Broncho pulmonary dysplasia(bpd)


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Broncho pulmonary dysplasia(bpd)

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