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Back groundBack 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 groundBack 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 .
PathophysiologyPathophysiology
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 BPDStages 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 BPDFrequency 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 BPDMortality/Morbidity of BPD
Infants with severe BPDIncreased risk of pulmonary morbidity & mortality within the first 2 years of life .
Pulmonary Complications of Pulmonary Complications of BPDBPD
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 & Volume trauma & BarotraumaBarotrauma
Rx 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-Barotrauma VolumetraumaLung injury secondary to
excess TV from increased PPV .
Volume trauma & Volume trauma & BarotraumaBarotrauma
Severity 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 & Volume trauma & BarotraumaBarotrauma
Increased PPV to recruit all alveoliCompliant alveoli & terminal bronchioles ruptureleaks air in to interstiumPIEIncrease risk of BPD
Using SIMV compared to IMV in infants <1000g showed less BPD .
O2 & AntioxidantsO2 & Antioxidants
O2 accept electrons in it’s outer ringForm O2 free radicalsCell membrane destruction
Antioxidants(AO)Antagonise O2 free radicals
Neonates-Relatively AO deficient Major antioxidants – super oxide dismutase ,
glutathione peroxidase & catalase
O2 & AntioxidantsO2 & Antioxidants
Antioxidant enzyme level increase during last trimester .
Preterm birthIncreased risk of exposure to O2 free radicals
InflammationInflammation
Activation of inflammatory mediatorsIn acute lung injury
Activation of leukocytes by O2 free radicals , barotrauma & infectionDestruction & abnormal lung repairAcute lung injuryBPD
Leukocytes & lipid byproducts of cell membrane destructionActivate inflammatory cascade
InflammationInflammation
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 mediatorsvasodilatationincreased capillary permeabilityalbumin leakage & inhibition of surfactant functionrisk of barotrauma
InflammationInflammation
Neutrophils – release collegenase & elastasedestroy lung tissue
Hydroxyproline & elastin recovered in urine of preterms who develops BPD
Di2ethylhexylphthalate(DEHP) degradation product of used ET tubeslung injury
A study in 1996 found that increased interleukin 6 in umbilical cord plasma
InfectionInfection
Maternal cervical colonization/ preterm neonatal tracheal colonization of U.urealyticum associated with high risk of BPD
NutritionNutrition
Inadequate nutrition supplementation of preterm compound the damage by barotrauma , inflammatory cascade activation & deficient AO stores
Acute stage of CLDincreased energy expenditure
New born ratsnutritionally depriveddecreased lung weight
NutritionNutrition
Cu , Zn , Mn deficiencypredispose 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
NutritionNutrition
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
GeneticsGenetics
Strong family history of asthma & atopy increase risk of development & severity of BPD
CVS ChangesCVS 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 ChangesCVS Changes
Persistent right ventricular hypertrophy/ fixed pulmonary hypertension unresponsive to supplemental O2 leads to poor prognosis
AirwayAirway
Trachea & main stem bronchi - abnormalities depend on duration & frequency of intubation & ventilation
Diffuse or focal mucosal edema , necrosis/ulceration occur
Earliest changes from light microscopyloss of cilia in columnar epithelium , dysplasia/necrosis of the cells
AirwayAirway
Neutrophils , lymphocyte infiltrate & goblet cell hyperplasiaincreased mucus production
Granulation tissue & upper airway scarring from deep suctioning & repeated ET intubation results in laryngotracheomalacia , subglottic stenosis & vocal cord paralysis
AirwayAirway
Necrotizing bronchiolitis – results from edema , inflammatory exudate & necrosis of epithelial cells .
Inflammatory cells , exudates & cellular debris obstruct terminal airways
Activation & proliferation of fibroblastsperibronchial fibrosis & obliterative fibroproliferative bronchiolitis
Radiologic FindingsRadiologic Findings
Decreased lung volumes Areas of atelectasis Hyperinflation Lung haziness PIE
Histologic FindingsHistologic Findings
In 1996 Cherukupalli & colleagues described 4 pathologic stages
Acute lung injury Exudative bronchiolitis Proliferative bronchiolitis Obliterative fibroproliferative bronchiolitis
Medical care in BPDMedical care in BPD
Prevention Mechanical ventilation O2 therapy Nutritional support Medications
Mechanical VentilationMechanical 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 VentilationMechanical 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 VentilationMechanical Ventilation
When weaning from vent & O2 difficult – when adequate TV & low FiO2 achievedtrial of extubation & NCPAP
Commonly extubation failuresecondary 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 TherapyO2 Therapy
Chronic hypoxia & airway remodelingpulmonary HT & cor pulmanale
O2stimulate production of NOsmooth muscle relaxationvasodilatation
O2 TherapyO2 Therapy
Repeated desats secondary to hypoxia results from- decreased respiratory drive
- altered pulmonary mechanics
- excessive stimulation
- bronchospasm Hyperoxiaworsen BPD as preterms have
a relative deficiency of AO
O2 TherapyO2 Therapy
O2 requirement increase during stressful procedures & feedingstherefore wean O2 slowly
Keep sats 88% - 92% High altitudesmay require O2 many
months PRBC transfusionincrease O2 carrying
capacity in anemic(hct<30%) preterms
O2 TherapyO2 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 byerythropoetin , iron supplements & decreased phlebotomy requirements
Nutritional SupportNutritional 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 linesmaximize calories in TPN
Nutritional SupportNutritional Support
Rapid & 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 SupportNutritional Support
Cu , Mn , & Zn essential cofactors in AO defenses
Early initiation of small enteral feeds with EBM , slow & steady increase in volumefacilitate tolerance of feeds
Needs 120 – 150 Kcal/kg/day to gain weight
DiureticsDiuretics
Furesemide (Lasix) Rx of choice Decrease PIE & pulmonary vascular
resistance Facilitate weaning from PPV , O2 /both Adverse effects – hyponatremia ,
hypokalemia , hypercalciuria , cholelithiasis , nephrocalcinosis & ototoxicity
DiureticsDiuretics
Careful parenteral & enteral supplements compensate adverse effects
Thiazide & spiranolactone for long term Rx
Systemic BronchodilatorsSystemic Bronchodilators
Methylxanthines – increase respiratory drive , decrease apnea , improve diaphragmatic contractility
Smooth muscle relaxation – decrease pulmonary vascular resistance & increase lung compliance
Exhibit diuretic effects
Systemic BronchodilatorsSystemic Bronchodilators
Theophyline – metabolized primarily to caffeine in liver
Adverse effects – increase heart rate , GER , agitation & seizures
PrognosisPrognosis
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