnosis. CT is reserved for infants with unexpectedly severe or atypical disease, or where structural airway abnormality or tracheobronchomalacia is suspected.
Other tests
Echocardiography to screen for pulmonary hypertension in moderate-to-severe disease. Overnight or continuous oximetry to set and wean home oxygen. Bronchoscopy where malacia or acquired subglottic stenosis is suspected. Infant and, later, childhood lung function in specialist follow-up, typically showing reduced forced expiratory flows.
Management
Prevention — where the real gains are
- Antenatal corticosteroids for anticipated preterm birth — among the most effective interventions in perinatal medicine.
- Early CPAP rather than routine intubation. Large trials found that starting on CPAP, with selective surfactant, reduces death or BPD compared with routine intubation and prophylactic surfactant.3
- Less-invasive surfactant administration via a thin catheter in a spontaneously breathing infant, avoiding intubation altogether.
- Caffeine citrate, started early, reduces BPD and improves neurodevelopmental outcome at 18–21 months — benefits still detectable at 5 and 11 years.4
- Volume-targeted ventilation and avoidance of hypocapnia where ventilation is unavoidable.
- Careful oxygen targeting, avoiding both hyperoxia and prolonged hypoxaemia.
- Vitamin A supplementation gives a small reduction in BPD, though supply issues limit its use in some settings.
Established disease
- Nutrition — high-energy feeds and close growth monitoring. Lung growth requires somatic growth; nutrition is arguably the single most important therapy after the acute phase.
- Oxygen to maintain saturations in the target range set by the neonatal team, continued at home where necessary and weaned against oximetry.
- Postnatal corticosteroids — genuinely difficult territory. Systemic dexamethasone facilitates extubation and reduces BPD but has been associated with cerebral palsy at higher, earlier doses; low-dose late regimens and hydrocortisone are used selectively where the risk of ongoing ventilation is judged to outweigh the neurological risk.5
- Diuretics and inhaled bronchodilators — widely used, weakly supported. Both may produce short-term improvement in compliance or resistance; neither has been shown to change duration of support or long-term outcome.
- Pulmonary hypertension — managed by the neonatal and cardiology teams, with attention to hypoxaemia, aspiration and airway obstruction as reversible contributors.
- RSV prevention — nirsevimab and maternal RSV vaccination have substantially changed the outlook for this group; see the RSV guide.
- Immunisation and smoke-free environment — unglamorous and among the most effective steps a family can take.
BPD is a disease of impaired alveolar and vascular growth, not of secretion retention. Routine chest physiotherapy in preterm infants has no demonstrated benefit, is poorly tolerated, causes desaturation and destabilisation, and has historically been associated with harm.6 Physiotherapy for this population is developmental, positional, feeding-related and rehabilitative — not percussive. Airway clearance is reserved for a specific, identified problem such as a lobar collapse or an infant with a tracheostomy and genuine secretion load, and is then delivered by a paediatric-experienced clinician.
Living with bronchopulmonary dysplasia
The first two years
For most families, the first two years are the hardest. Practical priorities are keeping the baby away from respiratory infection during the first winter without isolating the family entirely, protecting feeding and growth, learning to recognise the difference between a normal cold and a deteriorating chest, and managing home oxygen equipment if it is needed. A written action plan — what normal looks like for this baby, what to watch for, who to call — reduces both admissions and anxiety.
Beyond infancy
Beyond infancy, most children are active and well. They may tire more quickly than their peers and be more affected by chest infections, but exercise should be encouraged rather than restricted; physical activity in childhood is associated with better later lung function, and avoidance leads to deconditioning that is easily mistaken for lung disease.
Prognosis
Improvement through the preschool years
Respiratory symptoms improve steadily through the preschool years as new alveoli continue to form — alveolarisation continues into at least the second year of life and probably well beyond. Most children come off oxygen within the first year, and readmission rates fall sharply after age two.
Lung function into adult life
Lung function, however, does not fully normalise. Survivors of BPD reach school age and adulthood with reduced forced expiratory flows, and follow-up cohorts show a group that enters adult life with a lower peak lung function than their peers.7 Because chronic obstructive lung disease in later life depends on both the peak attained and the subsequent rate of decline, this group is at increased risk of meeting COPD criteria in mid-life without ever having smoked. Whether this reflects a fixed structural deficit or an accelerated decline is not yet resolved — but it is a strong argument for never smoking, avoiding occupational exposures, and maintaining lifelong physical activity.
Role of the physiotherapist
In the neonatal unit
The physiotherapist's role is primarily developmental and positional: supportive positioning that promotes flexion and midline orientation, minimal handling and clustered care to limit desaturation, prone positioning where appropriate to improve oxygenation, and guidance to parents on handling. Chest physiotherapy is used sparingly and for a defined indication. Assessment of tone, movement and early neurodevelopment identifies infants needing early intervention.
After discharge
The contribution shifts to developmental follow-up, family education, and recognising the child whose “asthma” is not responding because the underlying problem is structural rather than inflammatory. Supporting feeding, positioning and parental confidence with home oxygen equipment is a substantial part of the first year.
In later childhood and adolescence
Physiotherapy here is exercise medicine: assessing exercise capacity, distinguishing true ventilatory limitation from deconditioning or dysfunctional breathing, and prescribing training that builds fitness in a group who have often been treated as fragile by everyone around them. Given that this cohort enters adult life with a lower peak lung function, establishing lifelong activity habits in adolescence is a genuinely preventive intervention.
Where there is a genuine secretion problem
Where a child has a tracheostomy, neuromuscular weakness or a demonstrable secretion load, the full airway clearance skill set applies — sized, timed and delivered for a small child, by a clinician with paediatric experience. This is the exception that defines the rule rather than a reason to treat routinely.
Part 1 · References
- Jensen EA, Dysart K, Gantz MG, et al. The diagnosis of bronchopulmonary dysplasia in very preterm infants: an evidence-based approach. Am J Respir Crit Care Med 2019;200:751–9.
- Northway WH, Rosan RC, Porter DY. Pulmonary disease following respirator therapy of hyaline-membrane disease: bronchopulmonary dysplasia. N Engl J Med 1967;276:357–68.
- SUPPORT Study Group of the Eunice Kennedy Shriver NICHD Neonatal Research Network. Early CPAP versus surfactant in extremely preterm infants. N Engl J Med 2010;362:1970–9.
- Schmidt B, Roberts RS, Davis P, et al. Caffeine therapy for apnea of prematurity. N Engl J Med 2006;354:2112–21.
- Doyle LW, Cheong JL, Hay S, et al. Late (≥7 days) systemic postnatal corticosteroids for prevention of bronchopulmonary dysplasia in preterm infants. Cochrane Database Syst Rev 2021;11:CD001145.
- Hough JL, Flenady V, Johnston L, Woodgate PG. Chest physiotherapy for reducing respiratory morbidity in infants requiring ventilatory support. Cochrane Database Syst Rev 2008;3:CD006445.
- Simpson SJ, Turkovic L, Wilson AC, et al. Lung function trajectories throughout childhood in survivors of very preterm birth: a longitudinal cohort study. Lancet Child Adolesc Health 2018;2:350–9.
References are numbered in citation order (Vancouver/BMJ style) and were current at the time of writing. Guidelines are living documents — verify against the latest version before clinical use.
Supervised exercise, breathing technique and self-management education are the mainstay of cardiorespiratory physiotherapy for this condition.
Clinical evidence
Part 1 covers the same condition without the technical detail. What follows is the evidence base behind it, written for clinicians — the literature, the reasoning and the gaps.
For clinicians: this summary supports clinical reasoning and is not a protocol. Check current guidelines and local policy before applying it, and read it alongside the key references and guidelines directory.
Framing. BPD is the paediatric condition most often mismanaged by adult-trained cardiorespiratory physiotherapists, because the name suggests a chronic suppurative airway disease and the treatment reflex is airway clearance. It is not that disease. New BPD is arrested alveolarisation and dysmorphic pulmonary vascular development in a lung that stopped growing; the deficit is gas-exchange surface area and vascular bed, not mucus. Recognising this changes the intervention from percussion to positioning, development, nutrition advocacy and, later, exercise.
Prevention: the evidence that changed the disease
The interventions with genuine outcome data are preventive and mostly not physiotherapeutic. Early CPAP with selective surfactant, rather than routine intubation and prophylactic surfactant, reduced the composite of death or BPD in large randomised trials and shifted practice internationally.1 The Caffeine for Apnea of Prematurity trial randomised over 2,000 infants and found reduced BPD, reduced patent ductus requiring treatment, and less cerebral palsy and cognitive delay at 18–21 months, with benefits still evident at later follow-up — one of the largest effect sizes in neonatal medicine.2 Postnatal corticosteroids remain the clearest example of a treatment whose respiratory benefit and neurological risk must be weighed individually rather than by protocol.3
Chest physiotherapy in the preterm infant
Systematic review of chest physiotherapy in ventilated and recently extubated neonates found no evidence of benefit for the outcomes that matter — reintubation, duration of oxygen, length of stay — alongside consistent evidence of physiological destabilisation during treatment, and historical reports of an association between vigorous percussion techniques and encephaloclastic porencephaly.4 The appropriate inference is not that airway clearance is never indicated in a preterm infant, but that it requires a specific identified indication, a paediatric-competent clinician, and a plan to stop when the indication resolves. The default is minimal handling.
Long-term respiratory trajectory
Follow-up cohorts consistently show persistent airflow obstruction into school age and adulthood in BPD survivors, with reduced FEV1 and mid-expiratory flows relative to term-born peers, incomplete bronchodilator response, and evidence of small-airway disease and gas trapping on imaging.5 Because adult COPD risk is determined jointly by peak lung function attained in early adulthood and the subsequent rate of decline, a preterm-born adult may reach diagnostic criteria for airflow obstruction without accelerated decline at all. Exercise capacity in this group is frequently reduced out of proportion to spirometry, implicating deconditioning, peripheral muscle factors and, in some, pulmonary vascular limitation.6
Physiotherapy implications
- Default to developmental and positional care, not percussion. Cluster handling; treat desaturation with handling as a clinical finding, not an inconvenience.
- Airway clearance requires a named indication — documented lobar collapse, an artificial airway with secretion load, or an intercurrent infection with retained secretions — and a stop date.
- Advocate for nutrition and growth in ward rounds: somatic growth drives lung growth, and no physiotherapy technique substitutes for it.
- In the child or adolescent with a BPD history, assess exercise capacity properly before attributing breathlessness to the lungs. Deconditioning, dysfunctional breathing and exercise-induced laryngeal obstruction are all common in this group and all treatable.
- Counsel explicitly about smoking, vaping and occupational exposure in adolescence — this cohort starts adult life with less reserve than their peers.
Clinical reasoning
When a preterm infant deteriorates, ask what has changed before reaching for a technique: reflux and aspiration, an evolving infection, airway malacia, pulmonary hypertension and simple fatigue all present as increased work of breathing, and none of them respond to chest physiotherapy. When an older child with a BPD history presents with exertional symptoms, resist the assumption that the lungs are the limiting organ — measure it. And when a family have been told their child has “chronic lung disease”, take the time to explain the growth model: what is limited now can improve, and what they do about activity, infection and smoke exposure genuinely alters the trajectory.
Evidence gaps
There is no trial evidence to guide physiotherapy in BPD specifically — the neonatal chest physiotherapy literature is small, old and largely conducted before current definitions and ventilation practice. Optimal exercise prescription for children and adults born preterm has not been established, and it is unknown whether structured training in adolescence alters the adult lung function trajectory or only fitness. The relative contribution of pulmonary vascular disease to exercise limitation in adult survivors is unquantified. Diuretics and inhaled bronchodilators remain in routine use with no long-term outcome data, and the optimal oxygen saturation target after discharge is still debated.
References for the clinical evidence summary
- SUPPORT Study Group of the Eunice Kennedy Shriver NICHD Neonatal Research Network. Early CPAP versus surfactant in extremely preterm infants. N Engl J Med 2010;362:1970–9.
- Schmidt B, Roberts RS, Davis P, et al. Caffeine therapy for apnea of prematurity. N Engl J Med 2006;354:2112–21.
- Doyle LW, Cheong JL, Hay S, et al. Late (≥7 days) systemic postnatal corticosteroids for prevention of bronchopulmonary dysplasia in preterm infants. Cochrane Database Syst Rev 2021;11:CD001145.
- Hough JL, Flenady V, Johnston L, Woodgate PG. Chest physiotherapy for reducing respiratory morbidity in infants requiring ventilatory support. Cochrane Database Syst Rev 2008;3:CD006445.
- Simpson SJ, Turkovic L, Wilson AC, et al. Lung function trajectories throughout childhood in survivors of very preterm birth: a longitudinal cohort study. Lancet Child Adolesc Health 2018;2:350–9.
- Edwards MO, Kotecha SJ, Lowe J, et al. Effect of preterm birth on exercise capacity: a systematic review and meta-analysis. Pediatr Pulmonol 2015;50:293–301.
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