2. INTRODUCTION
• Most common chronic lung disease of childhood.
• First described by Northway et al
• Definition : 1. NIH definition (2001)
2. Physiological definition
• Old and New BPD
9. Pathogenesis of BPD :
premature lung with developmental deficiencies
(surfactant,nitric oxide,immune defence) and immature alveoli
hyperoxia Mechanical ventilation
Infection Pulmonary Oedema
Lung injury
Nutrophil influx Macrophage influx
Increased proinflammatory cytokines
and altered growth factor
Genetic susceptibility
Surfactant dysfunction,failure of alveologenesis,
increased airway and vascular resistance,abnormal repair
Bronchopulmonary Dysplasia
10.
11. Etiological factors:
Host Susceptibility and genetic factors :
• 50 – 80 % variance in BPD is due to genetic factors
• Family h/o asthma increases the risk of BPD
• SNP for genes involved in inflammatory response, innate immunity,
angiogenesis, surfactant function, and extracellular matrix production
are associated with BPD
12. Inflammation :
• Fetal inflammation play a major role.
• May be derived by microbial infection of amniotic cavity or sterile
histological acute chorioamnionitis.
• IL-6 level increase are hallmark of Fetal inflammation.
• Tracheal aspirate from day 2 of life shows increase of
proinflammatory markers.
13. Neonatal Infection:
• Airway microbial colonization specially by Ureaplasma urealyticum
and Mycoplasma is associated with BPD.
Oxygen toxicity and oxidative stress :
• Mediated by ROS
• Altered oxidant – antioxidant balance in BPD
15. Pulmonary edema and PDA :
• Higher fluid intake and lesser fluid loss in 1st 10 days of life.
• Persistant left to right shunt with delayed closure of PDA
Inadequate nutrition :
• Increased susceptibility to infection
• Deficiency of Vit A and Vit E
16. Surfactant dysfunction :
• Common after a week of intubation
• Infection or respiratory deterioration is associated with worsening
surfactant function
Adrenal insufficiency :
• Premature infant have less mature HPA axis leading to inadequate
response to inflammatory lung injury
23. Prevention of BPD
1. Prevention of prematurity and RDS.
2. Reducing exposure to risk factors.
24. • Ventilation strategies :
Minimizing ventilator support
Prefer non – invasive mode
If invasive ventilation used:
1. Volume targeted ventilation
2. Patient triggered ventilation
3. Low tidal volume
4. Moderate PEEP
5. Slightly high Ti
6. Permissive hypercapnia
25. Saturation target :
• The surfactant, positive pressure, and oxygenation randomization trial
(SUPPORT)
• Canadian oxygen trial (COT)
• Postmenstrual age target oxygen saturation:
Gestational Age Target spo2 on oxygen Target spo2 off oxygen
<32 weeks 90-95% 90-100%
32-36 weeks 92-97% 92-100%
>36 weeks 94-98% 94-100%
26. Surfactant replacement therapy
• Prophylactic surfactant therapy in infants born before 30 weeks of
gestation has not been shown to reduce the incidence of BPD
• However, surfactant treatment for established RDS in infants born at
or after 30 weeks gestation is associated with significant reduction in
incidence of BPD
• The apparent lack of effect in 1st group could probably due to the
increased survival of more immature infants.
27. Vitamin A – is accumulated predominantly in 3rd trimester ,
preterm infants have deficient store of this vitamin
Dose: 5000 IU thrice weekly for 4 wk
Route: IM
Caffeine citrate –
Loading dose 20mg/kg
Maintenance dose 5mg/kg
Reduction of BPD incidence
28. iNO
• Most clinical studies in preterm infants with severe respiratory failure
have not demonstrated any reduction in the risk of death or CLD with
iNO
• Might be beneficial in a select group of preterm infants
• NIH and AAP do not recommend routine use
29. Treatment of BPD
1. Respiratory support
I. Supplemental oxygen
II. Positive-pressure ventilation
30. 2. Improving lung function
i. Fluid restriction :
Restricting fluid to 120 mL/kg/d
concentrating proprietary formulas to 24 cal/oz
addition of fat and carbohydrate.
31. ii. Diuretic therapy
• Diuretics:
Loop diuretics
Thiazide
• Clear evidence that diuretics improves lung mechanics and gas
exchange in well established BPD
• However there is no evidence of long term benefit
32. iii. Bronchodilator therapy
• With established BPD, there is a significant increased in airway
obstruction, and there may also be persistent and intermittent
wheezing may be related to increased airway tone or bronchospasm
• Several studies of either short term, inhaled or parenteral BAA have
demonstrated improvement in lung function.
• Albuterol is used most commonly
• Nebulized ipratropium bromide can also be used as combination
33. iv. Corticosteroids:
• Prenatal
• Postnatal – does not have substantial impact on long term pulmonary
outcomes, such as duration of supplemental oxygen requirement,
length of hospital stay or mortality.
Routine use discouraged due to potential harm. Treatment
reserved for infants with progressive respiratory failure that is
refractory to all therapy.
one approach to prevention is to estimate the risk of developing
BPD by NICHD BPD outcome estimator.
34. 3. Growth and nutrition
Infants with BPD frequently have high caloric needs.
Concentrated formula is often necessary to provide sufficient
calories and prevent pulmonary edema.
specific micronutrient supplementation.
