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1. PRESENTED BY,
MS.L.SOUNDARYA
M.SC.NURSING (PEDIATRICS)
BRONCHO-PULMONARY
DYSPLASIA

2. • Broncho-pulmonary dysplasia is chronic
lung disease of the neonate that typically is
caused by prolonged ventilation and is
further defined by age of prematurity and
extent of O 2 requirement.(OR)

3. • A progressive chronic pulmonary condition
characterized by pulmonary edema and a
prolonged requirement of oxygen in infants
who have been treated for respiratory
distress syndrome.

4. CAUSES
Significant risk factors include
• Prolonged mechanical ventilation
• High concentrations of inspired O 2
• Infection (eg, chorio-amnionitis or
sepsis)
• Degree of prematurity

5. Additional risk factors include
• Pulmonary interstitial
emphysema
• High peak inspiratory pressures
• Large end-tidal volumes

6. • Repeated alveolar collapse
• Increased airway resistance
• Increased pulmonary artery pressures

7. pathophysiology
4-pathological changes:
STAGE –I (MILD):
Clinically identical to
IRDS lasts from 2-3 days
during this time, there are
profuse hyaline
membrane,
 patchy mucosal cilia and
 slight edema of the
interstitium but no
necrosis of alveolar cells.

8. STAGE-II (MODERATE):
it last from 4-10 days, during
this time, there are hyaline
membrane present, but
extensive loss of cilia,
Some focci of atelectasis
Small amount of esino-philic
exudates in the brochioles,
Wide spread edema of the
interstitium
Necrosis of alveolar cells are
evident.

9. STAGE-III (SEVERE):
Lasts from 10-20 days.
Increased of alveolar cells
and bronchiolar mucosa
Wide spread alveolar
collapse
Increased interstitial
fibrosis
Hypertensive changes
occur in arterioles and
arteries
Oxygenation is difficult.

10. STAGE-IV (ADVANCE
CHRONIC):
Lasts for a month
Wide spread necrosis,
interstitial fibrosis
Emphysema present
Pulmonary failure
 cardiomegaly with
cor-pulmonale

11. ASSESSMENT
IT is evident when there is increased
need of oxygen
Crepitant rales and diminished
breathing sounds
Barrel shape chest appearance
Emphysema
Oxygenation difficult and carbon
dioxide retention
Respiratory acidosis occurs

12. DIAGNOSTIC EVALUATION
History collection
Physical examination
Radiological findings
Blood investigations for o2
tension, and acidosis

13. TREATMENT
•Nutrition supplementation
•Fluid restriction
•Diuretics
•O 2 supplementation as
needed
•Respiratory syncytial virus
(RSV) monoclonal antibody

14. NURSING MANAGEMENT
•Oxygen therapy can be
provided
•Supportive measurements-
*Nutritional supplementation,
*Fluid restriction, diuretics,
* Bronchodilators.

15. PREVENTION
• Use of antenatal corticosteroids
• Prophylactic use of exogenous
surfactant in selected high-risk
infants (eg, weighing < 1000 g and
requiring ventilator support)
• Early therapeutic continuous
positive airway pressure
• Early use of surfactant for
treatment of RDS

16. • Prophylactic use of methylxanthines
(eg, caffeine 5 to 10 mg/kg po
once/day), particularly when birth
weight is < 1.250 kg
• Permissive hypercarbia and
hypoxemia to achieve low ventilator
pressures, volumes, or both
• Prophylactic use of vitamin A (5000
units IM 3 times/wk for a total of 12
doses) for infants with birth weight <
1000 g

17. PROGNOSIS
•Prognosis varies with severity.
•Infants who still depend on mechanical
ventilation at 36 wk gestation have a 20
to 30% mortality rate in infancy.
•1/3rd of affected infants die by 7-8
months of age.

18. • If the child is survive –
corpulmonary function can be
expected by 5-6 years.
• Infants are at increased risk of
lower respiratory tract infections
(particularly viral pneumonia or
bronchiolitis) and may quickly
develop respiratory
decompensation if pulmonary
infection occurs.

19. THANK YOU