The Hive 2017

Combating chronic lung disease in prematurely born infants

Trish Lowe MACN, ACN Nurse Educator

Of the 310,330 live babies born in Australia in 2014, approximately 91% were born at term (37–41 weeks) and 9% were pre-term (before 37 completed weeks’ gestation) (Australian Institute of Health and Welfare (AIHW) 2016, p. 4). Premature birth is associated with a range of adverse outcomes – most notably lung dysfunction – which has the potential to impact on the health of effected individuals throughout their lifespan (Carter, Granty & Carter, 2016, p. 921). As the survival rates of prematurely born infants continues to rise, interdisciplinary cooperation is being directed towards improving the quality of survivors’ lives. This article describes the pathological processes leading to lung disease in prematurely born infants and some of the initiatives being implemented to enhance respiratory outcomes.

Foetal lung development commences at three weeks’ gestation and occurs in stages (Blackburn, 2013, p. 311). By 24–26 weeks, terminal air sacs emerge as outpouching of the terminal bronchioles (Blackburn, 2013, p. 311). During this “saccular phase”, the number of terminal sacs increase dramatically – from 240,000 at 24 weeks to four million at 32–36 weeks – as does lung surface area and volume (Blackburn, 2013, p. 311). It is at this stage that surfactant synthesis begins.

Surfactant is a phospholipid which reduces surface tension, the inspiratory force required to inflate the lungs and maintain residual functional capacity (Carlson, 2014, p. 364). Surfactant synthesis occurs in early gestation but escalates dramatically in the weeks preceding birth, to the highest level of any time in life (Carlson, 2014, p. 364). This process, along with respiratory movements in utero and the secretion of thyroid hormone and growth factors, prepares the infant for independent respiration (Carlson, 2014, p.364). The capacity for optimal gas exchange is enhanced, as developing blood vessels stretch the pulmonary epithelium, bringing pulmonary capillaries and alveolar surfaces into close proximity (Blackburn, 2013, p. 311).

Babies born prior to 30 weeks gestation are at risk of developing hyaline membrane disease, bronchopulmonary dysplasia and chronic lung disease. Hyaline membrane disease (HMD) occurs as a result of the pulmonary underdevelopment described and surfactant insufficiency (Carlson, 2014, p. 364). Due to linear lung development, the risk of HMD is inversely related to gestational age, with an incidence of 60% at 29 weeks, falling to 20% by 34 weeks gestation (Carlson 2014, p. 458). Broncho-pulmonary dysplasia (BPD) is a chronic lung disease first reported by Northway, Rosan and Porter, in 1967. It is a condition which develops as a result of barotrauma, following the mechanical ventilation and oxygen therapy used to treat respiratory distress and hyaline membrane disease, in premature infants (Davidson & Berkelhamer, 2017).

Respiratory Distress Syndrome (RDS) presents as rapid, labored breathing and sub-optimal oxygenation. It is best treated by the provision of minimally injurious respiratory support, early exogenous surfactant administration, the judicious use of supplementary oxygen and early closure of the patent ductus arteriosus (Carlson, 2014, p. 458; Davidson & Berkelhamer, 2017). As indicated, the condition is most commonly attributable to HMD. However, with sepsis, congenital cardiac disease and renal impairment, neurological and metabolic causes must be excluded as contributing causes (Gallacher, Hart & Kotecha, 2016, p. 32). Serial radiology and echocardiography are crucial to identify the underlying cause, and to direct and monitor treatment (Gallacher, Hart & Kotecha, 2016, p. 32).

Treating respiratory distress, paradoxically interferes with alveolarisation and vascularisation, leading to “arrested lung development” (Gardner, Enzman Hines & Nyp, 2016, p. 604). Therefore, the provision of minimally invasive respiratory support to maximise gas exchange, whilst protecting the developing lung tissue, is required (Gallacher, Hart & Kotecha, 2016, p. 32). Notwithstanding this awareness, chronic and recurring lung injury, alveolar haemorrhage, micro-atelectasis, hyper-expansion and oedema, continue to feature as pre-cursors to the development of chronic lung disease in prematurely born infants (Gardner Enzman Hines & Nyp, 2016, p. 604). Even during the post-acute phase, barotrauma, chronic inflammation and infection, further damage lung tissue (Gardner, Enzman Hines & Nyp, 2016, p. 604). Medications such as steroids and diuretics, feature heavily in treatment regimens and may be required to manage acute exacerbations of chronic conditions (Gallacher, Hart & Kotecha, 2016, p. 32).

The terms broncho-pulmonary dysplasia (BPD) and chronic lung disease (CLD) are often used interchangeably. However, BPD is only one of many conditions with the capacity to chronically impact on respiratory health. Others include pulmonary atresias, pneumonia, congenital heart disease and meconium aspiration syndrome (Gardner, Enzman Hines & Nyp, 2016, p. 603). Definitive diagnosis is made based upon an infant’s requirement for supplemental oxygen at 28 days of life – and/or 36 weeks corrected gestational age – with the length of supplemental oxygen dependency, used to indicate disease severity (Gallacher, Hart & Kotecha, 2016, p. 34; Gardner, Enzman Hines & Nyp, 2016, p. 604). It is not uncommon for prematurely born infants to be discharged home on supplemental oxygen and to require regular hospitalisations for acute exacerbations of respiratory conditions, throughout infancy.

The increased survival rate of prematurely born babies has been attributed to: birth in hospital, maternal steroid administration, exogenous surfactant use, fewer days’ mechanical ventilation (with associated reduction in risk of barotrauma), improved oxygenation and oxygen saturation targeting (Gardner, Enzman Hines & Nyp, 2016, p. 603). However, notwithstanding recent theoretical and technological advances, BPD remains the most common morbidity associated with prematurity. Incidence rates remain at approximately 40% for babies born at – or less than – 28 weeks’ gestation (Carter, Granty & Carter 2016, p. 921).

Therefore, interdisciplinary cooperation is being targeted towards addressing the ongoing pulmonary, nutritional, pharmacological and neurodevelopmental requirements of effected infants (Davidson & Berkelhamer, 2017). Most notably, research has focussed upon refining methods of non-invasive respiratory support. For example, a new continuous positive airway pressure (CPAP) protocol developed in Canberra, named CICADA (CeasIng Cpap At standarD criteriA) has shown promising results.

Heath, Jeffery, Broom, Shadbolt and Todd (2016, p. 321) studied babies born at less than 30 weeks, over three distinct time periods, spanning January 2004 – December 2012. Their findings highlighted the benefits of ceasing CPAP altogether, when clinical stability was evident, rather than following a protocol of slow weaning. Study findings revealed significantly reduced CPAP duration, time to wean, oxygen duration and CLD rates (Heath Jeffrey et al., 2016, p. 321). Early cessation also expedited positive outcomes, such as the transition to full feeds and transfer from neonatal intensive care to the special care nursery (Heath Jeffrey et al., 2016, p. 321).

Post discharge outcomes associated with low birth weight and BPD have traditionally included: pulmonary hypertension, growth failure, recurrent hospitalisations, adverse neurological outcomes, low tone, early motor delay and cerebral palsy (Carter, Granty & Carter 2016, p. 921). As medical management results in increasing numbers of adult “survivors”, it is possible that resultant pulmonary dysfunction, asthma-like symptoms and exercise intolerance may lead to significant long-term pulmonary sequalae and present a burden for patients, their families and the health system (Davidson & Berkelhamer, 2017). Therefore, any advancement in treatment protocols such as that described by Heath Jeffrey et al., (2016) are extremely encouraging and welcomed.

Almost 1:10 babies are born prematurely with ongoing lung dysfunction, impacting throughout the life span. As survival rates increase, the need to minimise lung damage and vigilantly avoid treatment regimens known to negatively impact on lung development, are required. One of the ways this can be achieved is by the employment of minimally injurious, non-invasive, respiratory support. To this end, interdisciplinary cooperation is being directed towards the finessing of treatment regimes to improve neonatal outcomes and the respiratory health of survivors.

Editor’s note: Trish designs and develops our Graduate Certificate in Neonatal Care. This graduate certificate will expand your knowledge and skills for the provision and coordination of evidenced-based care for the neonate and their family. Visit our website for more information.

REFERENCES
Australian Institute of Health and Welfare, 2016, Australia’s mothers and babies 2014—in brief, Perinatal statistics, series no. 32. Cat no. PER 87, AIHW, Canberra

Blackburn, ST, 2013, Maternal, fetal & neonatal physiology: a clinical perspective, Elsevier: Saunders, Maryland Heights, MO

Carlson, B 2014, Human embryology and developmental biology, 5th edn., Philadelphia, PA

Carter, A, Granty L & Carter, BS, 2016, ‘Chapter 31: Discharge planning and follow up of the neonatal intensive care infant’, in SL Gardner, BS Carter, M Enzman Hines & JA Hernandez (eds), Merenstein & Gardner’s Handbook of Neonatal Intensive Care, 8th edn., Elsevier, St. Louis. Missouri Davidson, LM & Berkelhamer, SK, 2017, ‘Bronchopulmonary Dysplasia: Chronic Lung Disease of Infancy and Long-Term Pulmonary Outcomes’, Journal of Clinical Medicine, vol. 6, no. 4, doi:10.3390/jcm6010004, p20

Gallacher, DJ, Hart, K & Kotecha, S, 2016, ‘Common respiratory conditions of the newborn’, Breathe, vol. 12, no. 1, pp. 30-42

Gardner, SL, Enzman Hines & Nyp, M, 2016 ‘Chapter 23: Respiratory Diseases’, in SL Gardner, BS Carter, M Enzman Hines & JA Hernandez (eds), Merenstein & Gardner’s Handbook of Neonatal Intensive Care, 8th edn., Elsevier, St. Louis, Missouri

Heath Jeffrey, RC, Broom, M, Shadbolt, B & Todd, DA, 2016, ‘CeasIng Cpap At standarD criteriA (CICADA): Implementation improves neonatal outcomes, Journal of Paediatrics and Child Health, vol. 52, pp. 32-326

Northway, WH Jr., Rosan, RC, Porter, DY, 1967, ‘Pulmonary disease following respiratory therapy of hyaline-membrane disease. Bronchopulmonary dysplasia’, New England Journal of Medicine, vol. 276, pp. 357–368

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