Broncho Pulmonary Dysplasia

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Broncho Pulmonary Dysplasia

  1. 1. Bronchopulmonary Dysplasia(BPD) Kumari Weeratunge M.D. PL - 2
  2. 2. Back ground <ul><li>Develops in neonates treated with O2 & PPV . </li></ul><ul><li>Originally described by Northway in 1967 using clinical , radiographic & histologic criteria . </li></ul><ul><li>Bancalari refined definition using ventilation criteria , O2 requirement @ 28days to keep PaO2>50mmhg & abnormalities in chest x –ray . </li></ul>
  3. 3. Back ground <ul><li>Shennan proposed in 1988 criteria of O2 requirement @ 36 weeks corrected GA . </li></ul><ul><li>Antenatal steroids , early surfactant Rx & gentle modes of ventilation minimize severity of lung injury . </li></ul>
  4. 4. Pathophysiology <ul><li>Multifactorial </li></ul><ul><li>Major organ systems - lungs & heart </li></ul><ul><li>Alveolar stage of lung development - 36wks GA to 18 months post conception </li></ul><ul><li>Mechanical ventilation & O2 interferes with alveolar & pulmonary vascular development in preterm mammals . </li></ul><ul><li>Severe BPD  Pulmonary HT & abnormal pulmonary vascular development . </li></ul>
  5. 5. Stages of BPD <ul><li>Defined by Northway in 1967 </li></ul><ul><li>Stage 1 - similar to uncomplicated RDS </li></ul><ul><li>Stage 2 - pulmonary parenchymal opacities with bubbly appearance of lungs </li></ul><ul><li>Stage 3 & 4 – areas of atelectasis , hyperinflation & fibrous sheaths </li></ul><ul><li>Recently CT & MRI of chest – reveals more details of lung injury </li></ul>
  6. 6. Frequency of BPD <ul><li>Dependent on definition used in NICU . </li></ul><ul><li>Using criteria of O2 requirement @ 28 days frequency range from 17% - 57% . </li></ul><ul><li>Survival of VLBW infants improved with surfactant  Actual prevalence of BPD has increased . </li></ul>
  7. 7. Mortality/Morbidity of BPD <ul><li>Infants with severe BPD  Increased risk of pulmonary morbidity & mortality within the first 2 years of life . </li></ul>
  8. 8. Pulmonary Complications of BPD <ul><li>Increased resistance & airway reactivity evident in early stages of BPD along with increased FRC . </li></ul><ul><li>Severe BPD  Significant airway obstruction with expiratory flow limitations & further increased FRC secondary to air trapping & hyperinflation </li></ul>
  9. 9. Volume trauma & Barotrauma <ul><li>Rx of RDS – surfactant replacement , O2 , CPAP & mechanical ventilation . </li></ul><ul><li>Increased PPV required to recruit all alveoli to Px atelectasis in immature lungs  Lung injury  Inflammatory cascade . </li></ul><ul><li>Trauma secondary to PPV-  Barotrauma </li></ul><ul><li>Volumetrauma  Lung injury secondary to excess TV from increased PPV . </li></ul>
  10. 10. Volume trauma & Barotrauma <ul><li>Severity of lung immaturity & effects of surfactant deficiency  determines PPV . </li></ul><ul><li>Severe lung immaturity  Alveolar number is reduced  increased PP transmitted to distal bronchioles . </li></ul><ul><li>Surfactant deficiency  some alveoli collapse while others hyper inflate . </li></ul>
  11. 11. Volume trauma & Barotrauma <ul><li>Increased PPV to recruit all alveoli  Compliant alveoli & terminal bronchioles rupture  leaks air in to interstium  PIE  Increase risk of BPD </li></ul><ul><li>Using SIMV compared to IMV in infants <1000g showed less BPD . </li></ul>
  12. 12. O2 & Antioxidants <ul><li>O2 accept electrons in it’s outer ring  Form O2 free radicals  Cell membrane destruction </li></ul><ul><li>Antioxidants(AO)  Antagonise O2 free radicals </li></ul><ul><li>Neonates-Relatively AO deficient </li></ul><ul><li>Major antioxidants – super oxide dismutase , glutathione peroxidase & catalase </li></ul>
  13. 13. O2 & Antioxidants <ul><li>Antioxidant enzyme level increase during last trimester . </li></ul><ul><li>Preterm birth  Increased risk of exposure to O2 free radicals </li></ul>
  14. 14. Inflammation <ul><li>Activation of inflammatory mediators  In acute lung injury </li></ul><ul><li>Activation of leukocytes by O2 free radicals , barotrauma & infection  Destruction & abnormal lung repair  Acute lung injury  BPD </li></ul><ul><li>Leukocytes & lipid byproducts of cell membrane destruction  Activate inflammatory cascade </li></ul>
  15. 15. Inflammation <ul><li>Lipoxigenase & cyclooxigenase pathways are involved in the inflammatory cascade </li></ul><ul><li>Inflammatory mediators are recovered in tracheal aspirate of newly ventilated preterm who later develops BPD </li></ul><ul><li>Metabolites of mediators  vasodilatation  increased capillary permeability  albumin leakage & inhibition of surfactant function  risk of barotrauma </li></ul>
  16. 16. Inflammation <ul><li>Neutrophils – release collegenase & elastase  destroy lung tissue </li></ul><ul><li>Hydroxyproline & elastin recovered in urine of preterms who develops BPD </li></ul><ul><li>Di2ethylhexylphthalate(DEHP) degradation product of used ET tubes  lung injury </li></ul><ul><li>A study in 1996 found that increased interleukin 6 in umbilical cord plasma </li></ul>
  17. 17. Infection <ul><li>Maternal cervical colonization/ preterm neonatal tracheal colonization of U.urealyticum associated with high risk of BPD </li></ul>
  18. 18. Nutrition <ul><li>Inadequate nutrition supplementation of preterm compound the damage by barotrauma , inflammatory cascade activation & deficient AO stores </li></ul><ul><li>Acute stage of CLD  increased energy expenditure </li></ul><ul><li>New born rats  nutritionally deprived  decreased lung weight </li></ul>
  19. 19. Nutrition <ul><li>Cu , Zn , Mn deficiency  predispose to lung injury </li></ul><ul><li>Vit A & E prevent lipid peroxidation & maintain cell integrity </li></ul><ul><li>Extreme prematurity – large amounts of H2O needed to compensate loss from thin skin </li></ul>
  20. 20. Nutrition <ul><li>Increased fluid administration  increased risk of development of PDA & pulmonary edema(PE) </li></ul><ul><li>High vent settings & high O2 needed to Rx PDA & PE </li></ul><ul><li>Early PDA Rx – improve pulmonary function but no effect on incidence of BPD </li></ul>
  21. 21. Genetics <ul><li>Strong family history of asthma & atopy increase risk of development & severity of BPD </li></ul>
  22. 22. CVS Changes <ul><li>Endothelial cell proliferation </li></ul><ul><li>Smooth muscle cell hypertrophy </li></ul><ul><li>Vascular obliteration </li></ul><ul><li>Serial EKG – right ventricular hypertrophy </li></ul><ul><li>Echocardiogram – abnormal right ventricular systolic function & left ventricular hypertrophy </li></ul>
  23. 23. CVS Changes <ul><li>Persistent right ventricular hypertrophy/ fixed pulmonary hypertension unresponsive to supplemental O2 leads to poor prognosis </li></ul>
  24. 24. Airway <ul><li>Trachea & main stem bronchi - abnormalities depend on duration & frequency of intubation & ventilation </li></ul><ul><li>Diffuse or focal mucosal edema , necrosis/ulceration occur </li></ul><ul><li>Earliest changes from light microscopy  loss of cilia in columnar epithelium , dysplasia/necrosis of the cells </li></ul>
  25. 25. Airway <ul><li>Neutrophils , lymphocyte infiltrate & goblet cell hyperplasia  increased mucus production </li></ul><ul><li>Granulation tissue & upper airway scarring from deep suctioning & repeated ET intubation results in laryngotracheomalacia , subglottic stenosis & vocal cord paralysis </li></ul>
  26. 26. Airway <ul><li>Necrotizing bronchiolitis – results from edema , inflammatory exudate & necrosis of epithelial cells . </li></ul><ul><li>Inflammatory cells , exudates & cellular debris obstruct terminal airways </li></ul><ul><li>Activation & proliferation of fibroblasts  peribronchial fibrosis & obliterative fibroproliferative bronchiolitis </li></ul>
  27. 28. Radiologic Findings <ul><li>Decreased lung volumes </li></ul><ul><li>Areas of atelectasis </li></ul><ul><li>Hyperinflation </li></ul><ul><li>Lung haziness </li></ul><ul><li>PIE </li></ul>
  28. 30. Histologic Findings <ul><li>In 1996 Cherukupalli & colleagues described 4 pathologic stages </li></ul><ul><li>Acute lung injury </li></ul><ul><li>Exudative bronchiolitis </li></ul><ul><li>Proliferative bronchiolitis </li></ul><ul><li>Obliterative fibroproliferative bronchiolitis </li></ul>
  29. 33. Medical care in BPD <ul><li>Prevention </li></ul><ul><li>Mechanical ventilation </li></ul><ul><li>O2 therapy </li></ul><ul><li>Nutritional support </li></ul><ul><li>Medications </li></ul>
  30. 34. Mechanical Ventilation <ul><li>O2 & PPV life saving </li></ul><ul><li>Aggressive weaning to NCPAP eliminate need of PPV </li></ul><ul><li>Intubation primarily for surfactant therapy & quickly extubation to NCPAP decrease need for prolong PPV </li></ul><ul><li>If infant needs O2 & PPV gentle modes of ventilation employed to maintain pH 7.28 – 7.40 , pCo2 45 – 65 , pO2 50- 70 </li></ul>
  31. 35. Mechanical Ventilation <ul><li>Pulse oximetry & transcutaneous Co2 mesurements – provide information of oxygenation & ventilation with minimal patient discomfort </li></ul><ul><li>SIMV – provide information on TV & minute volumes which minimize O2 toxicity & barotrauma/volumetrauma </li></ul><ul><li>SIMV – allow infant to set own IT & rate </li></ul>
  32. 36. Mechanical Ventilation <ul><li>When weaning from vent & O2 difficult – when adequate TV & low FiO2 achieved  trial of extubation & NCPAP </li></ul><ul><li>Commonly extubation failure  secondary to atrophy & fatigue of respiratory muscles </li></ul><ul><li>Optimization of nutrition & diuretics – contribute to successful weaning from vent </li></ul><ul><li>Meticulous nursing care – essential to ensure airway patency & facilitate extubation </li></ul>
  33. 37. O2 Therapy <ul><li>Chronic hypoxia & airway remodeling  pulmonary HT & cor pulmanale </li></ul><ul><li>O2  stimulate production of NO  smooth muscle relaxation  vasodilatation </li></ul>
  34. 38. O2 Therapy <ul><li>Repeated desats secondary to hypoxia results from- decreased respiratory drive </li></ul><ul><li>- altered pulmonary mechanics </li></ul><ul><li>- excessive stimulation </li></ul><ul><li>- bronchospasm </li></ul><ul><li>Hyperoxia  worsen BPD as preterms have a relative deficiency of AO </li></ul>
  35. 39. O2 Therapy <ul><li>O2 requirement increase during stressful procedures & feedings  therefore wean O2 slowly </li></ul><ul><li>Keep sats 88% - 92% </li></ul><ul><li>High altitudes  may require O2 many months </li></ul><ul><li>PRBC transfusion  increase O2 carrying capacity in anemic(hct<30%) preterms </li></ul>
  36. 40. O2 Therapy <ul><li>Study in 1988 found increased O2 content & systemic O2 transport , decreased O2 consumption & requirement after blood Tx </li></ul><ul><li>Need for multiple Tx & donor exposures decreased by  erythropoetin , iron supplements & decreased phlebotomy requirements </li></ul>
  37. 41. Nutritional Support <ul><li>Infant with BPD- increased energy requirements </li></ul><ul><li>Early TPN – compensate for catabolic state of preterm </li></ul><ul><li>Avoid excessive non N calories  increase CO2 & complicate weaning </li></ul><ul><li>Early insertion of central lines  maximize calories in TPN </li></ul>
  38. 42. Nutritional Support <ul><li>Rapid & early administration of increased lipids  worsen hyperbillirubinemia & BPD through billirubin displacement from albumin & pulmonary vascular lipid deposition respectively . </li></ul><ul><li>Excessive glucose load  increase O2 consumption , respiratory drive & glucoseuria. </li></ul>
  39. 43. Nutritional Support <ul><li>Cu , Mn , & Zn essential cofactors in AO defenses </li></ul><ul><li>Early initiation of small enteral feeds with EBM , slow & steady increase in volume  facilitate tolerance of feeds </li></ul><ul><li>Needs 120 – 150 Kcal/kg/day to gain weight </li></ul>
  40. 44. Medical Therapy <ul><li>Diuretics </li></ul><ul><li>Systemic bronchodilators </li></ul>
  41. 45. Diuretics <ul><li>Furesemide (Lasix) Rx of choice </li></ul><ul><li>Decrease PIE & pulmonary vascular resistance </li></ul><ul><li>Facilitate weaning from PPV , O2 /both </li></ul><ul><li>Adverse effects – hyponatremia , hypokalemia , hypercalciuria , cholelithiasis , nephrocalcinosis & ototoxicity </li></ul>
  42. 46. Diuretics <ul><li>Careful parenteral & enteral supplements  compensate adverse effects </li></ul><ul><li>Thiazide & spiranolactone for long term Rx </li></ul>
  43. 47. Systemic Bronchodilators <ul><li>Methylxanthines – increase respiratory drive , decrease apnea , improve diaphragmatic contractility </li></ul><ul><li>Smooth muscle relaxation – decrease pulmonary vascular resistance & increase lung compliance </li></ul><ul><li>Exhibit diuretic effects </li></ul>
  44. 48. Systemic Bronchodilators <ul><li>Theophyline – metabolized primarily to caffeine in liver </li></ul><ul><li>Adverse effects – increase heart rate , GER , agitation & seizures </li></ul>
  45. 49. Prognosis <ul><li>Pulmonary function slowly improves  secondary to continued lung & airway growth & healing </li></ul><ul><li>Northway- Airway hyperactivity , abnormal pulmonary functions , hyperinflation in chest x ray persists in to adult hood </li></ul><ul><li>A study in 1990 found gradual decrease in symptom frequency in children 6 – 9 yrs </li></ul>

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