Management of Bronchopulmonary dysplasia

Introduction
BPD or bronchopulmonary dysplasia represents a chronic ailment of the lungs, largely occurring among premature babies requiring oxygen therapy and mechanical ventilation for treating severe respiratory distress. It may also develop among immature babies displaying symptoms of early lung-related illness or babies born at their term but requiring rigorous ventilator therapy to treat serious lung ailments. In the last four decades, prenatal steroid administration, surfactant therapy, better nutrition, novel ventilator strategies and other modern treatments have led to significant progress in the medical course and results of premature babies suffering from respiratory distress syndrome (RDS). But in spite of the above advancements, BPD prevalence, on the whole, has remained the same over the last ten years (Gien & Kinsella, 2011).
Bronchopulmonary dysplasia pathophysiology
Babies displaying the greatest likelihood of BPD diagnosis are born at a time when their lungs haven’t yet transitioned to the saccular stage from the canalicular stage. Considering the complex lung development process and the various perinatal factors resulting in BPD development, the condition lacks a straightforward pathophysiology. Owing to the scant available histo-pathological information from BPD patients and preterm babies, current insights into the condition’s pathophysiology have largely emerged from a number of large and small animal models that analyze perinatal inflammation, mechanical ventilation, and oxygen toxicity impacts on babies’ lung development. While the aforementioned simplified BPD models merely approximate the condition among human patients, they have contributed significantly to improving insights into the condition’s pathophysiology (Collins et al., 2017).
Current and past management strategies
Though antenatal steroids, caffeine therapy, protective ventilation approaches, optimized nutrition, focused oxygen saturation targets, and treatment with vitamin A have, certainly, modestly improved BPD outcomes, a majority of modern treatments are supportive.
Surfactant
Administering surfactants featured one among the most salient treatments for decreasing preterm child mortality and altering BPD characteristics. Initial surfactant administration enabled instant extubation to the less-intensive ventilator techniques, thereby decreasing BPD development risks. Formerly, administration of surfactants was linked strictly to mechanical ventilation and intubation. At present, animal-lung surfactants, sometimes modi?ed through lipid addition, are utilized. The steep cost of production of such preparations and scant raw material availability has led to numerous attempts at producing synthetic surfactants. Apparently, synthetic surfactants with a relatively more complex composition of phospholipids and two peptides can work as imminent replacements for natural surfactants. However, more experiments are needed prior to drawing conclusions regarding their ideal composition (Tropea & Christou, 2012).
Diuretics
Diuretics are commonly utilized to treat BPD. One key BPD aspect is interstitial alveolar edema which, in excess, may reduce lung compliance. Factors playing a role in pulmonary edema development include capillary leaks owing to ventilator-produced lung injury or infection-linked inflammation, iatrogenic fluid administration increase, and overload of volume on account of left-right shunting across the ductus arteriosus. The potential advantages of diuretics include increased fluid reabsorption from lungs (Collins et al., 2017).
Bronchodilators
BPD increases airway resistance on account of smooth-muscle hyper-reactivity and hypertrophy. Bronchodilators commonly help relieve bronchospasms among asthmatics. Their utility has also been examined among the BPD population. Researchers reveal bronchospasms play a role in intensifying pulmonary resistance among preterm babies, with bronchodilators improving dynamic compliance through reducing pulmonary resistance. These drugs have, broadly, been grouped into anticholinergic and adrenergic agents. They have a transitory impact, with both groups significantly improving compliance and decreasing pulmonary resistance among BPD patients. Variability in patients’ ?-agonist response can be genetically established [27–29]. A lone Cochrane database trial involved bronchodilators use in preventing BPD and a measurement of long-term results. Ipratropium and albuterol are the most commonly-administered bronchodilators. Among -sympathomimetic agents’ possible adverse effects are hyperglycemia, hypokalemia, tachycardia, and arrhythmias. Additionally, inhalation of anticholinergic agents reduces gastrointestinal motility, besides making respiratory secretions thick and dry. Ipratropium and albuterol have historically been prescribed in combination for achieving synergism effects. Research has yet to investigate whether anticholinergic- ?-agonist medication, combined, improves BPD patient outcomes as compared with albuterol prescribed alone (Collins et al., 2017).
Steroids
Inflammation contributes significantly to BPD pathogenesis. Owing to corticosteroids’ powerful anti-inflammatory properties, several trials by scholars have studied steroid usage in treating BPD. Systemic administration of steroids is linked to decreased inflammatory reaction, easy weaning from therapy using mechanical ventilation, and swift pulmonary function improvements with improved gas exchange. Besides their anti-inflammatory impacts, steroids have the following positive impacts: increased surfactant generation, capillary leakage stabilization, reduced lung fibrosis, on the whole, reduced airway edema, and amplified ?-adrenergic activity. The role of inhaled as well as systemic corticosteroids in preventing and treating BPD among preterm babies has enjoyed extensive scholarly analysis. Steroid trials can be classified based on administration time. Preliminary administration is that which takes place within 8 days of birth. According to a Cochrane database meta-analysis, 28 randomized controlled trials assessed the impacts of preliminary dexamethasone treatment on BPD prevalence. Steroids reduced BPD prevalence and facilitated extubation (Collins et al., 2017).
Personal experience managing Bronchopulmonary dysplasia
Severe BPD-diagnosed children on oxygen therapy are carefully supervised within outpatient facilities. While utilizing home-based pulse oximeters usually proves vital, it may be stressful to caregivers owing to oximeters’ tendency to frequently raise false alarms. In supplemental oxygen weaning, the fundamental principle is: pulse oximetry ought to be utilized, with oxygen saturations being ?92 percent, especially in case of presence of pulmonary hypertension. At patient homes, 100% oxygen may be delivered through the nasal cannula; hence, the titration of flow rate in the weaning stage. Few researches have attempted to ascertain the right flow rate for safe oxygen discontinuation. Abman and colleagues’ prospective research revealed that babies on ?20 mL/kg oxygen enjoyed greater success when weaning to the room’s air. In case of poor growth, extended nocturnal oxygen use might be necessary. To sum up, for a number of sBPD-diagnosed babies, safe outpatient supplemental-oxygen usage may facilitate continued infant progress at home rather than within neonatal ICU settings (Abman et al., 2017).
Bronchopulmonary dysplasia protocol
Prevention and Management of BPD
Antenatal:
Premature birth prevention is considered the ideal BPD prevention measure. It is imperative to provide sound antenatal care incorporating strategies for preterm labor prevention and appropriate prenatal corticosteroid, tocolysis, and erythromycin usage for high-risk patients (Patel & Cherian, 2016).
Postnatal:
It is crucial to adopt an all-inclusive, non-ventilatory- and ventilatory-based approach. Respiratory management ought to:
• Follow existing preterm-baby stabilization/resuscitation guidelines, appropriately utilize surfactants, and personalize early RDS-linked respiratory management (non-invasive vs. invasive respiratory support).
• The following ventilatory goals ought to be set: gentle ventilation, adequate oxygenation and permissive hypercapnia, with large, regular oxygenation swings avoided (Patel & Cherian, 2016).
Fluid and nutrition:
· Careful fluid management, with extreme care taken to avoid fluid overload.
· Gastro esophageal reflux management
· Nutritional management for supporting optimum growth. This should encompass head circumference and weight monitoring on a weekly basis. The daily caloric consumption goal ought to be 120-150 kcal/kg. BPD babies’ growth failure is largely because of malnutrition, exacerbating the condition through compromised lung growth and potential lung injury repairs (Patel & Cherian, 2016).
Caffeine:
Infants being treated using mechanical ventilation seem to benefit more from caffeine, particularly if it is started within the first three days after birth.
· Every premature baby weighing extremely low at birth, particularly babies on non-invasive support and mechanical ventilation ought to be administered caffeine commencing from three days after birth up to 34-36 weeks PMA (postmenstrual age) unless contraindicated.
· Dosage: Caffeine citrate – 20mg/kg loading and subsequent 5-10 mg/kg/day (Patel & Cherian, 2016)
Diuretics:
Furosemide (loop diuretics) as well as diuretics like spironolactone and thiazide that act on distal renal tubules facilitate reabsorption of lung fluids and bring about pulmonary mechanics improvements. Their short-run benefits include; greater lung compliance, reduced oxygen requirement, and transitory airway resistance improvement.
· Diuretics might be considered in case of fluid overload symptoms among ventilator dependent babies with established or developing BPD and high oxygen-needing non-ventilated BPD babies (Patel & Cherian, 2016).
Corticosteroids:
Systemic postnatal corticosteroids, which reduce lung inflammation, have facilitated BPD prevention and treatment for the last three decades. Steroids decrease: polymorphonuclear leucocyte recruitment to lungs, pulmonary edema, vascular permeability, inflammatory mediator (e.g., prostaglandin) production, and fibrosis thereby modulating repair.
Hydrocortisone displays mild anti-inflammatory properties, a short half-life of 8-12 hours, and high mineralocorticoid activity. Existing evidence reveals hydrocortisone to be the first-line postnatal systemic corticosteroid utilized among ventilator-dependent babies (Patel & Cherian, 2016).
DOSAGE: Hydrocortisone regime: 5 mg/kg/day in four divided doses for a week, and subsequently 3.75 mg/kg/day for five days, 2.5 mg/kg/day for five days and 1.25 mg/kg/day for five days. The overall dosage is: 72.5 mg/kg over twenty-two days.
· Carefully monitor adverse effects and progress, aiming for earliest possible extubation.
· Use dexamethasone only for “rescue” purpose
Multidisciplinary discharge planning
· Explicit feeding regime. If required, the input of dietetic and SALT teams ought to be sought
· Home oxygen: Refer to CPR training, separate guidelines, and parent-focused health education
· Immunization: influenza and regular inoculation at the right age; also, RSV protection using Palivizumab
· Follow-up appointments with outpatient physicians, together with compulsory neurodevelopmental evaluation
· Community support on the part of neonatal outreach personnel, and arrangement for swift access during emergencies (Patel & Cherian, 2016)
Conclusion
While a significant growth in data on BPD pathogenesis has been achieved of late, not every mechanism resulting in lung damage has been comprehensively understood. This explains why theoretically-sound therapeutic strategies have enjoyed partial success or even failure. But prematurity prevention, caffeine and surfactant administration, and systematic nonaggressive ventilator usage may appreciably decrease BPD development risk.














References
Abman, S. H., Collaco, J. M., Shepherd, E. G., Keszler, M., Cuevas-Guaman, M., Welty, S. E., ... & Kirpalani, H. (2017). Interdisciplinary care of children with severe bronchopulmonary dysplasia. The Journal of pediatrics, 181, 12-28.
Collins, J. J., Tibboel, D., de Kleer, I. M., Reiss, I. K., & Rottier, R. J. (2017). The future of bronchopulmonary dysplasia: emerging pathophysiological concepts and potential new avenues of treatment. Frontiers in medicine, 4, 61.
Gien, J., & Kinsella, J. P. (2011). Pathogenesis and Treatment of Bronchopulmonary Dysplasia. Current Opinion in Pediatrics, 23(3), 305–313. http://doi.org/10.1097/MOP.0b013e328346577f
Patel, V. & Cherian S. (2016). Management of Bronchopulmonary Dysplasia / Chronic lung disease. Retrieved 17 May 2018 from http://www.cardiffnicu.com/Portal/Respiratory/Chronic%20lung%20disease%20guideline.pdf
Tropea, K., & Christou, H. (2012). Current pharmacologic approaches for prevention and treatment of bronchopulmonary dysplasia. International journal of pediatrics, 2012.