BRONCHOPULMONARY

DYSPLASIA
DR.AATHIRA AJAYKUMAR

3/13/2021 1
 Definition
•Bronchopulmonary dysplasia (BPD) is a chronic
lung disease most commonly seen in premature
infants who required mechanical ventilation and
oxygen therapy for acute respiratory distress.

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 Incidence of Bronchopulmonary Dysplasia
● The incidence of BPD in surviving infants less than or
equal to 28 weeks gestational age has been relatively
stable at approximately 40% over the last few decades

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 CLINICAL PRESENTATION

● Physical examination- tachypnea, retractions, and rales on auscultation.

● Arterial blood gas (ABG) analysis shows hypoxemia and hypercarbia
● chest radiograph -diffuse haziness, increased density, normal-to-low lung
volumes,inhomogeneous regions of opacification with hyperinflation.
● Cardiac evaluation- Electrocardiogram (ECG) can show persistent or progressive right
ventricular hypertrophy if cor pulmonale develops, echocardiography may be useful in
excluding left-to-right shunts (see Chapter 41) and Pulmonary hypertension.
● Infant pulmonary function testing (iPFT)-Increased respiratory system resistance and
decreased dynamic compliance are hallmarks of BPD.

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CLINICAL COURSE- Early phase
Early phase- upto 1 post natal week

Scenario 1- preterm baby with RDS requiring intubation/ surfactant

Successful extubation in a few days to SNIPPV/CPAP( MILD BPD)

Scenario 2- preterm baby with RDS requiring intubation/ surfactant,post extubation

Gets intubated and requires high ventilation pressures and FiO2

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Evolving phase (>1 postnatal week to 36 weeks)

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Established phase(>36 weeks)

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STAGE1 BPD

Diffuse reticulogranular
appearance with air
bronchogram
,indistinguishable from
RDS

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Stage 2 BPD

Homogenous opacification
of lung fields with coarse
confluent densities

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Stage 3 BPD

Expanded lucent vacuoles in the

lung fieldsappearing as aircysts
among dense patches of the
lung.

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Stage 4 BPD

Bubbly appearance of lung with

expansion of air cysts.Opacities
reduced to strands and streaks.

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 OLD and NEW BPD

● “Old” BPD (pre surfactant era) affected infants with mean gestational age of
33 weeks and birth weight of 2,000 g, the pathology of nonsurvivors showed
predominantly small airway injury, fibrosis, and emphysema.

● In contrast, in the postsurfactant therapy era, “new” BPD affects mostly

extremely preterm infants and the most significant pathologic finding is
decreased alveolarization with fewer and larger alveoli and decreased
pulmonary vascular development.

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MANAGEMENT OF BPD
ANTENATAL INTERVENSIONS
1.Antenatal steroids- most effective interventon for lung maturation.

2.Antenatal antibiotics - antenatal interventions to treat chorioamnionitis.

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GOLDEN HOUR INTERVENTIONS
1.Initial FiO2 -0.3 for preterms
2.Oxygen saturation targeting
3.Delayed cord clamping
4.Trial of CPAP/NIPPV
5.Intubate for resuscitation or severe respiratory distress orto
administer surfactant
6.Early surfactant administration-INSURE/LISA
7.Sustained lung inflation may be considered
8.Avoid hypo/hyperthermia

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 POSTNATAL INTERVENTIONS

OXYGEN supplementation
Maintain target saturation 88-92%( acute phase)and 90-95% ( chronicphase)
(SUPPORT Trial)
GESTTIONAL AGE(weeks) TARGET SpO2 on O2(%) TARGETSpO2 off O2(%)

<32 90-95% 90-100%

32-36 92-97% 92-100%

>36 94-98% 94-100%

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 MANAGEMENT OF BPD

CAFFEINE- (20 mg/kg loading dose and 5 mg/kg daily maintenance)

started during the first 10 days after birth reduces the risk of BPD. Recent
evidence suggests that beginning caffeine therapy within the first 72 hours
of age and a higher loading and maintenance dose results in the greatest
reduction in the BPD risk.

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EARLY PHASE-VENTILATOR STRATEGY
1.Ensure antenatal steroids
2.Initial FiO2 of 0.3-0.4
3.attempt to stabilise the infannton CPAP/SNIPPV
4.Early surfactant administration
5.Give loading doseof Caffeine
6.If ventilated use
a)short inspiratory time(0.24-0.4s)
b)rapid rates(40-60/min)
c)low PIP(14-20cmH2O)
d)moderate PEEP(4-6cm H2O)
e)low tidal volumes (3-6ml/kg)

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BLOOD GAS TARGETS - EARLY PHASE

pH 7.25-7.35

PaO2 40-60

PaCO2 45-55

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EVOLVING PHASE-VENTILATOR STRATEGY
1. Maximise NIV (CPAP/NIPPV) for respiratory support
2. Wean PIPand rates ,attempt to use the lowest MAP
3. In case of worsening of distress,rule out a PDA/ Ventillator
associated pneumonia
4. Consider using diuretic therapy
5. After 3-4 weeks ,can consider using a short course of
dexamethasone
6. Inspiratory time- 0.35-0.45s
7. Tidal volume- 4-6ml/kg
8. PEEP- 4-6 cmH2O

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BLOOD GAS TARGETS- EVOLVING PHASE

pH 7.25-7.35

PaO2 40-60

PaCO2 45-55

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ESTABLISHED PHASE-VENTILATOR STRATEGIES
1. Attempt to minimise ventilator settings/use NIV
2. Continue chronic diuretic therapy
3. Use of inhaled steroids/bronchodialators
4. Screen for pulmonary hypertension
5. Inspiratory time(Ti )- 0.4-0.5s
6. Tidal volume - 4-6ml/kg
7. PEEP - 5-7cm H2O

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BLOOD GAS TARGETS-ESTABLISHED PHASE

pH 7.25-7.35

PaO2 50-70

PaCO2 50-65

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SEVERE BPD-VENTILATOR STRATEGY
1.Chest Xray shows uniform dense haziness
2.Oxygenation is the basic problem
3.Aim for higher MAP
PEEP 6-12 cm H2O

TV 8-12 ml/kg

Ti >0.5s

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 EARLY BPD EVOLVING BPD ESTABLISHED BPD

Ti(s) 0.24-0.4 0.35-0.45 0.4-0.5

TIDAL VOLUME(ml/kg) 3-6 4-6 5-7

PEEP(cmH2O) 6-8 6-10 6-18

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 PHARMACOLOGICAL STRATEGIES-SURFACTANT

1.Early rescue surfactant administration in preterm babies with RDS is

beneficial.
2.Administration of a surfactant avoiding standard endotracheal
intubation such as less invasive surfactant administration (LISA) or
minimally invasive surfactant therapy, has been shown to reduce BPD .

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 VITAMIN A :

● A relative deficiency of Vitamin Ain very preterm infants is associated

with BPD.
● Vitamin A improves lung healing,increases number of alveoli,decrease
susceptibility to infection
● Dose- 5,000 IU intramuscular [IM], three times weekly for the first 28
days of age

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 DIURETICS
● The clinical improvement-- due to decreased lung water content, with
decreased interstitial and peribronchial fluid resulting in less resistance
and better compliance.
○1.Furosemide-- 1.0 mg/kg/dose IV (or 2mg/kg/dose PO) daily.
○ 2.If a trial of furosemide given on 3 consecutive days suggests clinical
improvement, treatment with chlorothiazide (20 to40 mg/kg/day PO,
Q12H) or hydrochlorothiazide (2 to 4 mg/kg/day PO, Q12H) to avoid
furosemide toxicities.
○ Spironolactone- aldosterone antagonist -1.5-3mg/kg/day Q12H
○ Monitor electrolytes

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 POSTNATAL STEROIDS
● DEXAMETHASONE: dexamethasone resulted in increased compliance,
decreased resistance, and diminished O2 requirement, and facilitated earlier
extubation.
● early dexamethasone (<7 days) - reduced BPD risk but it is not recommended
due to side effects such as GI perforation, hypertrophic cardiomyopathy,
hypertension,cerebral palsy, and major neurosensory disability.
● “late” dexamethasone (>7 days) -less reduction of BPD but lesser CNS side
effects

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DART Regime
TIME DOSE(mg/kg/dose) FREQUENCY(hourly)

DAY 1-3 0.075 12

DAY 4-6 0.050 12

DAY 7 and 8 0.025 12

DAY 9 and 10 0.01 12

DoylelwDoyle, L. W., Davis, P. G., Morley, C. J., McPhee, A., Carlin, J. B., Kaimakamis, M., Callanan, C., Yu, V., Hayes,
M., Li, R., Fraser, S., Gill, A., Lontis, R., Goodchild, L., French, N., Evans, N., Reid, S., Darlow, B., Kuschel, C., ... Sinclair,
J. C. (2006). Low-dose dexamethasone facilitates extubation among chronically ventilator-dependent infants: A multicenter,
international, randomized, controlled trial. Pediatrics, 117(1), 75-83. https://doi.org/10.1542/peds.2004-2843

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 HYDROCORTISONE: (PREMILOC trial )
● The hydrocortisone group received 1 mg/kg of hydrocortisone
hemisuccinate per day divided into two doses per day for 7 days,
followed by one dose of 0·5 mg/kg/day for 3 days.
● BPD-free survival was improved and there were no short-term or
neurodevelopmental adverse effects.
● Side effect : higher sepsis rates among the most preterm infants (24 to
25 weeks)
Robin Steinhorn, MD, reviewing Baud O et al. JAMA 2017 Apr 4 Marlow N. JAMA 2017 Apr 4

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 INHALED STEROIDS - the NEuroSIS trial

● Neonatal European Study of Inhaled Steroids

● Inhaled steroids demonstrates improved BPD-free survival

● Intratracheal budesonide combined with surfactant holds promise in

preventing BPD.
www.nejm.org/doi/full/10.1056/NEJMoa1501917

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 Bronchodilators
● Nebulized β-adrenergic agonists such as albuterol and
nebulized ipratropium bromide, a muscarinic agent,results in
decreased resistance and increased compliance.
● Albuterol- 0.1-0.5mg/kg Q2-6H
● Levalbuterol- 0.31mg Q8H

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 Fluid management
● Initial fluid intake --adequate to maintain urine output of at least 1
mL/kg/hour and serum sodium concentration of 140 to 145 mEq/L.
● In the chronic phase-- limit fluids to 130 mL/kg/day with monitoring for

adequate urine output and attention to higher-caloric-density nutrients

● Ensure adequate calorie intake

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 INITIATION INCREMENTS MAINTENANCE

FLUIDS(ml/kg/day) 80-100 10-20 130-140

CALORIES(Kcal/kg/ 40-60 10-15 120

day)

CARBOHYDRATE( 4-6 1 10-12

mg/kg/min)

PROTEIN(g/kg/day) 1.5-3 0.5-1 4

LIPID(gl/kg/day) 0.5-1 0.5-1 3-4

SODIUM(meq/kg/da minimal 2(4-6 daysof life) 3 (after 6 days)

y)

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 PDA
● Treatment of a hemodynamically significant PDA in infants
who have respiratory decompensation or cannot be
weaned from mechanical ventilation reduces BPD risk
● Indomethacin/ Brufen/ Acetaminophen
● Surgical closure of PDA is associated with increased risk of
BPD.

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 HUMAN MILK

● Recent studies have shown that breast milk reduces the

risk of BPD. The odds of BPD reduced by 9.5% for every
10% increase in the use of mother’s own milk (MOM).
● Give expressed breast milk fortified with HMF and add on
MCT oil for better calorie intake.

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 OUTCOME
● Mortality in severe BPD is estimated at 10% to 20% during the first year
of life.
● PULMONARY- infants with BPD are at an increased risk for reactive
airway disease, bronchiolitis and pneumonia.The rehospitalization rate
for respiratory illness during the first 2 years of life in infants with BPD
is twice that in control infants.
● CNS-Children with BPD have motor,cognitive,educational and
behavioral impairments.
● Delayed growth

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 REFERENCE
● Clohery and Starks manual of neonatal care-SAE 8th edition -2021
● Goldsmith,Karotkin,Keszler Assisted Ventillation of the Neonatesixth edition
● Averys Neonatology- Pathophysiology and management of the newborn seventh edition
● Bronchopulmonarydysplasia: definition,pathogenesis,clinical management -up to date
● https://www.ncbi.nlm.nih.gov/portal/utils/pageresolver.fcgi?recordid=604c0ced2b776044fbca8af3
● zoe michel,helen christou et al Bronchopulmonary Dysplasia: An Update of Current Pharm
● https://pubmed.ncbi.nlm.nih.gov/28774356/acologic Therapies and New Approaches
● AIIMS Protocols in neonatology -second edition -2019
● Essentials of neonatal ventilation -Rajiv,Vidyasagar,Lakshminrusimha 2019
● www.nejm.org/doi/full/10.1056/NEJMoa150191
● Robin Steinhorn, MD, reviewing Baud O et al. JAMA 2017 Apr 4 Marlow N. JAMA 2017 Apr 4
● DoylelwDoyle, L. W., Davis, P. G., Morley, C. J., McPhee, A., Carlin, J. B., Kaimakamis, M., Callanan, C., Yu,
V., Hayes, M., Li, R., Fraser, S., Gill, A., Lontis, R., Goodchild, L., French, N., Evans, N., Reid, S., Darlow, B.,
Kuschel, C., ... Sinclair, J. C. (2006). Low-dose dexamethasone facilitates extubation among chronically
ventilator-dependent infants: A multicenter, international, randomized, controlled trial. Pediatrics, 117(1),
75-83. https://doi.org/10.1542/peds.2004-2843

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THANK
YOU

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