Bronchopulmonary Dysplasia

Introduction

• BPD is a chronic lung disease affecting both the alveoli and the pulmonary vasculature. It is the most common sequela of premature birth at less than 37 weeks gestational age.¹
• Major global cohort studies demonstrate BPD prevalence between 11-50% in premature infants, with the wide range in values attributed to differences in gestational age or birth weight criteria used to determine a BPD diagnosis.²
• The strongest risk factors for BPD include premature birth and low birth weight.2 Other risk factors include intrauterine growth restriction, antenatal infection, and maternal tobacco usage.¹

Etiology and Pathophysiology

Classic BPD^1,3

• “Classic BPD,” first described in 1967 by Northway and colleagues, referred to a severe lung injury resulting from barotrauma and oxygen injury in preterm infants with respiratory distress syndrome requiring positive pressure ventilation.
  • The average gestational age of infants in this original cohort was 34 weeks. Thus, lung development was interrupted during alveolar development (Figure 1).
  • Northway described four stages of BPD:
    • Acute respiratory distress syndrome
    • Development of pulmonary edema due to the presence of a persistent ductus arteriosus with increased left-to-right shunt
    • Progression to chronic disease with development of pulmonary vascular remodeling and fibroproliferative changes
    • Manifestation of irreversible chronic lung disease, often associated with a high mortality as a result of severe respiratory failure and cor pulmonale
  • Patients with classic BPD had characteristic chest radiograph findings showing alternating areas of lung overinflation and fibrosis (Figure 2).

• The definition and clinical characteristics of BPD have evolved over time with advancements in neonatal care, such as antenatal steroid administration, surfactant therapy, and improved ventilator strategies designed to avoid barotrauma.
• These strategies have allowed for the survival of more preterm infants, including extremely low gestational age newborns (born at less than 28 weeks gestational age) and extremely low birth weight infants (birth weight less than 1,000 grams).²

New BPD^1,3,4

• “New BPD” is caused by arrested lung development rather than acute lung injury.
  • The average gestational age of infants with new BPD is 28 weeks or less.
  • Lung development is interrupted much earlier, during the time of canalicular and saccular development (Figure 1). This growth arrest results in:
    • Simplified alveoli with reduced alveolar surface area for gas exchange.
    • Thickened muscular layers between the alveoli and pulmonary arterioles, leading to an increase in pulmonary vascular resistance (PVR) and the development of PH.
    • Pulmonary inflammatory reaction caused by infection, mechanical ventilation, or oxygen toxicity during the perinatal period.
  • Chest radiographs are less likely to reveal the severe fibrosis and cystic changes characteristic of classic BPD (Figure 3).
  • The current National Institutes of Health definition of BPD uses postmenstrual age (gestational age + time elapsed from birth) and supplemental oxygen requirement to assign disease severity (Table 1).

Complications of BPD^1,3,5,6

• Patients with BPD experience persistent airway obstruction and hyperreactivity.
• Infants requiring prolonged tracheal intubation and mechanical ventilation may develop tracheomalacia and/or bronchomalacia. Subglottic stenosis, airway granulomas, and pseudopolyps can also result from prolonged tracheal intubation.
• Rehospitalization for respiratory illness occurs at increased frequency in patients with BPD less than 2 years of age. Common causes include reactive airway disease, pneumonia, or respiratory syncytial virus.
• “BPD spells” are acute cyanotic events caused by increases in central airway compliance. They are seen in older infants with BPD.
• The incidence of PH in mild, moderate, and severe BPD is estimated at 5%, 18%, and 41%, respectively, in a 2025 meta-analysis. Mortality is significantly higher in BPD infants who develop PH.

Preanesthetic Evaluation

Respiratory Status³

• The preoperative history should specifically investigate:
  • Prior anesthetic history
  • Cough or sputum production
  • Baseline home oxygen use and recent changes in oxygen requirements
  • Exercise tolerance: poor exercise tolerance may present as diaphoresis or cyanosis during feeding in infants
  • Current medications/allergies with specific attention paid to inhaled bronchodilators or steroids, diuretics, and pulmonary vasodilators (e.g., sildenafil, bosentan, calcium channel blockers)
  • Prior hospitalizations, including the need for tracheal intubation.
• Physical examination should evaluate:
  • Vital signs, including baseline room air oxygen saturation.
  • Presence of wheezing, cough, or cyanosis
  • Accessory muscle use
  • Hydration status
  • Nutritional status

PH3

• Patients with moderate or severe BPD should be screened for PH via echocardiography or cardiac catheterization.
• A continued need for positive pressure ventilation, oxygen requirement out of proportion to the degree of lung disease, failure to thrive, recurrent cyanotic episodes, frequent hospitalizations, and elevated PaCO₂ should also prompt screening for PH.

Additional Sequelae of Prematurity⁷

• Patients should be screened for additional complications of premature birth such as retinopathy of prematurity, patent ductus arteriosus, intraventricular hemorrhage, necrotizing enterocolitis, or persistent apneas/bradycardias as these conditions may also affect anesthetic management.

Anesthetic Management

• Anesthetic management focuses on avoiding bronchospasm or increases in PVR.
• Patients with BPD should not undergo general anesthesia for elective procedures during acute respiratory infections due to the high risk of bronchospasm.³
• Premedication with oral midazolam aids in reducing anxiety-induced bronchospasm. Caution is advised in patients with PH or upper airway disease, as oversedation may lead to hypercarbia, hypoxemia, and airway obstruction.³
• Consider stress-dose steroids in children with a history of systemic corticosteroid use.²
• Airway management technique (mask vs. laryngeal mask airway vs. endotracheal tube) depends on procedural needs and existing lung morbidity. Children with severe BPD may require endotracheal tube placement and mechanical ventilation due to low lung compliance.¹
• Tracheal intubation may precipitate bronchospasm. Ensure a deep plane of anesthesia prior to airway manipulation. Consider nebulized β2-adrenergic agonists for patients with reactive airway disease before the induction of anesthesia. Consider regional or neuraxial anesthesia whenever possible.²
• Modern ventilation strategies target low peak inspiratory pressures (14-20 cm H2O) and moderate peak end-expiratory pressure (4-6 cm H2O). SpO₂ levels between 90% and 95%, as well as arterial CO₂ levels of 55-65 mmHg, are accepted if pH greater than 7.3 can be maintained with the ventilator settings.^1,8
• Intraoperative bronchospasm or airway collapse poses serious risks and can quickly lead to profound hypoxemia, acute PH, right-sided heart strain, arrhythmias, and death.^2,3,6
• Increases in PVR must be treated aggressively to avoid descent into a pulmonary hypertensive crisis. Moderate hyperventilation with 100% oxygen, correction of metabolic and respiratory acidosis, improved analgesia, and the administration of pulmonary vasodilators should be initiated.^2,3,6
• Inhaled nitric oxide is typically the pulmonary vasodilator of choice given its rapid onset and ease of administration. Inotropic support should be initiated for persistent systemic hypotension despite the initiation of pulmonary vasodilator therapy.^2,3,6
  • Consider the possibility of intensive care unit admission and mechanical ventilation postoperatively, depending on the nature of the procedure, its length, and the severity of the disease.²