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    Ppt bpd Ppt bpd Presentation Transcript

    • Bronchopulmonary dysplasia( chronic lung disease) Dr prathik
      • First defined by northway in 1967
      • Incidence
      • In 1970 s----30-40% of neonates who received mechanical ventilation
      • Recently incidence is increased – increased survival of VLBW babies
      • Acc to NICHD database(2003) incidence is about
      • < 1000 grams---23.2%
      • 1000-1249 g---8.4%
      • 1250-1499 g---5.4%
      • No indian database
      • Study from PGI
      • < 1000 grams---50%
      • 1000-1249 g---8.1%
      • 1250-1499 g---2.3%
    • DEFINITION
      • Initially defined as continous oxygen dependency for first 28 days with compatible clinical and radiologic findings
      • Bronchopulmonary dysplasia:clinicalpresentation. J Pediatr 1979
      • Later, it was proposed to use the need for supplemental oxygen at 36 weeks postmenstrual age (PMA) as the diagnostic criterion especially in preterm very low birth weight (VLBW) infants
      • Abnormal pulmonary outcomes in premature infants: prediction from oxygen requirement in the neonatal period. Pediatrics 1988
    • NIH DEFINITION < 32 weeks > 32 weeks Time point of assessment 36 weeks PMA or discharge* > 28 days but < 56 days postnatal age or discharge* Treatment with oxygen > 21% for at least 28 days > 21% for at least 28 days Mild Breathing room air at 36 weeks PMA or discharge Breathing room air at 56 days postnatal age or discharge* Moderate Need for <30% oxygen at 36 weeks PMA or discharge Need* for <30% oxygen at 56 days postnatal age or discharge Severe Need for > 30% oxygen and/or positive pressure (IMV/CPAP) at 36 weeks PMA or discharge Need for > 30% oxygen and/or positive pressure (IMV/CPAP) at 56 days postnatal age or discharge
    • Etiology
      • Multifactorial
      • The major risk factors include
      • prematurity
      • oxygen therapy,
      • mechanical ventilation,
      • infection( u urealyticum)
      • patent ductus arteriosus (PDA)
      • Excessive early intravenous fluid administration
      • genetic predisposition ( inadequate activity of antioxidant enzymes sod, catalase, glutathione peroxidase and ceruloplasmin --- predisposes to o2 toxicity)
      • Familial airway hyperreactivity
      • Increased inositol clearance
    • pathogenesis
      • The most important factor in the pathogenesis of CLD is prematurity
      • Exposure of immature lungs to high O2 concentrations and positive pressure ventilation results in oxidative stress and ventilator induced lung injury (barotrauma/volutruma)
    • Infection
      • Intrauterine infection (chorioamnionitis)
      • Inflammatory cytokines(IL-1,IL6 and TNF alfa)
      • Lung injury and arrest of lung growth
      • U urealyticum is most commonly implicated
      • Several large clinical studies have found a strong correlation between the presence of BPD and the development of late-onset sepsis, usually with organisms such as staphylococcus epidermidis
    • Barotrauma/Volutrauma
      • The most immediate and frequent cause of BPD is the lung injury imposed by mechanical ventilatory support.
      • positive-pressure mechanical ventilation
      • Immature lung
      • Surfactant def
      • Injury to endothelium
      • increased permaebility of serum protiens
      • Inhibition of surfactant
      • Increased surface tension, unequal areation, collapse of alveoli
      • Increased pressure to distend saccules->lung injury, PIP ,pneumothorax.
      • Studies have shown that overdistension of the lung (not increased pressure) is responsible for lung injury in the surfactant-deficient lung
      • volutrauma and not barotrauma is the primary determinant of VILI.
    •  
    • Inflammation
      • oxygen free radicals, pulmonary barotrauma, infectious agents
      • attraction and activation of leukocytes.
      • excessive oxygen free radicals ,tumour necrosis factor, interleukin-1, interleukin-8 (IL-8), and transforming growth factor (TGF)-1
      • breakdown of capillary endothelial integrity and leakage of macromolecules (e.g., albumin) into alveolar spaces.
      • Albumin leakage and pulmonary edema inhibit surfactant function
      • The release of elastase and collagenase from activated neutrophils directly destroys the elastin and collagen framework of the lung.
    • Genetics
      • neonates were more likely to develop BPD if there was a strong family history of atopy and asthma
      • Nickerson found a positive family history of asthma in 77% of infants with RDS who subsequently developed BPD, compared with only 33% who did not .
      • Clark and associates found that only infants with HLA-A2 developed BPD.
    • Clinical and radiologic features
      • Respiratory signs in infants with CLD include fast but shallow breathing, retractions, and paradoxical breathing. Rales and coarse rhonchi are usually heard on auscultation
      • Old BPD, as originally described by Northway, had four distinct stages:
    • Stage I
      • Hyaline membrane.
      • Alveolar and interstitial oedema.
      • Necrosis of bronchial mucosa.
    • Stage II
      • Areas of emphysema
      • Atelectasis
      • Areas of necrosis and repair of bronchial mucosa .
    • Stage III
      • Cystic areas with hyperinflation.
      • Bronchial metaplasia and hyperplasia.
      • Interstitial oedema.
    • Stage IV
      • Hyperinflation,
      • Interstitial streak densities
      • Flatter chest
      • Infants with new BPD show only haziness reflecting diffuse loss of lung volume or increased lung fluid.
      • Occasionally they have dense areas of segmental or lobar atelectasis or pneumonic infiltrates, but they do not show severe over inflation.
    • Old vs New BPD
      • OLD BPD is seen in infants who received aggressive ventilation and were exposed to high inspired oxygen concentration from birth
      • emphysema, atelectasis and fibrosis, and marked epithelial metaplasia and smooth muscle hypertrophy in the airways and in the pulmonary vasculature.
      • NEW BPD occurs in infants who had only mild respiratory failure requiring shorter duration of ventilation and or oxygen therapy immediately after birth.
      • Seen in VLBW infants, earlier stages of gestation , before alveolarization has been completed and associated with antenatal infection.
      • Due to ARREST IN ALVEOLAR DEVELOPMENT
    • Histo-Pathologic characteristics of the ‘New BPD’
      • Decreased, large and simplified alveoli (alveolar hypoplasia)
      • Decreased number and dysmorphic capillaries
      • Variable interstitial fibroproliferation
      • Negligible airway epithelial lesions
      • Variable airway smooth muscle hyperplasia
    • Prevention of BPD
      • BEFORE BIRTH
      • Prenatal antibiotics and infection prevention
      • Prompt treatment of chorioamnionitis with antibiotics.
    • Prevention of bpd
      • Antenatal steroids
      • Use of antenatal steroids in mothers at risk for delivering a premature infant reduces the incidence of neonatal deaths and RDS but does not reduce the incidence of CLD.
      • Antenatal thyrotropin-releasing hormone (TRH) has not been effective in prevention of BPD.
      • Cochrane Database Syst Rev 2004;
    • Practices in delivery room
      • The goal in babies being resuscitated at birth,whether born at term or preterm, should be an oxygen saturation value in the interquartile range of preductal saturations
      • These targets may be achieved by initiating resuscitation with air or a blended oxygen and titrating the oxygen concentration to achieve an SpO2 in the target range using pulse oximetry
      • If blended oxygen is not available, resuscitation should be initiated with air
      • If the baby is bradycardic (HR 60 per minute) after 90 seconds of resuscitation------ increase to 100 % o2.
      • Use lower target inflation pressure range between 20- 25 cm h2o
    • Ventilatory strategies
      • Continuous positive airway pressure (CPAP ):
      • Early initiation of nasal CPAP has been shown to reduce the need for intubation and mechanical ventilation
    • Nasal intermittent positive pressure ventilation (NIPPV)
      • NIPPV is a method of augmenting NCPAP by delivering ventilator breaths via the nasal prongs.
      • Improves the tidal and minute volumes and decrease the inspiratory effort required by neonates as compared to nCPAP
      • The Cochrane review that included three RCTs found a trend towards reduction in rates of chronic lung disease.
      • Nasal intermittent positive pressure ventilation (NIPPV) versus nasal continuous positive airway pressure (NCPAP) for preterm neonates after extubation. Cochrane Database of Systematic Reviews
    • Patient-triggered ventilation (PTV):
      • Patient triggered modes (SIMV, assist-control, and pressure support ventilation) improve the infant-ventilator asynchrony.
      • The Cochrane review concluded that though PTV is associated with shorter duration of ventilation, it does not reduce the incidence of BPD.
      • Synchronized mechanicalventilation for respiratory support in newborn infants. Cochrane Database of SystematicReviews2008
    • High-frequency ventilation (HFV):
      • Animal studies indicate that HFV could lead to less lung injury when compared to conventional ventilation
      • A recent meta-analysis that included 17 RCTs of conventional versus high frequency ventilation found no significant difference in the incidence of BPD
      • Ventilation strategies and outcome in Randomised Trials of High Frequency Ventilation Arch Dis Child. 2005
    • Volume targeted ventilation
      • The Cochrane review that included four RCTs found significant reduction in the duration of ventilation and pneumothorax rates but only a borderline reduction in the incidence of BPD.
      • Volume-targeted versus pressure-limited ventilation in the neonate. Cochrane Database of Systematic Reviews 2005
      • PERMISSIVE HYPERCAPNIA :
      • Hypocapnia that occurs during assisted ventilation is an independent risk factor for BPD
      • Co2 targets of 45-55 mm hg are now recommended in order to reduce the days of ventilation.
      • Permissive hypoxemia: A ccepting lower oxygen saturation values is associated with decreased incidences of CLD and ROP
      • BOOST-trial and STOP-ROP trial indicate that maintaining higher oxygen saturation (>95%) is associated with increased need for oxygen at 36 weeks PMA and greater use of postnatal steroids and diuretics in premature infants (when compared to maintaining lower oxygen saturation of 89-94%).
      • Spo2 b/w 85-93% ---- < 32 wks
      • 87-94%---->32 wks
    • Fluid restriction
      • The systematic review of studies on fluid restriction has not found any significant reduction in the incidence of BPD
      • The amount of fluid restriction in VLBW infants is not definitely known.
      • Fluid restriction for treatment of preterm babies with chronic lung disease. (Protocol) Cochrane Database of Systematic Reviews 2005;
    • Nutrition
      • Aggressive parenteral nutrition and early enteral feeding decreases the incidence of BPD in VLBW infants
      • ( The role of nutrition in the prevention and management of bronchopulmonary dysplasia. Semin Perinatol 2006 )
      • Enteral feeding is often delayed in these infants due to gastrointestinal immaturity, parenteral nutrition with proteins and lipids should be initiated as soon as possible after birth.
      • .
      • Metabolic rate and energy expenditure are elevated in BPD
      • Infants developing BPD require 20 to 40% more calories than their age-matched healthy controls .
      • caloric requirement varies from 120 to 150 Kcal/kg/day
      • More calories– lipids( mct oil)> carbohydrates, lowers respiratory quotient and decreases co2 production.
      • When enteral feeding is started --- give only EBM.
      • Addition of HMF will also increase the calories and make up the deficiencies of protiens and minerals.
      • Mct oil and glucose polymers can also be added.
    • Pharmacological strategies
      • Exogenous surfactant
      • Prophylactic surfactant therapy in infants born before 30 weeks of gestation has not been shown to reduce the incidence of BPD. However, surfactant treatment for established RDS ( ‘rescue therapy’) in infants born at or after 30 weeks of gestation is associated with significant reduction in the incidence of BPD
      • American Academy of Pediatrics Committee on Fetus and Newborn.Surfactant-replacement therapy for respiratory distress in the preterm and term neonate. Pediatrics 2008;
    •  
    • Role of vit A
      • Vitamin A ---integrity of respiratory tract epithelial cells.
      • Very preterm infants are relatively deficient in vitamin A which has been shown to associated with CLD.
      • large dose of intramuscular vitamin A (5000 units three times a week for 4 weeks from birth) decreases the incidence of CLD.
      • (Cochrane Database Syst Rev 2007)
      • All ELBW infants with respiratory distress requiring supplemental oxygen or mechanical ventilation at 24 hours of age should recieve vit A
      • Vit E – antoxidant, no role in prevention of bpd
      • Role of superoxide dismutase :
      • sod antioxidant --eliminates the free radicles
      • Preterms – deficient in antioxidant enzymes and sucesptible to oxidant injury.
      • A RCT enrolled around 300 infants proved the safe nature of the drug CuZnSOD,
      • But did not find any difference in the primary outcome of BPD at 36 weeks PMA.
      • SOD treated infants-- fewer episodes of respiratory illness at I year of age.
      • Cochrane review on this subject conclude that “The use of superoxide dismutase to prevent chronic lung disease of prematurity is not recommended”
    • Methylxanthines
      • caffeine – reduced incidence of BPD .
      • In a multicenter trial , infants < 1,250 g who received caffeine had lower BPD rates than infants who did not receive it.
      • Duration of ventilaton, need for CPAP, and supplemental oxygen were reduced by caffeine administration.
      • ( Adjunctive therapies in chronic lung disease:examining the evidence. Semin Fetal Neonatal Med 2008)
      • Another large RCT that used caffeine for these indications in infants with birth weights of 500-1250g has shown a significant decrease in the incidence of BPD.
      • Caffeine for Apnea of Prematurity Trial Group. Caffeine therapy for apnoea of prematurity. N Engl J Med 2006
      • The authors attributed this rather unexpected finding to reduced duration of mechanical ventilation in the caffeine treated group
    • Indomethacin / Ibuprofen therapy for PDA:
      • Patent ductus arteriosus is one of the major risk factors for BPD.
      • prevention or treatment of PDA should ideally reduce its risk.
      • However, prophylactic use of indomethacin in very low birth weight infants has failed to show any reduction in the incidence of BPD despite a significant reduction in the incidence of PDA
      • (Long-term effects of indomethacin prophylaxis in extremely-low-birth-weight infants. N Engl J Med 2001)
      • Similar results are obtained with ibufrofen.
      • Treatment of symptomatic PDA could possibly reduce the incidence of BPD .
      • Recommendations for the postnatal use of indomethacin: an analysis of four
      • separate treatment strategies. J Pediatr. 1996
    • ROLE OF STEROIDS
      • inflammation ----pathogenesis of BPD
      • Early : During the first 96 hrs after birth
      • Moderately early :Between postnatal days 7 and 14.
      • Delayed :After 3 weeks of age
      • Most commonly used steroid is :dexamethasone
      • AMERICAN ACADEMY OF PEDIATRICS Committee on Fetus and Newborn
    • Systemic Early Postnatal Corticosteroid Therapy <96 Hours
      • preterm, respiratory distress syndrome, and required mechanical ventilation with oxygen at the time of enrollment
      • Corticosteroids (dexamethasone)intravenously within 96 hours after birth.
      • The most commonly used dosages were 0.5 mg/kg of body weight per day for 3 days, followed by a tapering course
      • The combined outcome of death or CLD at 28 days PNA or at 36 weeks’PMA was significantly decreased by early corticosteroid treatment
      • Weaning from mechanical ventilation was more successful in infants treated with dexamethasone.
      • incidences of hypertension, hyperglycemia, insulin therapy for hyperglycemia, gastrointestinal bleeding or perforation, and hypertrophic obstructive cardiomyopathy were increased by early corticosteroid treatment.
      • Borderline increased risk of PVL in steroid group
    • Moderately Early Postnatal Corticosteroid Therapy (7–14 Days PNA)
      • The combined outcome of death or CLD was decreased at 28 days’ PNA and at 36 weeks’ PMA.
      • There was increase in incidence of hyperglycemia, gastrointestinal bleeding, hypertrophic obstructive cardiomyopathy, and infection.
      • AMERICAN ACADEMY OF PEDIATRICS Committee on Fetus and Newborn
    • Systemic Delayed Postnatal Corticosteroid Therapy (>3 Weeks)
      • The incidence of CLD at 36 wks PMA was decreased by steroid therapy.
      • Same side effects.
      • AMERICAN ACADEMY OF PEDIATRICS Committee on Fetus and Newborn
      • The use of inhaled steroids, as well as the use of systemic steroids cannot be recommended as a part of standard practice for ventilated preterm infants to prevent CLD
      • ( Inhaled versus systemic corticosteroids for preventing chronic lung disease in ventilated very low birth weight preterm Neonates Cochrane Database of Systematic Reviews 2008)
    • Inhaled nitric oxide
      • pulmonary vasodilatation ,reduces lung inflammation and promotes lung growth
      • iNO as rescue therapy for the very ill preterm infant does not appear to be effective.
      • Early routine use of iNO in preterm infants with respiratory disease does not improve survival without BPD
      • Inhaled nitric oxide for respiratory failure in preterm infants. Cochrane Database of Systematic Reviews 2010, Issue 12
    • Diuretic therapy:
      • MOA: decreases interstitial and peribronchial fuid--- dec resistance and improves compliance
      • Response: acute response – 1 hr, max clinical response– 1 wk
      • Indication: clinical/radiographic features of pulmonary edema in an infant with evolving or established BPD Pharmacological strategies in the prevention and management of bronchopulmonary dysplasia. Semin Perinatol 2006
      • Dose: 0.5-1 mg/kg, stop after 24- 48 hours if no improvement in clinical condition.
      • no effects on mortality or the incidence of BPD
    • Mast cell stabilizers
      • Cromolyn sodium
      • decrease neutrophil migration and activation ----minimizes inflammation in the lungs
      • Dose: 10-20 mg 6-8 hr , nebulization.
      • 2 trials– no benefit in prevention and treatment.
      • Cromolyn sodium for the prevention of chronic lung disease in preterm infants. Cochrane Database Syst Rev. 2001
    • Associted complications
      • Cor pulmonale
      • Systemic hypertension
      • Systemic to pulmonary shunting
      • Metabolic imbalance– sec to diuretics
      • Infection-- urealasma and mycoplasma----rx with erythromycin
      • Viral infections and fungal infections are also common
      • Cns dysfunction: a neurologic syndrome presenting with EPS signs has been described
      • Hearing loss
      • ROP
      • Nephrocalcinosis
      • Growth failure
    • Discharge planning
      • Spo2 maintained > 92-94%
      • No significant period of desaturation during feeding or sleep
      • Good weight gain
      • Stable respiratory status
    • Immmunization
      • In addition to standard immunization , infants with CLD should receive penumocoocal, influenza and palivizumab
      • AAP RECOMMENDATIONS FOR PALIVIZUMAB
      • Administer monthly beginning in early november for 5 months
      • Dose: 15mg/kg IM
    • OUTCOME
      • MORTALITY: 10-20% in first year of life (infection)
      • Morbidity: increased risk of reactive airway disease , bronchiolitis and pneumonia
      • Rehospitalization rate is twice that of matched controls in first 2 yr of life
      • Growth failure: delayed growth in 1/3 to 2/3 of these infants at 2 years.
    •