Successfully reported this slideshow.
We use your LinkedIn profile and activity data to personalize ads and to show you more relevant ads. You can change your ad preferences anytime.



Published on

Published in: Health & Medicine
  • Be the first to comment


  1. 1. Bronchopulmonary DysplasiaDr Varsha Atul Shah
  2. 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. 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.
  4. 4. Definition Old vs. New BPD
  5. 5. Incidence A review of Surfactant trials demonstrated a significant differences in incidence depending on the institution and definition used (17-57%).
  6. 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. 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. 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. 9. Pathophysiology Lung injury can occur as a result of any of the following.
  10. 10. Pathophysiology Surfactant deficiency  Results in collapse of saccules  Distention of distal alveolar ducts  Maldistribution of ventilation
  11. 11. Pathophysiology Pulmonary Edema  Almostalways present in RDS  Worsened by hypoproteinemia and increased pulmonary blood flow (think PDA)
  12. 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. 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. 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. 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…)
  16. 16. Pathophysiology Mechanical Ventilation  43,200
  17. 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. 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. 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. 20. Pathophysiology Infection  Inconsistent reports that colonization with Ureaplasma urealyticum may predispose and infant to BPD
  21. 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. 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. 23. Pathologic Changes Early changes include areas of altelectasis filled with proteinacious fluid alternating with areas of overexpansion
  24. 24. Pathologic Changes Continued airway injury is seen as a loss of epithelium and cilia
  25. 25. Pathologic Changes Late findings include interstitial fibrosis, cystic dilatation, atelectasis, intersitial edema, and lymphatic distention
  26. 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. 27. Diagnosis Often preceded by significant oxygen requirements and need for mechanical ventilation beyond the first week of life.
  28. 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. 29. Diagnosis Physical Examination  Enlarged liver secondary to right heart failure, or displacement secondary to hyperinflation
  30. 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. 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. 32. Management The management of BPD includes the preventive measures to decrease the incidence of the disease and treatment modalities once it is present
  33. 33. Management Prevention  Decrease the risk of prematurity  Decrease risk factors  Prematurity  Genetic predisposition  Fluid overload  Patent ductus arteriosus  Infection  Inflammation  Air leak  Mechanical ventilation  Oxygen  Malnutrition
  34. 34. Management Prevention  Vitamin A supplementation?
  35. 35. Management Treatment  Prudent oxygen supplementation (premature infants <36wks O2 Sat 88-94% & >36wks O2 sat >95%)  Softer mechanical ventilation strategies (NCPAP vs. NSIMV)  Fluid restriction +/- diuretics
  36. 36. Management Treatment  Beta-2 agonist for acute exacerbations of CLD  Nutrition
  37. 37. Prognosis Depends on the degree of pulmonary disease and the presence of other medical conditions
  38. 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. 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
  40. 40. What’s the Evidence for how we Treat BPD?
  41. 41. Bronchodialators
  42. 42. Bronchodialators
  43. 43. Cromolyn Sodium
  44. 44. Early Inhaled Steroids
  45. 45. Early Inhaled Steroids
  46. 46. Early Inhaled Steroids No increased incidence of:  Infection  IVH  Hyperglycemia  PVL  Hypertension  NEC  GI bleeding  ROP  Cataracts  PDA
  47. 47. Early Post-natal (<96hrs) Steroids
  48. 48. Early Post-natal (<96hrs) Steroids
  49. 49. Early Post-natal (<96hrs) Steroids Increased  No change  Hyperglycemia  Infection  Hypertension  Severe IVH  NEC  Growth Failure  Pulmonary Hemorrhage  GI Bleeding  PVL  Intestinal Perforation  ROP  Baley PDI <70 in tested  EEG survivors  Blindness & Deafness  Abnormal Neuro exam  Decreased  Developmental Delay  Pulmonary Air Leak  Cerebral Palsy  PDA
  50. 50. Surfactant
  51. 51. Surfactant
  52. 52. Vitamin A
  53. 53. Vitamin A
  54. 54. Which of the following CXR findings are consistent with stage 4 of BPD?A) lung appears cystic with areas of hyperinflation & areas of atelectasisB) fibrosis and edema with areas of consolidation & areas of overinflationC) low volumes with diffuse fine granular opacitiesD) opaque lung fields with air bronchograms & possibly interstitial airE) normal
  55. 55. Which of the following organisms have been implicated in the pathogenesis of BPD?A) MycoplasmaB) UreaplasmaC) Group B strepD) Borrelia burgdorferiE) Moraxella catarrhalis
  56. 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. 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) BronchodilatorsB) Thiazide DiureticsC) Loop DiureticsD) Inhaled CorticosteroidsE) None of the above
  58. 58. Which of the following is NOT a risk factor for bronchopulmonary dysplasia?A. PrematurityB. Female sexC. Patent ductus arteriosusD. Air leakE. Mechanical ventilation
  59. 59. How many breaths are delivered via positive pressure toan 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