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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 .

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bronchopulmonary dysplasia bpd

Bronchopulmonary Dysplasia(BPD)

Kumari Weeratunge M.D.

PL - 2

back ground
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 .
back ground1
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 .
pathophysiology
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 .
stages of bpd
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
frequency of bpd
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 .
mortality morbidity of bpd
Mortality/Morbidity of BPD
  • Infants with severe BPDIncreased risk of pulmonary morbidity & mortality within the first 2 years of life .
pulmonary complications of bpd
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
volume trauma barotrauma
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 .
volume trauma barotrauma1
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 .
volume trauma barotrauma2
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 .
o2 antioxidants
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
o2 antioxidants1
O2 & Antioxidants
  • Antioxidant enzyme level increase during last trimester .
  • Preterm birthIncreased risk of exposure to O2 free radicals
inflammation
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
inflammation1
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
inflammation2
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
infection
Infection
  • Maternal cervical colonization/ preterm neonatal tracheal colonization of U.urealyticum associated with high risk of BPD
nutrition
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
nutrition1
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
nutrition2
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
genetics
Genetics
  • Strong family history of asthma & atopy increase risk of development & severity of BPD
cvs changes
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
cvs changes1
CVS Changes
  • Persistent right ventricular hypertrophy/ fixed pulmonary hypertension unresponsive to supplemental O2 leads to poor prognosis
airway
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
airway1
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
airway2
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
radiologic findings
Radiologic Findings
  • Decreased lung volumes
  • Areas of atelectasis
  • Hyperinflation
  • Lung haziness
  • PIE
histologic findings
Histologic Findings
  • In 1996 Cherukupalli & colleagues described 4 pathologic stages
  • Acute lung injury
  • Exudative bronchiolitis
  • Proliferative bronchiolitis
  • Obliterative fibroproliferative bronchiolitis
medical care in bpd
Medical care in BPD
  • Prevention
  • Mechanical ventilation
  • O2 therapy
  • Nutritional support
  • Medications
mechanical ventilation
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
mechanical ventilation1
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
mechanical ventilation2
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
o2 therapy
O2 Therapy
  • Chronic hypoxia & airway remodelingpulmonary HT & cor pulmanale
  • O2stimulate production of NOsmooth muscle relaxationvasodilatation
o2 therapy1
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
o2 therapy2
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
o2 therapy3
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
nutritional support
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
nutritional support1
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.
nutritional support2
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
medical therapy
Medical Therapy
  • Diuretics
  • Systemic bronchodilators
diuretics
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
diuretics1
Diuretics
  • Careful parenteral & enteral supplements compensate adverse effects
  • Thiazide & spiranolactone for long term Rx
systemic bronchodilators
Systemic Bronchodilators
  • Methylxanthines – increase respiratory drive , decrease apnea , improve diaphragmatic contractility
  • Smooth muscle relaxation – decrease pulmonary vascular resistance & increase lung compliance
  • Exhibit diuretic effects
systemic bronchodilators1
Systemic Bronchodilators
  • Theophyline – metabolized primarily to caffeine in liver
  • Adverse effects – increase heart rate , GER , agitation & seizures
prognosis
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