Improved neonatal survival and outcomes at borderline viability brings increasing ethical dilemmas

With improvements in neonatal intensive care over the past five decades, the limits of viability have reduced to around 24 weeks' gestation. While increasing survival has been the predominant driver leading to lowering the gestation at which care can be provided, these infants remain at significant risk of adverse long-term outcomes including neuro-developmental disability. Decisions about commencing and continuing intensive care are determined in partnership with parents, considering the best interests of the baby and the family. Occasionally, clinicians and parents come to an impasse regarding institution or continuation of intensive care. Inevitably, these ethical dilemmas need to consider the uncertainty of the long-term prognosis and challenges surrounding providing or withdrawing active treatment. Further reduction in the gestational age considered for institution of intensive care will need to be guided by short- and long-term outcomes, community expectations and the availability of sufficient resources to care for these infants in the neonatal intensive care unit and beyond

Effects of bias gas flow, lung compliance and airway resistance on pressure and flow in a test lung.

<p>(A) Effect of bias gas flow on the pressure wave in the ventilation circuit; dotted line indicates 200 msec after inflation onset and values indicate the pressure at this point, expressed as a percentage of the peak pressure. (B) Effect of lung compliance on gas flow into the lung at different bias gas flows. (C) Relationship between airway resistance and gas flow into the lung, measured at 3 different lung compliances and 4 different bias gas flows.</p

Effect of bias gas flow on ventilatory parameters.

<p>Values are mean ± SEM for inflation time (Ti), expiratory time (Te), peak inspiratory pressure (PIP), mean airway pressure (MAP), ventilator rate, tidal volume (TV), inspiratory flow, expiratory flow, rate of rise for inspiratory flow (Δ inspiratory flow), ventilator efficiency index (VEI) and resistance during ventilation at ventilator bias gas flows of 8, 18 or 28 L/min. Data are averaged for all time points. *p&lt;0.05; **<i>p</i>&lt;0.01 vs. flow 18 L/min,^†<i>p</i>&lt;0.05 and ^‡<i>p</i>&lt;0.01 vs. flow 28 L/min.</p

Quantitative analysis of the effect of bias gas flow on pulmonary histology.

<p>The proportion of lung tissue stained positive for elastin, αSMA and collagen, the proportion of Ki67-positive cells (labelling index, representing mitotic cells) and the proportion of each field of view occupied by tissue rather than air space (using a point counting technique) <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0047044#pone.0047044-Allison1" target="_blank">[7]</a> for age matched non-ventilated controls and animals ventilated at 8, 18 and 28 L/min. ^§<i>p</i>&lt;0.05 vs. control tissue, * <i>p</i>&lt;0.05 vs. flow 18 L/min, ^†<i>p</i>&lt;0.05 vs. flow 28 L/min.</p

Effect of bias gas flow on cardiorespiratory parameters.

<p>Values are mean ± SEM for heart rate (HR), mean arterial blood pressure (BP), PaO₂, PaCO₂, FiO₂ and pneumothorax (PNX) during ventilation at ventilator bias gas flows of 8, 18 or 28 L/min. Data are averaged for all time points. *p&lt;0.05 vs. flow 18 L/min,^†<i>p</i>&lt;0.05 vs. flow 28 L/min.</p

Effect of bias gas flow on mRNA levels of <i>CTGF</i>, <i>EGR1</i> and <i>CYR61</i>.

<p>mRNA levels, expressed as fold change relative to mRNA levels in age-matched un-ventilated control tissue (<i>n</i> = 8), of <i>CTGF</i> (A), <i>EGR1</i> (B) and <i>CYR61</i> (C) in lung tissue of lambs ventilated with a ventilator bias gas flow of 8 (<i>n = </i>11), 18 (<i>n = </i>11) or 28 L/min (<i>n = </i>14). * <i>p</i>&lt;0.05 vs. flow 18 L/min, ^§<i>p</i>&lt;0.05 vs. control tissue and ^§§<i>p</i>&lt;0.01 vs. control tissue.</p

Representative photomicrographs of lung tissue from age matched non-ventilated controls and ventilated animals.

<p>Photomicrographs of controls (<i>n</i> = 8) are shown in the first row (A, E, I), of lambs ventilated at 8 L/min (<i>n</i> = 5) in the second row (B, F, J), 18 L/min (<i>n</i> = 5) in the third row (C, G, K) and 28 L/min (<i>n</i> = 5) in the fourth row (D, H, L). Columns demonstrate elastin (stained black with Hart’s resorcin stain; A–D), differentiated myofibroblasts (stained brown using immunohistochemistry; E–H), and collagen type I and III fibres (stained black with Gordon-Sweet’s stain; I–L). Bar 10 µm. Arrows (↑) demonstrate secondary septal crests with elastin (A) or myofibroblasts (E) visible at the tip. Solid arrowheads (▴) demonstrate abnormal deposition of elastin and open arrowheads (Δ) demonstrate thickened interstitium (C, D, H) containing a finer meshwork of collagen fibres in tissue ventilated at 18 and 28 L/min (K, L).</p