\documentclass[10pt]{article}

\usepackage{fullpage}
\usepackage{setspace}
\usepackage{parskip}
\usepackage{titlesec}
\usepackage[section]{placeins}
\usepackage{xcolor}
\usepackage{breakcites}
\usepackage{lineno}
\usepackage{hyphenat}





\PassOptionsToPackage{hyphens}{url}
\usepackage[colorlinks = true,
            linkcolor = blue,
            urlcolor  = blue,
            citecolor = blue,
            anchorcolor = blue]{hyperref}
\usepackage{etoolbox}
\makeatletter
\patchcmd\@combinedblfloats{\box\@outputbox}{\unvbox\@outputbox}{}{%
  \errmessage{\noexpand\@combinedblfloats could not be patched}%
}%
\makeatother


\usepackage{natbib}




\renewenvironment{abstract}
  {{\bfseries\noindent{\abstractname}\par\nobreak}\footnotesize}
  {\bigskip}

\titlespacing{\section}{0pt}{*3}{*1}
\titlespacing{\subsection}{0pt}{*2}{*0.5}
\titlespacing{\subsubsection}{0pt}{*1.5}{0pt}


\usepackage{authblk}


\usepackage{graphicx}
\usepackage[space]{grffile}
\usepackage{latexsym}
\usepackage{textcomp}
\usepackage{longtable}
\usepackage{tabulary}
\usepackage{booktabs,array,multirow}
\usepackage{amsfonts,amsmath,amssymb}
\providecommand\citet{\cite}
\providecommand\citep{\cite}
\providecommand\citealt{\cite}
% You can conditionalize code for latexml or normal latex using this.
\newif\iflatexml\latexmlfalse
\providecommand{\tightlist}{\setlength{\itemsep}{0pt}\setlength{\parskip}{0pt}}%

\AtBeginDocument{\DeclareGraphicsExtensions{.pdf,.PDF,.eps,.EPS,.png,.PNG,.tif,.TIF,.jpg,.JPG,.jpeg,.JPEG}}

\usepackage[utf8]{inputenc}
\usepackage[english]{babel}



\usepackage{float}








\begin{document}

\title{Predictors of home oxygen duration in chronic neonatal lung disease}



\author[1]{Matthew Wong}%
\author[2]{Melissa Neylan}%
\author[1]{Gordon Williams}%
\author[2]{Syeda Zahir}%
\author[1]{Jasneek Chawla}%
\affil[1]{Children's Health Queensland Hospital and Health Service}%
\affil[2]{Queensland Health Centre for Children's Health Research}%


\vspace{-1em}



  
  \date{June 18, 2024}


\begingroup
\let\center\flushleft
\let\endcenter\endflushleft
\maketitle
\endgroup





\selectlanguage{english}
\begin{abstract}
\textbf{Aims:}~ In infants with chronic neonatal lung disease (CNLD), we
aimed to identify predictors of home oxygen duration, predictors of
discharge oxygen flow rates and the association of oxygen flow rates
with respiratory outcomes.

\textbf{Methods:}~ Retrospective review of infants with CNLD requiring
home oxygen in 2016 and 2017.~ Hazard ratios (HR) were estimated from
Cox proportional hazards regression models in the cohort.~ A multinomial
logistic regression model examined the effects of maternal and infant
variables on discharge oxygen flow rates.~ Kruskal-Wallis test with
univariate linear regression and Fisher's exact test with binomial
univariate logistic regression were used to examine associations between
oxygen flow groups and post-discharge clinical variables.

\textbf{Results:}~ 149 infants were included. ~Median corrected
gestational age (CGA) at oxygen cessation was 6.8 months (IQR 4.4) with
87.2\% of infants weaned by 12 months CGA.~ Shorter initial neonatal
intensive care unit (NICU) stay predicted faster oxygen weaning at 9
months (HR 0.99, 95\%CI 0.98-1.00, \emph{p}=0.02) and 12 months (HR
0.99, 95\%CI 0.98-1.00, \emph{p}=0.02).~ Infants with hypercarbia at
discharge or discharged from NICU at higher CGA had higher odds of
requiring [?]200mL/min relative to [?]125 mL/min oxygen.~ Infants discharged
with \textgreater{}250mL/min oxygen were more likely to have a
respiratory related admission before two years chronologic age.

\textbf{Conclusion:} ~Shorter initial NICU stay was the best predictor
of earlier home oxygen cessation. ~At NICU discharge, infants with
hypercarbia or a higher CGA may require more home oxygen and experience
more respiratory related hospital admission in the first two years of
chronological age.%
\end{abstract}%



\sloppy


\textbf{MAIN TEXT}

\textbf{Introduction}

Chronic neonatal lung disease (CNLD) is defined clinically as a need for
supplemental oxygen therapy or positive pressure support at 36 weeks
CGA, at 56 days chronological age if born at [?] 32 weeks gestational age)
or at time of hospital discharge.\textsuperscript{1}~ It is
pathologically known as bronchopulmonary dysplasia (BPD), a common
respiratory complication of low birth weight preterm infants who
experience arrested lung development and are susceptible to lung
inflammation secondary to early supplemental oxygen, positive pressure
ventilation, and sepsis in the postnatal period.\textsuperscript{2}
~CNLD and BPD are used interchangeably in the literature with CNLD (or
simply chronic lung disease) being the preferred terminology used by the
Australian and New Zealand Neonatal Network (ANZNN).\textsuperscript{3}~

~

The worldwide incidence of CNLD has been increasing since 1993 due to an
increased survival of extreme preterm infants.\textsuperscript{4} ~~The
2017 ANZNN prevalence of CNLD was 30.3\% with 418 (20.8\%) babies with
CNLD requiring home oxygen therapy.\textsuperscript{3}~ Of those
requiring home oxygen, 340 (81.3\%) also had very low birthweight
(\textless{}1,500g).\textsuperscript{3}~ In Canada and the United
States, the annual reported prevalence of extremely premature infants
with CNLD and chronic oxygen dependency is between 25 and
59\%.\textsuperscript{5-8}~ Home oxygen facilitates earlier hospital
discharge and is generally favored as it reduces the risk of nosocomial
infections and may improve quality of life in the comfort of a home
environment.\textsuperscript{9,10}~ Duration of home oxygen therapy
varies widely due to unstandardized weaning practices in
CNLD.\textsuperscript{5}

~

Population-based cohort studies have identified predictors of requiring
home oxygen at hospital discharge but to our knowledge, no studies have
evaluated predictors of home oxygen therapy duration in
CNLD.\textsuperscript{6,7} ~Thus, the primary aim of this study was to
identify predictors of home oxygen therapy duration in premature infants
with CNLD.~ Secondary aims were to identify predictors of home oxygen
flow rates at time of hospital discharge and to identify if discharge
oxygen flow rates were associated with post-discharge respiratory
outcomes up to two years chronological age.



\textbf{Methods}

\emph{Study Participants}

This retrospective cohort study identified all infants with a primary
diagnosis of moderate or severe CNLD, who required home oxygen therapy,
and were managed at the Queensland Children's Hospital (QCH) between
January 2016 and December 2017.~ All infants were managed according to
the standard home oxygen protocol within our center (Appendix
1)\textbf{. ~}Demographic and clinical information was obtained from the
patient's integrated electronic medical record (iEMR). ~Post-discharge
clinical variables were collected until the infants reached 24 months
chronological age.~ Small for gestational age (SGA) was defined as being
less than 10\textsuperscript{th} percentile for birth weight using the
Fenton preterm growth chart.\textsuperscript{11}~ This study was
approved by the Children's Health Queensland Hospital and Health Service
Human Research Ethics Committee.

\par\null

\emph{Outcomes}

The primary outcome of this study was all-cause home oxygen cessation at
three, six, nine, and twelve months corrected gestational age (CGA).
~Time on oxygen was calculated from birth to CGA at oxygen cessation
using CGA in days as a timescale. ~Infants who did not achieve the
outcome at 12 months CGA or those who were lost to follow up before the
end of study (n=20) were censored.~ ~

~

A secondary outcome was to assess maternal and infant predictors of home
oxygen flow rate required at hospital discharge.~ Another was to examine
how oxygen flow rates at discharge predicted various post-discharge
variables up to 24 months chronological age which included respiratory
related emergency department (ED) presentations, respiratory related
hospital admissions, doctor documented wheeze, prescribed oral
corticosteroids, prescribed inhaled corticosteroids, pediatric intensive
care unit (PICU) admissions, and pulmonary hypertension.

\par\null

\emph{Statistical Analyses}

The study population characteristics were described by summary
statistics (Table 1). ~For continuous variables, measures of central
tendency (mean/median) and spread (standard deviation/interquartile
range) were presented. Mean/standard deviation (SD) were presented for
normally distributed continuous variables and median/interquartile range
(IQR) for non-normally distributed variables. ~Normality was checked by
conducting the Shapiro-Wilks test and visual inspection of histograms.~
Frequencies and proportions were presented for categorical variables.~

\par\null

Cox proportional hazards regression models were used to estimate effects
of each \emph{a priori} predictor of home oxygen duration on home oxygen
cessation, with simultaneous adjustment for potential confounders in
multivariable models. ~Hazard ratios (HR) with 95\% confidence intervals
(CI) were calculated.~ Four Cox-models were built for four different
time on oxygen cut-off points: from baseline to three, six, nine, and
twelve months CGA respectively.~ The proportional hazards assumption was
assessed by examining the relationship between the scaled Schoenfeld
residuals and time on oxygen and the overall fit of the models was
tested by examining the Cox-Snell residuals and evidence of
non-proportional hazards for oxygen flow was found. ~Hence, the baseline
hazard function was stratified by oxygen flow group and proportional
hazards assumption was satisfied by fitting a stratified Cox-regression
model. ~Covariates included for adjustment in multivariable models were
GA, birth weight, partial pressure of carbon dioxide
(pCO\textsubscript{2}) at term CGA, invasive ventilation total
respiratory support and length of initial NICU hospital stay in days. ~

\par\null

We assessed the potential effects of different maternal and infant
variables on oxygen flow rates at hospital discharge using multinomial
logistic regression.~ Patients were grouped into three oxygen flow
groups based on their oxygen flow requirements at discharge: a) [?] 125
mL/min; b) 126 mL/min to 250 mL/min; c) 251 mL/min to 750 mL/min.~ Basic
inferential statistical tests were conducted to select variables with
significant differences between the three oxygen flow groups in the
final multinomial logistic regression model.~ A Kruskal-Wallis test was
used for continuous variables (i.e., birth weight in grams, pCO2 at term
CGA in mmHg, total duration of respiratory support in days, length of
hospital stay in days and CGA at hospital discharge in weeks).~ A
Chi-Square test was used for categorical variables including GA [?] 28
weeks and maternal PROM.~ Odds ratios (OR) with 95\% CI were calculated
and presented for the final multinomial logistic model.~ Modelled
estimates of the sensitivity, specificity, positive predictive value
(PPV) and negative predictive value (NPV) predictive values were derived
and presented as Appendix 2.

\par\null

The~ Kruskal-Wallis test was used to examine the association between the
three oxygen flow groups and continuous post-discharge variables.~ A
univariate linear regression was then conducted to identify the effect
of oxygen flow and continuous post-discharge variables.~ For oxygen flow
groups and categorical post-discharge variables, a Fisher's Exact test
and a binomial univariate logistic regression were used ~

\par\null

\textbf{Results}

A total of 149 infants (63.1\% males) were included in the analyses
(Table 1).~ In our cohort, infants with CNLD requiring home oxygen had a
median GA at birth of 26 weeks (IQR 3) and BW 779 grams (IQR 331) with
13 (8.7\%) born SGA.~ The median length of invasive ventilation during
the neonatal period was 17.9 days (IQR 29.4) and mean length of total
respiratory support was 73.3 days (SD 28.6) with 53\% requiring high
frequency oscillation ventilation.~ At term CGA, the mean
pCO\textsubscript{2} was 53.9 mmHg (SD 7.1).~ At discharge, the median
CGA was 42 weeks (IQR 4.5) with 70.5\% of infants requiring 250 mL/min
of oxygen flow or less at discharge.~ The median CGA of oxygen weaning
was 6.8 months CGA (IQR 4.4) with 87.2\% of infants able to wean off
oxygen by 12 months CGA.

~

Cox proportional hazards regression models for clinical predictors of
oxygen weaning at three, six, nine and twelve months CGA with \emph{a
priori} variables of GA, BW, pCO\textsubscript{2} at term CGA, duration
of invasive ventilation, total duration of respiratory support, length
of hospital stay and oxygen flow group at discharge are shown in Table
2.~ The models indicated that shorter length of hospital stay was a
statistically significant predictor of faster oxygen weaning at CGA 9
months (HR 0.99, 95\% CI 0.98--1.00, \emph{p}=0.02) and at 12 months (HR
0.99, 95\% CI 0.98--1.00, \emph{p}=0.02) (Table 2). ~Length of hospital
stay was not found to be a significant predictor of oxygen weaning at
CGA 3 months (HR 1.01, 95\% CI 0.97-1.05, \emph{p}=0.65) or 6 months (HR
0.99, 95\% CI 0.97-1.00, \emph{p}=0.16).~ Higher GA, higher BW, lower
pCO\textsubscript{2} at term CGA, fewer invasive ventilation days and
fewer total days on respiratory support were not significant predictors
of faster oxygen weaning at any time point (Table 2).

~

Our multinomial logistic regression (Table 3) indicated that infants has
higher odds of being discharged with 200-250 mL/min (OR 1.099, 95\% CI
1.02-1.19, \emph{p}=0.02) or 251-750 mL/min (OR 1.13, 95\% CI 1.04-1.23,
\emph{p}=0.004) home oxygen relative to [?] 125 mL/min with increasing
measured pCO2 at term CGA when all other variables were held constant.~
With each week increase in CGA at hospital discharge, there were higher
odds of being discharged on 200-250 mL/min (OR 1.34, 95\% CI 1.09-1.63,
\emph{p}= 0.005) or 251-750 mL/min (OR 1.51, 95\% CI 1.21-1.88,
\emph{p}\textless{}0.001) relative to [?] 125 mL/min when all other
variables were held constant.~ With every day increase in length of
hospital stay, infants had lower odds of being discharged on 200-250
mL/min (OR 0.95, 95\% CI 0.91-0.99, \emph{p}=0.02) or 251-750mL/min (OR
0.94, 95\% CI 0.90-0.99, \emph{p}=0.01) relative to [?] 125 mL/min when
all other variables were held constant.~ Our results also suggest that
infants born to mothers with PROM had lower odds of being discharged on
200-250 mL/min home oxygen (OR 0.36, 95\% CI 0.14-0.91, \emph{p}=0.032)
compared to mothers without PROM when all other variables were held
constant (Table 3).

~

For our model, accuracy was around 55\% (CI 46-63\%) with performance of
the model using diagnostic measures outline in Appendix 2.~ Sample sizes
were low in some groups which is reflected by the accuracy of the model.

~

We found significant associations of oxygen flow rate at discharge with
respiratory related hospital admissions (\emph{p}\textless{}0.01) and
PICU admissions (\emph{p}=0.05) up to two years of chronological age
(Table 4).~ ~We estimated that infants discharged on 251-750 mL/min of
home oxygen had 6.08 times higher odds (95\% CI, 2.20-18.48,
\emph{p}\textless{}0.001) of being admitted (at least once) with a
respiratory related illness within the first two years of chronological
age (Appendix 3).~



\textbf{Discussion}

Many of the variables that predict home oxygen in CNLD such as early
gestational age, low birth weight, invasive ventilation time or total
duration of respiratory support did not predict oxygen weaning within 12
months CGA.\textsuperscript{6,7}~ Our finding that infants who were
discharged on higher oxygen flow rates required home oxygen therapy for
longer is similar to what has been reported
previously.\textsuperscript{12}~ Variables typically associated with
severity of CNLD like high frequency oscillation ventilation, early
gestational age, or hypercapnia at term CGA did not correlate with the
duration of home oxygen therapy.~ Therefore, infants should not be
presumed to need longer oxygen therapy based on ventilation requirements
in NICU.

~

In our cohort, prolonged neonatal hospital stay was associated with
increased duration of home oxygen therapy.~ The reported duration of
home oxygen therapy in CNLD worldwide over the last 40 years is between
2 and 13.5 months (Table 5).\textsuperscript{12-24}~ When home oxygen
was initially introduced, weaning was based on a target partial pressure
of arterial oxyhemoglobin (PaO\textsubscript{2}) of 55-60
mmHg.\textsuperscript{13-15}~ Continuous overnight pulse oximetry has
become more commonly used to guide oxygen weaning with expert consensus
suggesting targeting a mean peripheral arterial hemoglobin saturation
(SpO\textsubscript{2}) \textgreater{} 93-95\% and [?] 5\% of the overnight
oximetry time spent with SpO\textsubscript{2} [?] 90\% or
SpO\textsubscript{2} [?] 93\%.\textsuperscript{25-28} ~However, there is a
significant lack of evidence supporting these recommendations and thus
home oxygen weaning in CNLD remains highly variable between health
services.\textsuperscript{29,30}~

~

Several service provision variables likely contribute duration of oxygen
therapy for these infants. ~This includes who oversees oxygen weaning
following discharge from neonatal care and the frequency of follow up
visits in the first year of life. ~Models of care differ across centers
with neonatology, general pediatrics, general practitioners,
respiratory, and sleep specialists all involved in patient care to
varying degrees. ~Some centers may even have oxygen weaning unsupervised
by a medical provider.\textsuperscript{12,30} ~At our center, infants
are reviewed every 6-8 weeks post-discharge (Appendix 1) and the median
age of home oxygen cessation was 6.8 months CGA (IQR 4.4), with 51\% of
infants discharged on oxygen flow rates of 200-250 mL/min (Table 1). ~In
contrast, centers where a clinical nurse undertakes weaning in the
community may wean oxygen slower and be affected by the follow up
frequency.~

~

Centers that rely on polysomnography (PSG) assessment for oxygen weaning
report prolonged duration of home oxygen therapy possibly due to PSG
waiting times (Table 5).\textsuperscript{12,31} ~In our experience, the
majority of infants with CNLD can be safely weaned using overnight
oximetry monitoring and PSG is reserved for infants requiring more than
500 mL/min of supplemental oxygen at time of discharge, infants with a
clinical suspicion of comorbid obstructive sleep apnea (OSA), or when
there is concern that an additional etiology contributes to hypoxemia. ~

~

The current lack of standardization of home oxygen initiation and
weaning makes it difficult to assess outcomes in these infants.
~Currently, no evidence exists to suggest that one method of weaning
supplemental oxygen therapy is superior to another and to our knowledge
no studies have been able to evaluate long-term outcomes following a
standardized weaning protocol.~ This highlights the need for prospective
longitudinal studies in view of the continued increase in the number of
preterm infants requiring home oxygen.\textsuperscript{32}{}

~

Infants with CNLD are known to be at higher risk of lower respiratory
tract infections (especially respiratory syncytial virus) and those
receiving home oxygen therapy are 10\% more likely to be readmitted for
a respiratory illness with 49-58\% of infants with severe CNLD requiring
readmission within the first two years of
life.\textsuperscript{5,33,34}~ In our study, infants discharged on
higher oxygen flow levels required more admissions (including PICU)
which is in keeping with findings in other studies.\textsuperscript{5}~
It is important for clinicians to monitor these higher risk infants
closely during this early period and ensuring families are aware of the
increased vulnerability if an infant is discharged on [?] 500 mL/min of
oxygen. ~The number of ED visits within the first two years did not
correlate with discharge oxygen flow rates, perhaps indicating that home
oxygen may help reduce severity of subsequent respiratory illnesses.

~

Wheeze and bronchial hyper-responsivity are well described following
preterm birth\textsuperscript{35-38} and infants with CNLD are more
likely to receive additional oxygen, bronchodilators and inhaled
steroids within the first year of life.\textsuperscript{23}~ In our
study, doctor documented wheeze and corticosteroid use (inhaled or oral)
in the first 2 years of life were not significantly associated with
duration of oxygen therapy or oxygen flow rates at discharge. ~Further
longitudinal follow up of our cohort would be required to determine if
such presentations occur later in genetically predisposed individuals,
with prematurity and CNLD increasing risk during pre-school years.~ All
infants with CNLD requiring home oxygen at our center receive
respiratory syncytial virus immunoglobulin prophylaxis during the winter
months which may have reduced wheezy hospital presentations compared to
other studies.

~

Infants were more likely to be discharge on higher levels of oxygen
therapy ([?] 200 mL/min) if they had higher pCO2 measured at term CGA and
increased CGA at hospital discharge.~ In our cohort, 30.9\% (n=46) had
moderate hypercapnia (pCO\textsubscript{2} 55-65 mmHg) and 6\% (n=9) had
severe hypercapnia (pCO\textsubscript{2} \textgreater{} 65 mmHg)
measured at term CGA (Table 1).~ Moderate to severe hypercapnia was not
predictive of home oxygen cessation but was significantly associated
with requiring \textgreater{}250mL/min oxygen at discharge (Table 3).~
In a sub-analysis, infants with pCO\textsubscript{2} [?] 55 mmHg had a
median time to oxygen weaning of 6.3 months (95\% CI, 5.7-7.0) whereas
patients with pCO\textsubscript{2} \textgreater{} 55 mmHg had a median
time of 8.4 months (95\% CI, 7.7-9.1) (Appendix 4).~ The differences
were statistically significant at our time on oxygen cut-off points of
CGA 6 months (\emph{p}=0.001), 9 months (\emph{p}=0.035), and 12 months
(\emph{p}=0.034).~ This information may be useful clinically to guide
parent's expectations of a longer duration of oxygen therapy in those
who have hypercarbia at term CGA. ~

~

It is unclear whether alternative or additional respiratory support
would be beneficial in infants with hypercarbia as there are no studies
assessing the impact of hypercarbia and level of respiratory support on
outcomes in CNLD. ~Centers may consider PSG to evaluate the need for
pressure support in infants who have evidence of alveolar
hypoventilation (more than 25\% of the total sleep time with
pCO\textsubscript{2} \textgreater{} 50 mmHg)\textsuperscript{41} but it
is unclear which infants with moderate to severe hypercapnia benefit
from pressure support over supplemental oxygen. ~A Canadian
retrospective cohort study identified that of infants born at GA
\textless{} 29 weeks, only 0.9\% and 0.6\% were discharged on
non-invasive ventilation (NIV) or tracheostomy ventilation
respectively.\textsuperscript{42} ~The indications for initiating NIV
were not stated.~ After laryngomalacia, CNLD was the second most common
indication for home CPAP over a period of 10 years at Westmead
Children's Hospital.\textsuperscript{43}~ No specific gas exchange or
PSG criteria for initiating CPAP was mentioned.~ Future work to explore
practices for NIV therapy in infants with CNLD across centers would be a
first step in determining whether this is an option that should be
offered more readily in this population and whether this impacts longer
term outcomes.

~

Our study is limited by its retrospective nature but is strengthened by
the inclusion of a reasonable sample size. ~The multinomial logistic
regression model to predict oxygen flow rates at discharge would need to
be validated on a larger cohort of patients as the lower accuracy was
affected by the smaller sample size in some comparative groups.~ There
is selection bias as only infants managed at a single center were
included for analysis.~ We recognize that length of oxygen therapy and
weaning practices are often based on the anecdotal experience of
individual clinicians due to the lack of evidence in this area. ~This is
consistent with practice in other centers as there are currently no
standardized protocols to guide weaning of home oxygen therapy in
infants with CNLD. ~Recall bias is minimized by our multidisciplinary
oxygen clinic following a consistent follow up and weaning process
(Appendix 1).~ Although our study only describes associations between
\emph{a priori} maternal and infant variable with home oxygen duration
and oxygen flow rates, it provides insightful information about which
infants may require prolonged oxygen therapy or experience more hospital
readmissions.~ \textbf{}



\textbf{Conclusions}

This study provides information which may be of use for clinicians when
advising families of infants with CNLD being discharged on home
supplemental oxygen therapy. ~Shorter length of initial NICU stay
appears to predict shorter duration of home oxygen therapy and was
associated with lower odds of needing [?] 200 mL/min at discharge.
~~Infants with higher CGA at discharge or hypercarbia were more likely
to need higher levels of home oxygen therapy.~ Close monitoring is
recommended for infants discharged on higher flows of oxygen therapy
(e.g. \textgreater{}250 mL/min) as these infants have a higher risk of
respiratory related hospital and PICU admissions within the first two
years.~ Additionally, our study highlights the variability in practice
and need for standardization of oxygen weaning process for infants with
CNLD in order to improve outcomes for this increasing population.



\textbf{References}

1.~~~~~~~~~ Jobe AH, Bancalari E. Bronchopulmonary dysplasia. \emph{Am J
Respir Crit Care Med.} 2001;163(7):1723-1729.

2.~~~~~~~~~ Thebaud B, Goss KN, Laughon M, et al. Bronchopulmonary
dysplasia. \emph{Nat Rev Dis Primers.} 2019;5(1):78.

3.~~~~~~~~~ Chow SSWC, P.; Chambers, G.M.; Lui, K. \emph{Report of the
Australian and New Zealand Neonatal Network 2017.} Sydney: UNSW;2019.

4.~~~~~~~~~ Stoll BJ, Hansen NI, Bell EF, et al. Trends in Care
Practices, Morbidity, and Mortality of Extremely Preterm Neonates,
1993-2012. \emph{JAMA.} 2015;314(10):1039-1051.

5.~~~~~~~~~ DeMauro SB, Jensen EA, Bann CM, et al. Home Oxygen and
2-Year Outcomes of Preterm Infants With Bronchopulmonary Dysplasia.
\emph{Pediatrics.} 2019;143(5).

6.~~~~~~~~~ Ejiawoko A, Lee HC, Lu T, Lagatta J. Home Oxygen Use for
Preterm Infants with Bronchopulmonary Dysplasia in California. \emph{J
Pediatr.} 2019;210:55-62 e51.

7.~~~~~~~~~ Lagatta J, Clark R, Spitzer A. Clinical predictors and
institutional variation in home oxygen use in preterm infants. \emph{J
Pediatr.} 2012;160(2):232-238.

8.~~~~~~~~~ Lodha A, Sauve R, Bhandari V, et al. Need for supplemental
oxygen at discharge in infants with bronchopulmonary dysplasia is not
associated with worse neurodevelopmental outcomes at 3 years corrected
age. \emph{PLoS One.} 2014;9(3):e90843.

9.~~~~~~~~~ Lau R, Crump RT, Brousseau DC, et al. Parent Preferences
Regarding Home Oxygen Use for Infants with Bronchopulmonary Dysplasia.
\emph{J Pediatr.} 2019;213:30-37 e33.

10.~~~~~~~ Balfour-Lynn IM, Primhak RA, Shaw BN. Home oxygen for
children: who, how and when? \emph{Thorax.} 2005;60(1):76-81.

11.~~~~~~~ Fenton TR, Kim JH. A systematic review and meta-analysis to
revise the Fenton growth chart for preterm infants. \emph{BMC Pediatr.}
2013;13:59.

12.~~~~~~~ Yeh J, McGrath-Morrow SA, Collaco JM. Oxygen weaning after
hospital discharge in children with bronchopulmonary dysplasia.
\emph{Pediatr Pulmonol.} 2016;51(11):1206-1211.

13.~~~~~~~ Pinney MA, Cotton EK. Home management of bronchopulmonary
dysplasia. \emph{Pediatrics.} 1976;58(6):856-859.

14.~~~~~~~ Campbell AN, Zarfin Y, Groenveld M, Bryan MH. Low flow oxygen
therapy in infants. \emph{Arch Dis Child.} 1983;58(10):795-798.

15.~~~~~~~ Abman SH, Accurso FJ, Koops BL. Experience with home oxygen
in the management of infants with bronchopulmonary dysplasia. \emph{Clin
Pediatr (Phila).} 1984;23(9):471-476.

16.~~~~~~~ Hudak BB, Allen MC, Hudak ML, Loughlin GM. Home oxygen
therapy for chronic lung disease in extremely low-birth-weight infants.
\emph{Am J Dis Child.} 1989;143(3):357-360.

17.~~~~~~~ Sauve RS, McMillan DD, Mitchell I, Creighton D, Hindle NW,
Young L. Home oxygen therapy. Outcome of infants discharged from NICU on
continuous treatment. \emph{Clin Pediatr (Phila).} 1989;28(3):113-118.

18.~~~~~~~ Silva DT, Hagan R, Sly PD. Home oxygen management of neonatal
chronic lung disease in Western Australia. \emph{J Paediatr Child
Health.} 1995;31(3):185-188.

19.~~~~~~~ Baraldi E, Carra S, Vencato F, et al. Home oxygen therapy in
infants with bronchopulmonary dysplasia: a prospective study. \emph{Eur
J Pediatr.} 1997;156(11):878-882.

20.~~~~~~~ Bertrand P, Alvarez C, Fabres J, Simonetti M, Sanchez I.
{[}Home oxygen therapy in children with chronic respiratory failure{]}.
\emph{Rev Med Chil.} 1998;126(3):284-292.

21.~~~~~~~ Norzila MZ, Azizi BH, Norrashidah AW, Yeoh NM, Deng CT. Home
oxygen therapy for children with chronic lung diseases. \emph{Med J
Malaysia.} 2001;56(2):151-157.

22.~~~~~~~ Saletti A, Stick S, Doherty D, Simmer K. Home oxygen therapy
after preterm birth in Western Australia. \emph{J Paediatr Child
Health.} 2004;40(9-10):519-523.

23.~~~~~~~ Hennessy EM, Bracewell MA, Wood N, et al. Respiratory health
in pre-school and school age children following extremely preterm birth.
\emph{Arch Dis Child.} 2008;93(12):1037-1043.

24.~~~~~~~ Batey N, Batra D, Dorling J, Bhatt JM. Impact of a
protocol-driven unified service for neonates with bronchopulmonary
dysplasia. \emph{ERJ Open Res.} 2019;5(1).

25.~~~~~~~ Kapur N, Nixon G, Robinson P, et al. Respiratory management
of infants with chronic neonatal lung disease beyond the NICU: A
position statement from the Thoracic Society of Australia and New
Zealand. \emph{Respirology.} 2020.

26.~~~~~~~ Balfour-Lynn IM, Field DJ, Gringras P, et al. BTS guidelines
for home oxygen in children. \emph{Thorax.} 2009;64 Suppl 2:ii1-26.

27.~~~~~~~ Hayes D, Jr., Wilson KC, Krivchenia K, et al. Home Oxygen
Therapy for Children. An Official American Thoracic Society Clinical
Practice Guideline. \emph{Am J Respir Crit Care Med.}
2019;199(3):e5-e23.

28.~~~~~~~ Thoracic Society of A, New Z, Fitzgerald DA, et al. Infants
with chronic neonatal lung disease: recommendations for the use of home
oxygen therapy. \emph{Med J Aust.} 2008;189(10):578-582.

29.~~~~~~~ Wong MD, Chung H, Chawla J. Using continuous overnight pulse
oximetry to guide home oxygen therapy in chronic neonatal lung disease.
\emph{J Paediatr Child Health.} 2020;56(2):309-316.

30.~~~~~~~ Palm K, Simoneau T, Sawicki G, Rhein L. Assessment of current
strategies for weaning premature infants from supplemental oxygen in the
outpatient setting. \emph{Adv Neonatal Care.} 2011;11(5):349-356.

31.~~~~~~~ Kulkarni G, de Waal K, Grahame S, et al. Polysomnography for
the management of oxygen supplementation therapy in infants with chronic
lung disease of prematurity. \emph{J Matern Fetal Neonatal Med.}
2018:1-7.

32.~~~~~~~ Hayes D, Jr., Wilson KC, Balfour-Lynn IM. Need for
international standardization of home oxygen therapy in children.
\emph{Pediatr Pulmonol.} 2019.

33.~~~~~~~ Abman SH, Collaco JM, Shepherd EG, et al. Interdisciplinary
Care of Children with Severe Bronchopulmonary Dysplasia. \emph{J
Pediatr.} 2017;181:12-28 e11.

34.~~~~~~~ Carbonell-Estrany X, Quero J, Bustos G, et al.
Rehospitalization because of respiratory syncytial virus infection in
premature infants younger than 33 weeks of gestation: a prospective
study. IRIS Study Group. \emph{Pediatr Infect Dis J.}
2000;19(7):592-597.

35.~~~~~~~ Castro-Rodriguez JA, Forno E, Rodriguez-Martinez CE, Celedon
JC. Risk and Protective Factors for Childhood Asthma: What Is the
Evidence? \emph{J Allergy Clin Immunol Pract.} 2016;4(6):1111-1122.

36.~~~~~~~ Leps C, Carson C, Quigley MA. Gestational age at birth and
wheezing trajectories at 3-11 years. \emph{Arch Dis Child.}
2018;103(12):1138-1144.

37.~~~~~~~ Perez-Yarza EG, Moreno-Galdo A, Ramilo O, et al. Risk factors
for bronchiolitis, recurrent wheezing, and related hospitalization in
preterm infants during the first year of life. \emph{Pediatr Allergy
Immunol.} 2015;26(8):797-804.

38.~~~~~~~ Been JV, Lugtenberg MJ, Smets E, et al. Preterm birth and
childhood wheezing disorders: a systematic review and meta-analysis.
\emph{PLoS Med.} 2014;11(1):e1001596.

39.~~~~~~~ Berkelhamer SK, Mestan KK, Steinhorn R. An update on the
diagnosis and management of bronchopulmonary dysplasia (BPD)-associated
pulmonary hypertension. \emph{Semin Perinatol.} 2018;42(7):432-443.

40.~~~~~~~ Al-Ghanem G, Shah P, Thomas S, et al. Bronchopulmonary
dysplasia and pulmonary hypertension: a meta-analysis. \emph{J
Perinatol.} 2017;37(4):414-419.

41.~~~~~~~ Berry RQ, SF; Abreu, AR; et al for the American Academy of
Sleep Medicine. The AASM Manual for the Scoring of Sleep and Associated
Events: Rules, Terminology and Technical Specifications.~ Version 2.6.
In: Darien, IL: American Academy of Sleep Medicine; 2020.

42.~~~~~~~ Nassel D, Chartrand C, Dore-Bergeron MJ, et al. Very Preterm
Infants with Technological Dependence at Home: Impact on Resource Use
and Family. \emph{Neonatology.} 2019;115(4):363-370.

43.~~~~~~~ Al-Iede M, Kumaran R, Waters K. Home continuous positive
airway pressure for cardiopulmonary indications in infants and children.
\emph{Sleep Med.} 2018;48:86-92.

\selectlanguage{english}
\FloatBarrier
\end{document}

