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Bronchopulmonary Dysplasia John Salyer RRT-NPS, MBA, FAARC Director Respiratory Therapy Seattle Children’s Hospital and Research Institute

Bronchopulmonary Dysplasia

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Bronchopulmonary Dysplasia . John Salyer RRT-NPS, MBA, FAARC Director Respiratory Therapy Seattle Children’s Hospital and Research Institute. A Little History. Originally described by Northway in 1967 Report of a series of 32 patients in NEJM, average gestational age 32 weeks - PowerPoint PPT Presentation

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Page 1: Bronchopulmonary Dysplasia

Bronchopulmonary Dysplasia

John Salyer RRT-NPS, MBA, FAARCDirector Respiratory Therapy

Seattle Children’s Hospital and Research Institute

Page 2: Bronchopulmonary Dysplasia

A Little History

Originally described by Northway in 1967

• Report of a series of 32 patients in NEJM, average gestational age 32 weeks

• All were treated with 100% oxygen, then prolonged mechanical ventilation with 80-100% oxygen

• Before mechanical ventilation was available the usual course of RDS was several days of severe lung disease to which the infant either succumbed or recovered completely in 7-10 days

Page 3: Bronchopulmonary Dysplasia

History (cont.)

• The addition of mechanical ventilation led to appearance of a new syndrome– Stage I, days 1-3, HMD (RDS)

– Stage II, days 4-10, opacification of lungs, with bronchiolar and alveolar necrosis

– Stage III, days 10-20, transition to a CXR with a reticular network of small rounded areas of radiolucency, emphysematous and atelectatic airspaces, with pulmonary fibrosis

– Stage IV, hyperexpanded and cystic lungs. cor pulmonale

Page 4: Bronchopulmonary Dysplasia

Definition

• Shennan noted that if oxygen requirement at 36 weeks used as threshold over 50% of infants would have abnormal pulmonary follow-up (Shennan, 1988)

• Now usually defined as requirement for supplemental oxygen at:

– 36 weeks postmenstrual age if born at or before 32 weeks’ gestational age

– 4 weeks of age if born after 32 weeks’ gestational age

Page 5: Bronchopulmonary Dysplasia

Physiologic Test

• BPD if at 35-37 weeks post menstrual age:– receiving mechanical ventilation, or

– CPAP, or

– >30% oxygen with saturation <96%

– If infant is receiving <30% oxygen or ≥30% oxygen with saturation >96% then:

• Wean O2 to room air

• No BPD if saturation > 90% in room air for 30 minutes

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Pathology Classic BPD

• Airway injury

• Epithelial metaplasia with type II cell hyperplasia

• Smooth muscle hypertrophy

• Parenchymal fibrosis, alternating with emphysema

• Capillary dysplasia

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Low power view of lung from infant who died from BPD at 2.5 months of age. Note alternating areas of emphysema and atelectasis, and strands of fibrosis.

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Smooth Muscle Hyperplasia

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Albertine et al., Am J Respir Crit Care. 2008

Histology of BPD

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Classic BPD

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Classic vs. New BPD• Much of the histologic findings of “old

BPD” seen in animal models with oxygen toxicity

• New epidemiology– Most common in ELBW infants

– Risk factors: low gestational age, postnatal infection, maternal chorioamnionitis, PDA, mechanical ventilation

– Some ELBW infants do not have RDS, with minimal early oxygen or mechanical ventilation

Page 14: Bronchopulmonary Dysplasia
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Clinical Presentation “New” BPD

• Hazy lungs on CXR, with minimal cystic emphysema, or hyperinflation

• Less airway reactivity

• Less pulmonary hypertension (blue spells, “twits”)

• Pathology– Minimal fibrosis, minimal airway injury

– Decreased alveolar septation and microvascular development

Page 16: Bronchopulmonary Dysplasia

CXR New BPD Old BPD

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Division of Respiratory Bronchioles

• 20 to 32-36 weeks 3 generations of saccular septations, forming 524,000 respiratory bronchioles

• Hypothesized that the further septation of respiratory bronchioles disrupted by inflammation/injury in new BPD

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Pathology New BPDArrest of Alveolarization

• Increased saccular diameters, fewer saccules (alveoli)

• Collagen network disrupted, elastin not localized to fibers for secondary septation

• No severe inflammation

• Saccules lined with dysplastic type II cells

• Seen in post-natal mice and rats exposed to inflammation or hyperoxia

Page 19: Bronchopulmonary Dysplasia

Pathogenesis “New” BPD:Overview

• Immaturity of structure and function before about 32 weeks’ gestation– Poorly developed airway supporting

structures– Surfactant deficiency– Decreased compliance– Underdeveloped antioxidant mechanisms– Inadequate fluid clearance

• Inflammation– Mechanical ventilation– Oxygen toxicity– Infection

Page 20: Bronchopulmonary Dysplasia

Pathogenesis:Mechanical Injury

• Over-distension of airways and airspaces (Volutrauma)– Excessively large tidal volumes, not pressure

(Hernandez, 1989)– Association of decreased PCO2 with increased

risk BPD (Garland, 1995)– Maximum end-inspiratory volume more important

than tidal volume or FRC (Dreyfuss, 1993)– As few as 6 large manual inflations was enough to

increase the lung damage premature lambs (Bjorklund, 1997)

– Positive pressure causes bronchiolar lesions (Nilsson, 1978)

Page 21: Bronchopulmonary Dysplasia

Pathogenesis:Oxygen Toxicity

• Safe FiO2 level and duration are unknown

• Cell damage from reactive oxygen metabolites– Cell enzyme inactivation

• Preterm infants may have inadequate antioxidant defenses– Nutrient deficiencies– Immature enzyme development

Page 22: Bronchopulmonary Dysplasia

Pathogenesis:Infection

• Four-fold increase in BPD incidence with sepsis (Rojas, 1995)

• Due to increased concentration of proinflammatory cytokines in amniotic fluid?

• Association with Ureaplasma urealyticum (Hannaford, 1999)

• Maternal chorioamnionitis associated with decreased RDS, but increased risk of BPD

Page 23: Bronchopulmonary Dysplasia

Pathogenesis:Inflammation

• Macrophages, lymphocytes, platelets in lung will release inflammatory mediators– Cytokines– Lipid mediators– Platelet factors (Ozdemir, 1997)

• Complement activation• Increased vascular permeability• Protein leakage• Mobilization of neutrophils into interstitial

and alveolar compartments– Release of reactive oxygen radicals, elastase,

collagenase– Increased MIP-1 and IL-8, reduced IL-10 (Jobe

2001)

Page 24: Bronchopulmonary Dysplasia

Normal Alveolus

Injured Alveolus (Acute Phase)

Alveolar air spaceType I cell

Surfactant Layer

Type II cell

Interstitium

Capillary

Alveolar macrophage

Sloughing bronchial epithelium

Edema fluidNecrotic or Apoptotic Type I cell

Red cell

Cellular debris

Hyaline membrane

Fibrin

Widened, edematous interstitium(interstitial pneumonia)

TNFIL

Red cell

Inactivated surfactant

Activated neutrophil

Page 25: Bronchopulmonary Dysplasia

Cardiopulmonary function in BPD

• Decreased tidal volume• Increased airway resistance• Decreased dynamic lung

compliance• Uneven airway obstruction

– Gas trapping– Hyperinflation– Abnormal distribution of

ventilation• Bronchomalacia

Page 26: Bronchopulmonary Dysplasia

Pulmonary Edema in BPD

• Reduced cross sectional area of pulmonary vessels causes increased pulmonary vascular resistance

• Alveolar hypoxia induces local vasoconstriction

• Intact vessels must accept remaining pulmonary blood flow, which leads to– elevated pressure and RV afterload– increased fluid filtration in

interstitium

Page 27: Bronchopulmonary Dysplasia

Clinical Course of BPD

• Most: gradual improvement over weeks or months

• Some: marked pulmonary instability in first few weeks followed by weeks or months of ventilator dependence

• Few: pulmonary hypertension and cor pulmonale

Page 28: Bronchopulmonary Dysplasia

Prevention of BPD

• Antenatal glucocorticoid steroids - lead to decreased incidence RDS, but only modest decrease in BPD

• Nutrition – although poor growth is associated with BPD, no studies show impact of nutrition in altering risk for BPD

• Vitamin A – Slight decrease in BPD with IM supplementation in ELBW infants (Darlow, 2011), UW study showed increased sepsis with IM vit A (48.5% vs. 12%), but no decrease BPD

• Surfactant – decreases risk of pneumothorax, improves survival, decreases need for oxygen and ventilation, but no decrease in rate of BPD.

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Prevention of BPD (cont.)

• Limited oxygen – SUPPORT trial with lower oxygen targets saw decreased incidence of ROP, but increased mortality and no decrease in BPD

• Permissive hypercapnea – Target of pCO2>52 vs. <48 not associated with decreased BPD in ELBW, but decreased ventilation at 36 wks (Carlo, 2002)

• HFOV – not associated with decreased BPD compared to modern conventional ventilation

Page 30: Bronchopulmonary Dysplasia

Prevention of BPD (cont.)

• PDA treatment – incidence of PDA goes up with ligation (Chorne, 2007)

• Inhaled Nitric Oxide – NO-CLD trial showed decreased BPD in treatment group. Survival without BPD 43.9% vs. 36.8% (Ballard, 2006)

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Ventilation Strategy for CLDSettings

1. Slow Respiratory Rates– < 40 breaths/min

2. PIP (lowest required)– target VT 5-10 mL/kg– Not ECLS candidate

3. PSV/VG4. PEEP

– 5-6 (up to 12 for bad TM) 5. Short Inspiratory Times

– 0.4-0.7 s

Blood Gases

1. Permissive Hypercapnea– pCO2 levels 45-65*– pH 7.25-7.35

2. Less Aggressive Oxygenation Goals– paO2 45-55*– Saturations 85-92%

Page 32: Bronchopulmonary Dysplasia

p=< 0.05

Page 33: Bronchopulmonary Dysplasia

Management of established BPD:Bronchodilators

• Beta-2 agonists (albuterol, terbutaline) acutely decrease airway resistance and increase compliance

• Only one controlled clinical study of outcomes (Denjean, 1992)– 173 infants < 31 weeks, vent at 10 days– No effect on survival, severity of BPD,

duration of vent or oxygen use

Page 34: Bronchopulmonary Dysplasia

Management of established BPD:Bronchodilators

• Recommendation (not evidenced-based!)– Use albuterol for short-term

effects or to treat acute deterioration

– Discontinue if no improvement in gas exchange, work of breathing, or number of respiratory decompensations

– Watch for tachycardia, arrhythmia, hypokalemia, irritability

Page 35: Bronchopulmonary Dysplasia

Management of established BPD:Acute Exacerbations

• Consider viral infections (usually not bacterial)

• Consider tracheitis if purulent secretions

• Obtain CXR (although rarely helpful)• Culture and gram stain of tracheal

secretions if purulent (often misleading)

• Try dose of furosemide• Try inhaled albuterol, and if poor

response, try ipratropium• Consider inhaled corticosteroids• Consider systemic corticosteroids

for 5 days, esp. if at term corrected age

Page 36: Bronchopulmonary Dysplasia

Web Resources for Parents

• http://www.nhlbi.nih.gov/health/dci/Diseases/Bpd/Bpd_WhatIs.html– Excellent description of BPD for lay audience from the National

Heart Lung and Blood Institute

• http://www.nlm.nih.gov/medlineplus/ency/article/001088.htm– Very brief review of BPD from National Library of Medicine’s

Medline Plus website

• http://depts.washington.edu/growing/Assess/BPD.htm– Description of BPD with emphasis on home care and nutritional

issues from Donna Johnson at the University of Washington

Page 37: Bronchopulmonary Dysplasia

The End