2. Definition
Initially described in 1967
by Northway using
clinical, radiographic, and
histologic lung changes in
the preterm infant who
had been treated with
oxygen and ventilator
therapy. (Average age 34
wks, wt 2.2 kg.)
3. Definition
Definition initially required an oxygen
requirement at 28 days and an abnormal
chest radiograph. Currently, most authors
define BPD as an oxygen requirement at
36 wks CGA because of the increasing
survival of the ELBW infant.
5. Incidence
A review of Surfactant
trials demonstrated a
significant differences
in incidence
depending on the
institution and
definition used
(17-57%).
6. Incidence
The incidence however changes
dramatically with BW/GA increasing from
@7% in the 1001-1250 gm BW infant to
@64% in the 501-750 gm BW infant.
7. Risk Factors
Major risk factors
Prematurity
Genetic predisposition (male,
white, family history of atopy and
asthma, HLA-A2)
Fluid overload
Patent ductus arteriosus
Infection
Inflammation
Air leak
Mechanical ventilation
Oxygen
Malnutrition
8. Pathophysiology
BPD is a mutifactorial
disorder beginning
with an acute lung
injury in a susceptible
host followed by
continued injury and
abnormal repair.
9. Pathophysiology
Lung injury can occur as a result of any of
the following.
10. Pathophysiology
Surfactant deficiency
Results in collapse of saccules
Distention of distal alveolar ducts
Maldistribution of ventilation
11. Pathophysiology
Pulmonary Edema
Almostalways present in RDS
Worsened by hypoproteinemia and increased
pulmonary blood flow (think PDA)
12. Pathophysiology
Oxygen Exposure
Prolonged exposure to high [ ] can lead to
epithelial and endothelial cell damage, cilliary
dysfunction, decreased lung lymph flow,
altered surfactant synthesis, and inhibition of
lung growth
13. Pathophysiology
Oxygen Free Radicals
Inadequate concentrations of antioxidants
may predispose the premature infant to cell
membrane destruction and the unraveling of
nucleic acids
14. Pathophysiology
Mechanical Ventilation
Volutrauma (Thought to provoke a complex
inflammatory cascade that ultimately leads to
BPD)
Barotrauma (Increased pressure is
transmitted to terminal bronchioles and
alveolar ducts, dissects into the interstitium
where it is trapped, resulting in PIE)
15. Pathophysiology
Mechanical Ventilation
How many breaths do you deliver to a
newborn infant at a rate of 30 bpm?
(commonly seen in the NICU…)
17. Pathophysiology
Mechanical Ventilation
Important to note that there is ample
evidence demonstrating that excessive airway
pressures associated with large tidal volumes
can trigger the inflammatory cascade in the
lungs – the overdistention of the lungs
induces increased pulmonary vascular
resistance with retention of neutrophils and
release of inflammatory mediators
18. Pathophysiology
Infection
Often seen following the “honeymoon” period
(the several days after exogenous surfactant
treatment when often minimal or no oxygen
supplementation is needed
Increased risk of BPD seen in babies of
mothers who have chorioamnionitis
19. Pathophysiology
Infection
Neutrophils, macrophages, leukotrienes,
platelet-activating factor, interleukin-6,
interleukin-8, and tumor necrosis factor have
all been found in high concentrations in infant
who developed BPD
20. Pathophysiology
Infection
Inconsistent reports that colonization with
Ureaplasma urealyticum may predispose and
infant to BPD
21. Pathophysiology
Inflammation
The inflammatory process begins with an
initial stimulus, (oxygen free radicals,
pulmonary barotrauma, infectious agents,
etc…) and progresses with leukocyte
infiltration and a cascade of destruction and
abnormal repair – leading to the development
of chronic lung disease
22. Pathophysiology
Nutrition
The sick premature infant has an increased
nutritional requirement because of increased
metabolic needs and rapid growth
requirements – if the needs are not met the
infant will develop a catabolic state, probably
a major contributing factor in the
pathogenesis of BPD
23. Pathologic Changes
Early changes include
areas of altelectasis
filled with
proteinacious fluid
alternating with areas
of overexpansion
24. Pathologic Changes
Continued airway
injury is seen as a
loss of epithelium and
cilia
25. Pathologic Changes
Late findings include
interstitial fibrosis,
cystic dilatation,
atelectasis, intersitial
edema, and lymphatic
distention
26. Diagnosis
BPD is predominately
a disorder of the
surviving extremely
premature infant,
although it can be
seen in the term
infant with respiratory
failure.
27. Diagnosis
Often preceded by significant oxygen
requirements and need for mechanical
ventilation beyond the first week of life.
28. Diagnosis
Physical Examination
Worsening respiratory status manifested by
increased WOB, increased O2 requirement,
increased incidence of apnea-bradycardia
Retractions, diffuse rales, prolonged
expirations
Possible RV heave, single S2, or prominent P2,
signifying cor pulmonale
29. Diagnosis
Physical Examination
Enlarged liver secondary to right heart failure,
or displacement secondary to hyperinflation
30. Diagnosis
Laboratory and Radiographic Studies
ABG may reveal CO2 retention (although pH is
often normal with chronic lung disease - )
Abnormalities in the electrolytes may be the
result of the retained CO2 (elevated
bicarbonate), diuretic therapy (hypo-Na,
hypo-K, and hypo-Cl), and fluid restriction
(elevated BUN & Cr)
31. Diagnosis
Laboratory and Radiographic Studies
Chest X-ray can be quite variable from diffuse
haziness and hypoinflation to streaky
interstitial markings, altelectasis, cysts, and
hyperinflation
32. Management
The management of
BPD includes the
preventive measures
to decrease the
incidence of the
disease and treatment
modalities once it is
present
36. Management
Treatment
Beta-2 agonist for acute exacerbations of CLD
Nutrition
37. Prognosis
Depends on the
degree of pulmonary
disease and the
presence of other
medical conditions
38. Prognosis
Pulmonary outcome
Although there is a significant risk of needing
rehospitalization within the first year (@30%)
and many infant with BPD have increased
airway resistance and reactivity, the
pulmonary outcome is good
39. Prognosis
Neurodevelopmental outcome
Children
with BPD increased risk for adverse
outcome compared to infants without BPD
Increased hearing impairment
Increased ROP
Increased incidence of learning disabilities, ADHD,
and behavioral problems
54. Which of the following CXR findings are consistent with
stage 4 of BPD?
A) lung appears cystic with areas of hyperinflation &
areas of atelectasis
B) fibrosis and edema with areas of consolidation & areas
of overinflation
C) low volumes with diffuse fine granular opacities
D) opaque lung fields with air bronchograms & possibly
interstitial air
E) normal
55. Which of the following organisms have been implicated
in the pathogenesis of BPD?
A) Mycoplasma
B) Ureaplasma
C) Group B strep
D) Borrelia burgdorferi
E) Moraxella catarrhalis
56. Which statement about long term survivors with BPD
(school-age) is true?
A) They have an increased incidence of asthma.
B) They have airway hyper-responsiveness.
C) They have an increased incidence of atopy.
D) They have an increased incidence of hospital
admissions.
57. Which of the following treatments for Chronic Lung
Disease has been shown to improve the long term
outcome of this population (Need for ventilatory
support, length of hospital stay, long term
neurodevelopmental outcome)?
A) Bronchodilators
B) Thiazide Diuretics
C) Loop Diuretics
D) Inhaled Corticosteroids
E) None of the above
58. Which of the following is NOT a risk factor for
bronchopulmonary dysplasia?
A. Prematurity
B. Female sex
C. Patent ductus arteriosus
D. Air leak
E. Mechanical ventilation
59. How many breaths are delivered via positive pressure to
an infant on SIMV at a rate of 30 per day?
• 432
• 4,320
• 43,200
• 432,000
• 4,320,000
• 4.32 x 107
• 4.32 x 108
• 4.32 x 109
