Bronchopulmonary Dysplasia(BPD)

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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 . - PowerPoint PPT Presentation

Text of Bronchopulmonary Dysplasia(BPD)

  • Bronchopulmonary Dysplasia(BPD)Kumari Weeratunge M.D.PL - 2

  • Back groundDevelops 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 .

  • Back groundShennan 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 .

  • PathophysiologyMultifactorialMajor organ systems - lungs & heartAlveolar stage of lung development - 36wks GA to 18 months post conceptionMechanical ventilation & O2 interferes with alveolar & pulmonary vascular development in preterm mammals . Severe BPD Pulmonary HT & abnormal pulmonary vascular development .

  • Stages of BPDDefined by Northway in 1967Stage 1 - similar to uncomplicated RDSStage 2 - pulmonary parenchymal opacities with bubbly appearance of lungsStage 3 & 4 areas of atelectasis , hyperinflation & fibrous sheathsRecently CT & MRI of chest reveals more details of lung injury

  • Frequency of BPDDependent 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 .

  • Mortality/Morbidity of BPDInfants with severe BPDIncreased risk of pulmonary morbidity & mortality within the first 2 years of life .

  • Pulmonary Complications of BPDIncreased 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

  • Volume trauma & BarotraumaRx of RDS surfactant replacement , O2 , CPAP & mechanical ventilation . Increased PPV required to recruit all alveoli to Px atelectasis in immature lungsLung injuryInflammatory cascade . Trauma secondary to PPV-BarotraumaVolumetraumaLung injury secondary to excess TV from increased PPV .

  • Volume trauma & BarotraumaSeverity of lung immaturity & effects of surfactant deficiency determines PPV . Severe lung immaturityAlveolar number is reducedincreased PP transmitted to distal bronchioles . Surfactant deficiencysome alveoli collapse while others hyper inflate .

  • Volume trauma & BarotraumaIncreased PPV to recruit all alveoliCompliant alveoli & terminal bronchioles ruptureleaks air in to interstiumPIEIncrease risk of BPDUsing SIMV compared to IMV in infants
  • O2 & AntioxidantsO2 accept electrons in its outer ringForm O2 free radicalsCell membrane destructionAntioxidants(AO)Antagonise O2 free radicalsNeonates-Relatively AO deficientMajor antioxidants super oxide dismutase , glutathione peroxidase & catalase

  • O2 & AntioxidantsAntioxidant enzyme level increase during last trimester . Preterm birthIncreased risk of exposure to O2 free radicals

  • InflammationActivation of inflammatory mediatorsIn acute lung injuryActivation of leukocytes by O2 free radicals , barotrauma & infectionDestruction & abnormal lung repairAcute lung injuryBPDLeukocytes & lipid byproducts of cell membrane destructionActivate inflammatory cascade

  • InflammationLipoxigenase & cyclooxigenase pathways are involved in the inflammatory cascadeInflammatory mediators are recovered in tracheal aspirate of newly ventilated preterm who later develops BPDMetabolites of mediatorsvasodilatationincreased capillary permeabilityalbumin leakage & inhibition of surfactant functionrisk of barotrauma

  • InflammationNeutrophils release collegenase & elastasedestroy lung tissueHydroxyproline & elastin recovered in urine of preterms who develops BPDDi2ethylhexylphthalate(DEHP) degradation product of used ET tubeslung injuryA study in 1996 found that increased interleukin 6 in umbilical cord plasma

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

  • NutritionInadequate nutrition supplementation of preterm compound the damage by barotrauma , inflammatory cascade activation & deficient AO storesAcute stage of CLDincreased energy expenditureNew born ratsnutritionally depriveddecreased lung weight

  • NutritionCu , Zn , Mn deficiencypredispose to lung injuryVit A & E prevent lipid peroxidation & maintain cell integrityExtreme prematurity large amounts of H2O needed to compensate loss from thin skin

  • NutritionIncreased fluid administration increased risk of development of PDA & pulmonary edema(PE)High vent settings & high O2 needed to Rx PDA & PEEarly PDA Rx improve pulmonary function but no effect on incidence of BPD

  • GeneticsStrong family history of asthma & atopy increase risk of development & severity of BPD

  • CVS ChangesEndothelial cell proliferationSmooth muscle cell hypertrophyVascular obliterationSerial EKG right ventricular hypertrophyEchocardiogram abnormal right ventricular systolic function & left ventricular hypertrophy

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

  • AirwayTrachea & main stem bronchi - abnormalities depend on duration & frequency of intubation & ventilationDiffuse or focal mucosal edema , necrosis/ulceration occurEarliest changes from light microscopyloss of cilia in columnar epithelium , dysplasia/necrosis of the cells

  • AirwayNeutrophils , lymphocyte infiltrate & goblet cell hyperplasiaincreased mucus productionGranulation tissue & upper airway scarring from deep suctioning & repeated ET intubation results in laryngotracheomalacia , subglottic stenosis & vocal cord paralysis

  • AirwayNecrotizing bronchiolitis results from edema , inflammatory exudate & necrosis of epithelial cells . Inflammatory cells , exudates & cellular debris obstruct terminal airwaysActivation & proliferation of fibroblastsperibronchial fibrosis & obliterative fibroproliferative bronchiolitis

  • Radiologic FindingsDecreased lung volumesAreas of atelectasisHyperinflationLung hazinessPIE

  • Histologic FindingsIn 1996 Cherukupalli & colleagues described 4 pathologic stagesAcute lung injuryExudative bronchiolitisProliferative bronchiolitisObliterative fibroproliferative bronchiolitis

  • Medical care in BPDPreventionMechanical ventilationO2 therapyNutritional supportMedications

  • Mechanical VentilationO2 & PPV life savingAggressive weaning to NCPAP eliminate need of PPVIntubation primarily for surfactant therapy & quickly extubation to NCPAP decrease need for prolong PPVIf infant needs O2 & PPV gentle modes of ventilation employed to maintain pH 7.28 7.40 , pCo2 45 65 , pO2 50- 70

  • Mechanical VentilationPulse oximetry & transcutaneous Co2 mesurements provide information of oxygenation & ventilation with minimal patient discomfortSIMV provide information on TV & minute volumes which minimize O2 toxicity & barotrauma/volumetraumaSIMV allow infant to set own IT & rate

  • Mechanical VentilationWhen weaning from vent & O2 difficult when adequate TV & low FiO2 achievedtrial of extubation & NCPAPCommonly extubation failuresecondary to atrophy & fatigue of respiratory musclesOptimization of nutrition & diuretics contribute to successful weaning from ventMeticulous nursing care essential to ensure airway patency & facilitate extubation

  • O2 TherapyChronic hypoxia & airway remodelingpulmonary HT & cor pulmanaleO2stimulate production of NOsmooth muscle relaxationvasodilatation

  • O2 TherapyRepeated desats secondary to hypoxia results from- decreased respiratory drive - altered pulmonary mechanics - excessive stimulation - bronchospasmHyperoxiaworsen BPD as preterms have a relative deficiency of AO

  • O2 TherapyO2 requirement increase during stressful procedures & feedingstherefore wean O2 slowlyKeep sats 88% - 92%High altitudesmay require O2 many monthsPRBC transfusionincrease O2 carrying capacity in anemic(hct
  • O2 TherapyStudy in 1988 found increased O2 content & systemic O2 transport , decreased O2 consumption & requirement after blood TxNeed for multiple Tx & donor exposures decreased byerythropoetin , iron supplements & decreased phlebotomy requirements

  • Nutritional SupportInfant with BPD- increased energy requirementsEarly TPN compensate for catabolic state of pretermAvoid excessive non N calories increase CO2 & complicate weaningEarly insertion of central linesmaximize calories in TPN

  • Nutritional SupportRapid & early administration of increased lipidsworsen hyperbillirubinemia & BPD through billirubin displacement from albumin & pulmonary vascular lipid deposition respectively . Excessive glucose loadincrease O2 consumption , respiratory drive & glucoseuria.

  • Nutritional SupportCu , Mn , & Zn essential cofactors in AO defensesEarly initiation of small enteral feeds with EBM , slow & steady increase in volumefacilitate tolerance of feedsNeeds 120 150 Kcal/kg/day to gain weight

  • Medical TherapyDiureticsSystemic bronchodilators

  • DiureticsFuresemide (Lasix) Rx of choiceDecrease PIE & pulmonary vascular