1 / 49

Bronchopulmonary Dysplasia(BPD)

Bronchopulmonary Dysplasia(BPD). Kumari Weeratunge M.D. PL - 2. Back ground. Develops in neonates treated with O2 & PPV . Originally described by Northway in 1967 using clinical , radiographic & histologic criteria .

elina
Download Presentation

Bronchopulmonary Dysplasia(BPD)

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. Bronchopulmonary Dysplasia(BPD) Kumari Weeratunge M.D. PL - 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. 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. 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. 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. 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. Mortality/Morbidity of BPD • Infants with severe BPDIncreased risk of pulmonary morbidity & mortality within the first 2 years of life .

  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. 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. 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. 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. 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. O2 & Antioxidants • Antioxidant enzyme level increase during last trimester . • Preterm birthIncreased risk of exposure to O2 free radicals

  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. 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. 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. Infection • Maternal cervical colonization/ preterm neonatal tracheal colonization of U.urealyticum associated with high risk of BPD

  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. 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. 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. Genetics • Strong family history of asthma & atopy increase risk of development & severity of BPD

  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. CVS Changes • Persistent right ventricular hypertrophy/ fixed pulmonary hypertension unresponsive to supplemental O2 leads to poor prognosis

  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. 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. 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. Radiologic Findings • Decreased lung volumes • Areas of atelectasis • Hyperinflation • Lung haziness • PIE

  28. Histologic Findings • In 1996 Cherukupalli & colleagues described 4 pathologic stages • Acute lung injury • Exudative bronchiolitis • Proliferative bronchiolitis • Obliterative fibroproliferative bronchiolitis

  29. Medical care in BPD • Prevention • Mechanical ventilation • O2 therapy • Nutritional support • Medications

  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. 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. 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. O2 Therapy • Chronic hypoxia & airway remodelingpulmonary HT & cor pulmanale • O2stimulate production of NOsmooth muscle relaxationvasodilatation

  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. 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. 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. 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. 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. 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. Medical Therapy • Diuretics • Systemic bronchodilators

  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. Diuretics • Careful parenteral & enteral supplements compensate adverse effects • Thiazide & spiranolactone for long term Rx

  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. Systemic Bronchodilators • Theophyline – metabolized primarily to caffeine in liver • Adverse effects – increase heart rate , GER , agitation & seizures

  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

More Related