ARTICLE

The Epidemiology of Meconium Aspiration

Syndrome: Incidence, Risk Factors, Therapies,
and Outcome
Peter A. Dargaville, MBBS FRACP, MDa,b, Beverley Copnell, RN, RSCN, BAppSc, PhDb,c, for the Australian and New Zealand Neonatal Network

aDepartment of Pediatrics, Royal Hobart Hospital, Hobart, Australia; bNeonatal Research Group, Murdoch Children’s Research Institute, Melbourne, Australia; cDepartment

of Neonatology, Royal Children’s Hospital, Melbourne, Australia

The authors have indicated they have no financial relationships relevant to this article to disclose.

ABSTRACT
OBJECTIVE. We sought to examine, in a large cohort of infants within a definable
population of live births, the incidence, risk factors, treatments, complications, and
www.pediatrics.org/cgi/doi/10.1542/
outcomes of meconium aspiration syndrome (MAS). peds.2005-2215
DESIGN. Data were gathered on all of the infants in Australia and New Zealand who doi:10.1542/peds.2005-2215
were intubated and mechanically ventilated with a primary diagnosis of MAS Key Words
meconium aspiration syndrome, risk
(MASINT) between 1995 and 2002, inclusive. Information on all of the live births factors, gestational age, Apgar score, high-
during the same time period was obtained from perinatal data registries. frequency ventilation, nitric oxide,
pulmonary surfactants, pneumothorax
RESULTS. MASINT occurred in 1061 of 2 490 862 live births (0.43 of 1000), with a Abbreviations
decrease in incidence from 1995 to 2002. A higher risk of MASINT was noted at MAS—meconium aspiration syndrome
HFV— high-frequency ventilation
advanced gestation, with 34% of cases born beyond 40 weeks, compared with iNO—inhaled nitric oxide
16% of infants without MAS. Fetal distress requiring obstetric intervention was MSAF—meconium-stained amniotic fluid
noted in 51% of cases, and 42% were delivered by cesarean section. There was a ANZNN—Australian And New Zealand
Neonatal Network
striking association between low 5-minute Apgar score and MASINT. In addition, nCPAP—nasal or nasopharyngeal
risk of MASINT was higher where maternal ethnicity was Pacific Islander or continuous positive airway pressure
MASINT—meconium aspiration syndrome
indigenous Australian and was also increased after planned home birth. Uptake of requiring intubation
exogenous surfactant, high-frequency ventilation, and inhaled nitric oxide in- Accepted for publication Nov 7, 2005
creased considerably during the study period, with ⬎50% of infants receiving ⱖ1 Address correspondence to Peter Dargaville,
of these therapies by 2002. Risk of air leak was 9.6% overall, with an apparent MBBS FRACP, MD, Department of Paediatrics,
Royal Hobart Hospital, Liverpool Street, Hobart
reduction to 5.3% in 2001–2002. The duration of intubation remained constant TAS 7000, Australia. E-mail: peter.dargaville@
throughout the study period (median: 3 days), whereas duration of oxygen dhhs.tas.gov.au

therapy and length of hospital stay increased. Death related to MAS occurred in 24 PEDIATRICS (ISSN Numbers: Print, 0031-4005;
Online, 1098-4275). Copyright © 2006 by the
infants (2.5% of the MASINT cohort; 0.96 per 100 000 live births). American Academy of Pediatrics

CONCLUSIONS. The incidence of MASINT in the developed world is low and seems to be
decreasing. Risk of MASINT is significantly greater in the presence of fetal distress
and low Apgar score, as well as Pacific Islander and indigenous Australian ethnic-
ity. The increased use of innovative respiratory supports has not altered the
duration of mechanical ventilation.

1712 DARGAVILLE et al
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M ECONIUM ASPIRATION SYNDROME (MAS) is a dis-
ease of the term and near-term infant that is
associated with considerable respiratory morbidity. The
disease is characterized by early onset of respiratory
distress in a meconium-stained infant, with poor lung
compliance and hypoxemia clinically and patchy opaci-
fication and hyperinflation radiographically.1,2 At least
one third of infants with MAS require intubation and
mechanical ventilation,3,4 and newer neonatal therapies,
such as high-frequency ventilation (HFV), inhaled nitric
oxide (iNO), and surfactant administration are often
brought into play.5,6
In the past few decades, there seems to have been a
reduction in the incidence of MAS in many centers, at
least in the developed world.4,7,8 This observation has
largely been based on declining numbers in individual
centers, with only 1 population-based study examining
longitudinal trends in MAS incidence.7 The apparent
reduction in the risk of MAS has been attributed to
better obstetric practices, in particular, avoidance of
postmaturity and expeditious delivery where fetal dis-
tress has been noted.8
In previous epidemiologic studies, some important
risk factors for the development of MAS have been
identified, either within the general birth population or
among infants born through meconium-stained amni-
otic fluid (MSAF). The presence of fetal compromise,
indicated by abnormalities of fetal heart rate tracings
and/or poor Apgar scores, is known to increase the risk
of MSAF7,9,10 and of MAS in the meconium-stained in-
fant.8,9,11–15 Cesarean delivery is also associated with a
heightened incidence of MAS.16 There is an apparent
relationship between maternal ethnicity and risk of
MSAF7,10,17,18 and the suggestion in several reports of an
increased risk of MAS in black Americans and Afri-
cans7,17,19 and Pacific Islanders.18,20 Advanced gestation
has also been recognized as a risk factor, both for
MSAF10,17,21–23 and for MAS.8,11,12,20,23–25
Therapy for infants with MAS, in particular, those
requiring intubation, is evolving rapidly. There is, how-
ever, a paucity of longitudinal data examining the pro-
portional uptake of newer therapies in ventilated infants
with MAS. Similarly, whereas it is clear that severe MAS
is associated with a relatively high risk of pneumothorax
and a relatively long duration of respiratory support and
oxygen therapy,1,2 the specific factors that predict severe
disease and long ventilator course are incompletely char-
acterized. The mortality has been quoted as lying be-
tween 5% and 37%,1 with the marked disparity in pub-
lished figures being attributable to the difficulties in
identifying the cause of death (respiratory versus non-
respiratory) and the skewed populations in which the
mortality risk is calculated.
A complete understanding of the epidemiology of
MAS has been hampered by the lack of population-
based studies and by difficulties in assembling large co-
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horts of infants with confirmed disease. We have sought
to remedy this situation using the database of the Aus-
tralian and New Zealand Neonatal Network, supple-
mented by data from perinatal data registries. Our aims
with this study were to examine current indicators and
longitudinal trends for (1) the incidence of MAS, (2) the
risk factors for MAS among all live births, (3) the treat-
ments applied to ventilated infants with the disease, and
(4) the complications and outcomes. In view of the
difficulty in reliably recognizing cases of mild to moder-
ate MAS, this investigation focused on infants with rel-
atively severe disease in whom intubation and mechan-
ical ventilation were required.
METHODS
Data on infants with MAS were obtained from the da-
tabase of the Australian and New Zealand Neonatal Net-
work (ANZNN). This is a voluntary collaboration be-
tween all 28 level III NICUs that was established in 1994
to monitor the care of high-risk newborns. A minimum
data set has been developed, with any infant satisfying
any of the following criteria being included in the data-
base: (1) need for assisted ventilation either through an
endotracheal tube or via nasal/nasopharyngeal continu-
ous positive airway pressure (nCPAP), (2) need for ma-
jor surgery, (3) gestation ⬍32 weeks, and (4) birth
weight ⬍1500 g. Data are supplied to ANZNN in de-
identified form by the individual units and are checked
for errors. For each infant, a primary respiratory diag-
nosis is entered.
For this study, the ANZNN database for the years
1995–2002 was searched for infants ⬎35 weeks’ gesta-
tion with a primary respiratory diagnosis of MAS. The
ANZNN defines MAS in a meconium-stained infant as
respiratory distress within 12 hours of age, displaying
symptoms such as hypoxia, tachypnea, gasping respira-
tions, and signs of underlying asphyxia, with a chest
radiograph showing overexpansion of the lungs with
widespread coarse infiltrates.26 It is important to note
that the diagnosis of MAS is ascribed by the clinicians
responsible for supplying data to the ANZNN database.
This analysis focused on cases of MAS requiring intuba-
tion and mechanical ventilation (MASINT). Infants with
MAS treated with nCPAP only were excluded; such
infants, although meconium-stained, may have other
diagnoses as the predominant cause of respiratory dis-
tress, for example, transient tachypnea of the new-
born.27,28 All of the available antenatal and intrapartum
data and information pertaining to severity of the dis-
ease and medical management, were extracted from the
identified records. The presence of intrauterine growth
retardation was noted, defined as birth weight less than
the 10th percentile derived from Australian normative
data.29 For infants who died, the cause of death was
classified as being respiratory or nonrespiratory (ie, di-
rectly related or not related to the aspiration of meco-
PEDIATRICS Volume 117, Number 5, May 2006 1713
nium) based on the International Classification of Dis- to the entire birth population because of lack of access to
eases code numbers and additional diagnostic specific data from each individual without MASINT.
information entered in the ANZNN database.
Information regarding the total birth population in RESULTS
Australia and New Zealand was also obtained for the Between 1995 and 2002, 1061 infants were admitted to
years 1995–2002. Data were gathered on the total num- a level III NICU in Australia or New Zealand with
bers of live births and the incidence of potential risk MASINT, with the number ranging between 109 and 150
factors for MAS that could be matched to the ANZNN annually. An additional 107 infants with MAS treated
MASINT cohort. These factors included maternal ethnic- with nCPAP only were excluded along with 2 infants
ity, gender, place of birth, mode of delivery, gestational with a primary diagnosis of MAS in whom no respiratory
age, and condition at birth as indicated by 5-minute support was required. Median gestation for infants with
Apgar score. Australian data were obtained from the MASINT was 40 weeks (interquartile range: 39 – 41
annual reports of the Australian Institute of Health and weeks), median birth weight was 3400 g (interquartile
Welfare.30 Where variables were reported in terms of the range: 3000 –3700 g), and 52.4% were male. Overall,
number of confinements, the same percentage was used 42% of infants with MASINT were born in a tertiary
to project the number of live births. Variables treated in hospital, with the proportion being higher in New Zea-
this manner were indigenous births, home births, deliv- land than Australia (64% vs 31%; P ⬍ .001).
ery by cesarean section, and instrumental deliveries. During the study period, there were 2 490 862 live
Where data were stated to be missing or incomplete births in the 2 countries, giving an overall rate of MASINT
from some states or territories (eg, the classification of of 0.43 per 1000 live births. In Australia, there were 894
cesarean section as “emergency” or “elective”), the na- infants with MASINT in 2 038 666 live births and in New
Zealand, 167 cases in 452 196 live births, yielding rates
tional average and previous trends were used to calcu-
of MASINT of 0.44 and 0.37 per 1000 live births, respec-
late the totals.
tively. Combined longitudinal data from both countries
For New Zealand, the total number of live births for
revealed an overall decrease in the incidence of MASINT
each year and data on maternal ethnicity and infant
to a low of 0.35 per 1000 in 2002 (P ⫽ .0087). Analysis
gender were obtained from electronic documents made
by country shows a steady decrease in incidence in Aus-
available by Statistics New Zealand.31 Data on type of
tralia between 1995 and 2002, with considerable fluctu-
delivery between 1999 and 2002 and numbers of instru-
ation but no clear trend in incidence in New Zealand.
mental vaginal deliveries between 1995 and 1998 were
Figure 1 shows the rate of MASINT per 1000 live births
obtained from the Ministry of Health reports on mater-
at each week of gestation (Australian data only). Be-
nity (eg, refs 32 and 33). Numbers of emergency and
tween 36 and 40 weeks, the rate varied between 0.24
elective cesarean section deliveries were not separately
and 0.46 per 1000, with the lowest rate occurring at 38
reported in the years 1995-1998, and estimates have
weeks, and rose thereafter to a high of 1.42 per 1000 at
been made from subsequent trends. No reliable data on
home births in New Zealand were available. Summary
statistics on gestational age and 5-minute Apgar score
were reported differently from Australian data and could
not be included in the overall data set. For both coun-
tries, numbers of infants born in tertiary hospitals were
obtained from the annual reports of the ANZNN.26
Summary statistics were generated for all variables in
the MAS data set. The duration of intubation and nCPAP
were summed to give duration of respiratory support.
No assumptions were made about the distribution of
continuous variables. For binary and continuous vari-
ables, simple comparisons were made with ␹2 and
Mann-Whitney tests, respectively; longitudinal trends in
these variables were examined using the ␹2 test for trend
and linear regression, respectively. For all tests, a P ⬍ .05
was considered statistically significant. Within the
MASINT cohort, predictors of duration of respiratory sup-
port were sought using multiple linear regression anal-
ysis, with addition of all of the relevant variables to the FIGURE 1
Incidence of MASINT according to gestational age. Plot of incidence of MASINT at each
model in a stepwise manner. Binary variables were en- week of gestation; Australian data only. See text for comparisons between gestational
tered as 1 or 0. Multivariate analysis could not be applied age groups.

1714 DARGAVILLE et al
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42 weeks and beyond. Thirty-four percent of the MASINT
cohort were at ⬎40 weeks’ gestation and 6.5% at ⬎41
weeks’ compared with 16% and 2.0% of the total birth
population (P ⬍ .001 in both cases). Figure 2 shows the
trends in incidence of MASINT by gestational age group-
ing during the study period. A decrease in incidence was
noted over time at gestations ⬎40 weeks but not at
gestational ages between 36 and 40 weeks.
Antecedents of MASINT, with analysis by year and by
country, are shown in Table 1. More than half of the
infants were noted to have fetal distress prompting ob-
stetric intervention; 70% of these went on to deliver by
cesarean section or assisted vaginal delivery. Cesarean
section was the mode of delivery for 42% of the MASINT
infants overall. Fully 9.7% of the entire MASINT cohort
were delivered by cesarean section without labor, pre-
ceded by the recognition of fetal distress in 77% of cases
and of intrauterine growth restriction in an additional
6%. The proportion of assisted vaginal deliveries de-
creased during the study period. The number of MASINT
infants with 5-minute Apgar score ⬍7 and the number
requiring intubation in the delivery room also decreased.
Median Apgar scores at 5 minutes were lower among
infants born in New Zealand (6 vs 7; P ⫽ .0012), and
intubation in the delivery room for resuscitation was
more commonly required (59% vs 43%; P ⬍ .001).
The impact of selected antecedents on the risk of
MASINT, using combined data from all years, is shown in
Fig 3. There was a striking association between low
5-minute Apgar score and risk of MASINT, with an odds
ratio of 52. Among the demographic variables, infants
born to Pacific Islander mothers in New Zealand and
Aboriginal/Torres Strait Islander mothers in Australia
were ⬃3 times more likely to develop MASINT, whereas
FIGURE 2
Incidence of MASINT according to year in different gestational age groups: plot of inci-
dence of MASINT per 1000 live births for gestations 36 to 40 weeks and for gestations
beyond 40 weeks; Australian data only. a Decrease in incidence between 1995 and 2002
for infants beyond 40 weeks’ gestation (P ⫽ .010), with no discernible trend for 36 to 40
weeks. 䊐, ⱖ41 weeks; ‚, 36 to 40 weeks.
Downloaded from pediatrics.aappublications.org at Michigan State Univ on June 14, 2015
infants born to Maori mothers had no increased risk.
Gender of the infant was not a significant factor. All
forms of assisted delivery increased the risk of MASINT to
some extent, with infants undergoing emergency cesar-
ean section being at the highest risk, almost sixfold
higher than other modes of delivery. Planned home
birth was associated with a 2.7-fold increase in risk of
MASINT.
Figure 4 shows longitudinal trends in odds ratios for
selected risk factors during the study period. There was
considerable fluctuation in the odds ratio for most risk
factors, with no clear trend over time. The risk for infants
born to Aboriginal/Torres Strait Islander mothers did,
however, increase markedly from 1998, such that in
2002 the risk of MASINT was ⬎7 times that of the non-
indigenous population in Australia. Both emergency ce-
sarean section and birth in a tertiary center showed a
downward trend over the study period but continued to
be associated with an increased risk of MASINT. The odds
ratio for an assisted vaginal delivery decreased rapidly
and was ⬍1 after 1997.
With the knowledge of the antecedents of MASINT in
the birth population overall, we sought to identify
changes in the demography of live births that might
explain the decrease in incidence of MASINT in the latter
years of the study period. Compared with 1995, in 2002,
there were fewer deliveries beyond 41 weeks’ gestation
(1.6% vs 2.8%; P ⬍ .001) and fewer infants with a
5-minute Apgar score ⬍7 (1.4% vs 1.7%; P ⬍ .001).
These factors combined account for 62% of the reduc-
tion in MAS incidence noted in this time period.
Table 2 shows the therapies received by infants with
MASINT. More than half of infants overall received either
surfactant, HFV or iNO, with upward trends in the use of
all of these therapies during the study period. Infants
receiving ⱖ1 of surfactant, HFV, or iNO were intubated
for a median of 5 days and required respiratory support
for a median of 6 days, compared with 2 and 3 days,
respectively, for infants who received none of these
therapies. Only 1.1% of the MASINT cohort required
treatment with extracorporeal membrane oxygenation;
all infants treated with this therapy survived.
Table 3 shows the complications and outcomes for the
ANZNN MASINT cohort. Although no clear trend was
discernible for the whole study period, the incidence of
air leak seemed to decrease in 2001–2002, being signif-
icantly lower for these 2 years compared with all of the
other years (5.3% vs 10.8%; P ⫽ .013). Infants who
developed air leak required respiratory support for a
median of 5 days compared with 3.2 for those without
this complication. In the MASINT cohort overall, the
duration of intubation and of respiratory support re-
mained relatively constant during the study period;
however, the duration of oxygen therapy and the length
of hospital stay increased. The overall mortality was
6.6% (70 of 1061), with the majority of these deaths
PEDIATRICS Volume 117, Number 5, May 2006 1715
 TABLE 1 Antecedents of MAS Among the ANZNN MASINT Cohort
Variable All Years 1995–1997 1998–2000 2001–2002 Longitudinal Trend (P)a
Fetal distress noted, % of total 51.1 45.3 55.5 54.0 1 (.019)
All CS, % of total 41.8 40.4 39.9 47.1 Nil
CS in labor, % of total 32.0 30.6 31.9 34.8 Nil
Assisted vaginal delivery, % of total 11.1 16.1 7.8 7.9 2 (⬍.001)
Apgar scores
At 1 min, median, IQR 4 (2–6) 3 (2–6) 4 (2–6) 5 (2.5–6) 1 (.0017)
At 5 min, median, IQR 7 (5–8) 6 (5–8) 7 (5–8) 7 (5–8) 1 (.0029)
⬍7 at 5 min, % of total 46.7 50.7 47.2 39.2 2 (.017)
Intubated in delivery room, % of total 46.1 51.2 45.5 38.2 2 (.0063)
“Fetal distress noted” indicates any distress of the fetus leading to intervention by the obstetric team; “assisted vaginal delivery,” delivery with the aid of forceps or Ventouse extraction; “intubated
in delivery room,” intubation required for the purposes of resuscitation, not for airway clearance; CS, cesarean section; IQR, interquartile range; 1, increased over time; 2, decreased over time.
a Longitudinal trend analysis is in all cases based on comparison of data for each year from 1995–2002.

FIGURE 3
Risk factors for MASINT within the total birth population: plot of odds ratios (〫) and 95%
confidence interval (4 and 3) for selected risk factors for MASINT. Odds ratio (95%
confidence interval) also indicated as text. a Australian data only; b New Zealand data only.
TSI indicates Torres Strait Islander; “All CS,” all cesarean-section deliveries.

being because of perinatal asphyxia (n ⫽ 33) or congen-

ital anomalies (n ⫽ 6). Death directly attributable to
aspiration of meconium occurred in 24 infants, equiva-
lent to 2.5% of the total MASINT cohort and 0.96 per
100 000 live births. Mortality rates seemed to remain
constant during the study period. Of the 24 infants
whose death was directly related to MAS, 7 (29%) were
in relatively good condition at birth, not requiring im-
mediate intubation, and with a 5-minute Apgar ⱖ7. Air
leak occurred in 42% of MAS-related deaths compared
with 13% of infants dying from other causes (P ⫽ .037)
and 8.6% of survivors (P ⬍ .001). Infants dying of MAS
were more likely to have received surfactant, HFV, or
FIGURE 4
iNO (P ⫽ .037), but 5 infants received none of these Longitudinal trends in odds ratio for selected risk factors. Plot of odds ratio by year for
therapies. ethnicity (A), place and mode of delivery (B), and 5-minute Apgar score (C) are shown.
Forty-nine infants received home oxygen, with re- Odds ratios for Aboriginal/Torres Strait Islander (TSI) are specific for Australia, and those
for Pacific Islander are specific for New Zealand. “Emerg CS” indicates cesarean section in
quirement for this therapy increasing during the study labor; “Assist vag,” assisted vaginal delivery (defined in Table 1); other abbreviations as per
period. These infants had a longer duration of respira- Fig 3. a Increase in odds ratio for MASINT among Aboriginal/TSI during the study period (P
tory support, with a median of 7 days, compared with ⫽ .0091). b Decrease over time in odds ratio for birth in a tertiary center and assisted
vaginal delivery (P ⫽ .038 and 0.011, respectively). A, 䊐, Aboriginal/TSI; ‚, Pacific Is-
3.8 days for infants who did not require home oxygen (P lander; 〫, Maori. B, ‚, All CS; 䊐, Emerg CS; E, Assist vag; 〫, tertiary birth. C, 䊐, 5-min
⬍ .001). They were also more likely to receive surfac- Apgar ⬍7.

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 TABLE 2 Therapies Received by the ANZNN MASINT Cohort
Variable All Years 1995–1997a 1998–2000 2001–2002 Longitudinal Trend (P)
Surfactant, any type 30.8 20.1 35.7 42.9 1 (⬍.001)
HFV 19.1 14.9 16.0 29.5 1 (⬍.001)
INO 29.5 21.6 31.4 35.7 1 (⬍.001)
ECMO 1.1 1.1 0.7 1.8 Nil
Surfactant or HFV 42.4 29.2 41.3 53.3 1 (⬍.001)
Surfactant or HFV or iNO 50.6 39.2 50.8 58.8 1 (⬍.001)
NCPAP usedb 24.2 17.2 24.6 36.6 1 (⬍.001)
Data shown are % of total in each case. 1 indicates increased over time; 2, decreased over time.
a Data on HFV and iNO were not collected in 1995; all year percentages for these therapies, therefore, slightly underestimate the actual figures.

b Either before or after the period of intubation and mechanical ventilation.

TABLE 3 Respiratory Outcomes and Complications in the ANZNN MASINT Cohort

Variable All Years 1995–1997 1998–2000 2001–2002 Longitudinal Trend (P)
Air leak, % of total 9.6 11.0 10.5 5.3 Nil
Duration of intubation, median (IQR), d 3 (2–6) 3 (2–6) 3 (2–6) 3 (1.5–6) Nil
Duration respiratory support, median (IQR), d 4 (2–7) 4 (2–7) 4 (2–7) 3.1 (2–7) Nil
Duration oxygen therapy, median (IQR), d 6 (3–15) 6 (3–13) 6 (3–15) 7 (3–17) 1 (.036)
Length of hospital stay, median (IQR), d 13 (8–24) 10 (7–19) 14 (8–24) 17 (10–29) 1 (⬍.001)
Death, % of total 6.6 5.8 7.9 5.7 Nil
MAS-related death, % of total 2.5 2.3 2.5 3.2 Nil
Home oxygen, % of total 4.7 2.8 5.7 6.6 1 (.0093)
IQR indicates interquartile range; 1, increased over time; 2, decreased over time; “duration respiratory support,” the duration of intubation plus duration of nCPAP.

tant, HFV, or iNO (P ⫽ .026), although 16 infants re-
ceived none of these therapies.
In multiple linear regression analysis, duration of re-
spiratory support in MASINT survivors was found to be
predicted by the following binary variables: cesarean
section in labor (coefficient: 1.33; P ⫽ .003), fetal distress
(coefficient: 1.05; P ⫽ 0.012), indigenous Australian or
Pacific Islander ethnicity (coefficient: 1.38; P ⫽ 0.019),
and male gender (coefficient: 0.82; P ⫽ 0.040). Gesta-
tional age, intrauterine growth restriction, and 5-minute
Apgar score did not independently predict duration of
respiratory support when added to the model.
DISCUSSION
In this study we investigated the epidemiology of MAS
in a large cohort of ventilated infants, with reference to
available data for the entire birth population during the
same period. We found that during the period 1995–
2002, there was a reduction in the incidence of MASINT
to ⬍0.40 cases per 1000 live births, a strong association
of MASINT with low 5-minute Apgar score, a clear in-
crease in risk in Pacific Islander and indigenous Austra-
lian pregnancies, and a similar association with ad-
vanced gestation to that noted previously. A heightened
risk of MASINT was also noted after planned home birth.
Our data show a median duration of respiratory support
of 4 days, with 31%, 19%, and 30% of cases receiving
exogenous surfactant, HFV, and iNO, respectively. Mor-
tality directly attributable to MAS was 2.5% in the
MASINT cohort.
A strength of this study lies in the large numbers of
infants with MASINT in the ANZNN cohort (1061 in-
fants), in whom a relatively large individual data set has
been assembled. In addition, ANZNN data entry allows
only 1 primary respiratory diagnosis, with MAS being a
clearly defined and distinct entity. This allows exclusion
of meconium-stained infants with minimal evidence of
parenchymal disease in whom the main diagnosis is
PPHN. We have also had the advantage of obtaining data
from large perinatal data registries in both countries,
meaning that the findings in the ANZNN cohort can be
placed in the context of the total population of 2 490 862
live births in which the cases of MASINT occurred.
The low incidence of MASINT and its apparent reduc-
tion during the study period confirm that modern ob-
stetric practices can, for the most part, interrupt the
chain of events that results in significant aspiration of
meconium. The reduction in incidence cannot be as-
cribed to more zealous delivery room management, in
particular, tracheal suctioning. Indeed, in the latter part
of the study period, routine intubation of the trachea
after MSAF was largely abandoned in Australia and New
Zealand, contemporaneous with the publication of a
randomized, controlled trial finding no benefit from this
intervention in the vigorous infant.15 The decrease in
incidence parallels the findings of Yoder et al,8 who, in
selected birth cohorts from the same time period, found
a reduction in risk of MAS, attributed to avoidance of
postmaturity and more aggressive management of sus-
pected fetal distress. The reduced incidence of MASINT
over time in the present study would seem to relate to
similar factors, with advanced gestation and the propor-

PEDIATRICS Volume 117, Number 5, May 2006 1717

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tion of infants having a 5-minute Apgar score ⬍7 being
seen to decrease from 1995–2002.
Our data analysis allowed the computation of odds
ratios for a number of potential risk factors for MASINT in
the total birth population. In Australian live births, we
noted a very strong association with a 5-minute Apgar
score ⬍7, with an overall odds ratio of 52. This is, to our
knowledge, the first population-based study to quantify
the risk of MAS in relation to condition of the infant at
birth. The implication is that ⬃1.3% of all live-born
infants with a 5-minute Apgar score ⬍7 will subse-
quently be ventilated with MAS compared with 0.025%
of those with a 5-minute Apgar score ⱖ7. Other cohort
studies have documented the importance of condition at
birth in determining the risk of MAS developing in the
context of MSAF. For this latter association, Wiswell et
al,15 using stepwise linear regression, reported an odds
ratio of 21; others have found the risk to be approxi-
mately fourfold.8,12 There remains some dispute about
how this effect is mediated; the presence of fetal distress
requiring obstetric intervention in ⬎50% of the ANZNN
MASINT cohort suggests exaggerated fetal respiration and
in utero aspiration of meconium as a possible mecha-
nism.
The ethnology of MAS has been explored in this
study, with the finding of a 3 times greater risk of
MASINT in Pacific Islanders and indigenous Australians
and, in the latter group, an apparent upsurge in risk in
2001 and 2002. These findings complement those of
other investigators in identifying ethnic groups of
heightened risk of MSAF and MAS. Black Americans
and Africans have been found to have a risk of MSAF 1.5
to 2.6 times that of other ethnic groups,7,10,17,19 the ex-
planation for which may lie in earlier attainment of fetal
maturity and is not related to longer gestation.19 Pacific
Islanders in New Zealand have a 1.8-fold increase in risk
of MSAF.18 There are no published data regarding risk of
MSAF or MAS in indigenous Australians. Our popula-
tion-based estimate of the risk of MAS in Pacific Island-
ers (odds ratio: 2.7) is similar to that noted previously
within a single hospital (odds ratio: 3.6)20 and cannot be
entirely explained by the increase in the risk for MSAF
noted in this group. At least within the MASINT cohort,
we could not identify any other possible explanatory
factors, with fetal distress, Apgar score, and gestation
being equivalent among Pacific Islanders, indigenous
Australians, and others (data not shown). The mecha-
nism by which ethnicity imparts additional risk of MAS
requires additional study. We found, as have others,18 no
increase in the risk of MAS among the New Zealand
Maori population.
The risk of MASINT among live-born infants was in-
creased beyond 40 weeks’ gestation, with a 3.4-fold
increase in risk at ⬎41 weeks. Only 1 other population-
based study has examined the relationship between ges-
tation and risk of MAS, reporting an odds ratio of 2.9 for
1718 DARGAVILLE et al
Downloaded from pediatrics.aappublications.org at Michigan State Univ on June 14, 2015
the risk of MAS beyond 41 weeks.24 The propensity to
develop MAS at advanced gestation would seem to be
related both to a higher risk of MSAF10,17,21–23 and an
increased likelihood that MAS will occur in the presence
of MSAF,8,11,23 independent of other risk factors, such as
fetal distress and low Apgar scores.8
We found that place of birth was a predictor of
MASINT, with a higher risk for infants born in tertiary
centers (odds ratio: 1.65) and for planned home births
(odds ratio: 2.74). This latter finding is in contrast to the
reported outcome for planned home birth in Canada,
where no apparent increase in the risk of either MSAF or
MAS was noted.34 We also found cesarean delivery to be
associated with MASINT, as has been documented previ-
ously in a smaller birth cohort.16 The need for cesarean
delivery is also known to be associated with a higher risk
of subsequent MAS in the setting of MSAF.11,12,15 Fetal
growth restriction has been linked previously to MAS,24
and we found a doubling of risk for MASINT in growth-
restricted infants. Most infants with MASINT were, how-
ever, well-grown, with average birth weight being be-
tween the 25th and 50th percentile for gender and
gestation.29
A weakness of our investigation is that within the
total birth population it was not possible to ascertain the
incidence of MSAF, a requisite intermediary in the
pathogenesis of MAS. This limits, to some degree, our
capacity to distinguish whether the risk factors we de-
fined within the population exert their effect by increas-
ing the rate of MSAF, the risk of MAS in the presence of
MSAF, or both. Similarly, for this study we did not have
access to data from each individual in the total birth
population and, thus, can perform only univariate data
analysis. In the absence of multivariate regression anal-
ysis, it is not possible to define clearly whether the
heightened risks of MASINT related to ethnicity and ges-
tation are subsumed in a final common pathway of fetal
distress or low Apgar score. These questions clearly need
additional investigation in population-based epidemio-
logic studies.
Despite limited data to support the use of HFV and
exogenous surfactant in MAS, both of these treatments
were applied with increasing frequency over the study
period. Anecdotally, HFV in the form of oscillatory or jet
ventilation has been found to be effective in supporting
infants with MAS35,36 and may be a contributing factor to
the low requirement for extracorporeal membrane oxy-
genation in the ANZNN MASINT cohort. In a national
survey of neonatal units in continental France, Nolent et
al37 found high-frequency oscillatory ventilation to be
used for MAS in 27 of 29 units; a similar situation exists
in Australia and New Zealand (P.A.D., unpublished
data).
Of the trials of bolus surfactant therapy published
during the study period,38,39 only that of Findlay et al38
show clear benefits beyond an improvement in oxygen-
ation. It is, therefore, somewhat surprising that exoge-
nous surfactant therapy has found such a prominent
place in the treatment of MASINT. In the latter years of
the study period, exogenous surfactant was adminis-
tered to ⬃40% of all infants with MASINT. No data are
available in this study concerning surfactant dose and
retreatment.
Among the ANZNN MASINT cohort, 51% of infants
received ⱖ1 HFV, iNO, and exogenous surfactant, with a
documented increase in this proportion from 1996 to
2002. The uptake of these newer therapies over the
study period seems to have had no effect on the duration
of intubation, and the duration of oxygen therapy and
length of hospital stay have increased in the MASINT
cohort overall. These findings emphasize the supportive
rather than curative nature of these therapies in infants
with MASINT.
The mortality risk for ventilated infants with MAS in
Australia and New Zealand remains significant. Overall
mortality was 6.6%, with deaths directly attributable to
the respiratory illness occurring in 2.5% of the entire
MASINT cohort and 0.96 per 100 000 live births. This
latter figure compares favorably with other population-
based estimates of MAS-related mortality. Sriram et al7
found a mortality of 2.0 per 100 000 live-born infants in
the United States in 1998 –2000; Nolent et al37 report
1.03 deaths per 100 000 births in France in 2000 –2001,
but incomplete ascertainment of MASINT cases in this
study may limit the reliability of this estimate. These
population-based estimates of mortality from MAS are
generally markedly lower than those derived from hos-
pital birth cohorts. The largest of these, studying cases of
MAS in 7 hospitals in the United States during the years
1973–1987 (total birth population: 176 790), found a
mortality rate of 28 per 100 000 live births.4 Another
study found a mortality rate of 22 per 100 000 among
85 562 live births in 1 hospital in Saudi Arabia during
the period 1989 –1994.40 The apparent high mortality in
hospital-based studies is a reflection of the high-risk
birth populations from which the estimates are made
and can be presumed to also be related to the time period
in which the studies were done, before the advent of a
number of newer therapies that seem to have improved
outcome in MAS. Other more recent studies of smaller
hospital-based cohorts have shown lower mortality, in-
cluding, in several instances, no MAS-related deaths.8,41
Pneumothorax remains an important complication of
MAS, occurring in 9.6% of the MASINT cohort overall,
with an apparent reduction to ⬃5% in 2001–2002.
Other recent studies have reported an incidence of
pneumothorax in intubated infants of 8%,38 14%,42 and
20%,43 although this last study selected infants with
more severe disease. Despite the advances in respiratory
support for MAS, pneumothorax remains an important
indicator of disease severity, being present in 42% of
Downloaded from pediatrics.aappublications.org at Michigan State Univ on June 14, 2015
infants who ultimately died of MAS in the ANZNN co-
hort.
Durations of intubation and respiratory support did
not alter throughout the study period, although more
infants received nCPAP either before or after mechanical
ventilation. Disconcertingly, the duration of oxygen
therapy and length of hospital stay increased during the
study period, reaching a median of 8 and 17 days, re-
spectively, in 2002. These figures emphasize the consid-
erable burden that MAS continues to place on afflicted
infants, their families, and the health care system.
CONCLUSIONS
We found in this study that the incidence of MAS re-
quiring intubation in 2 countries in the developed world
is low and seems to be decreasing. The risk of MASINT is
significantly greater in the presence of fetal distress and
low Apgar score, as well as Pacific Islander and indige-
nous Australian ethnicity. MAS is now frequently
treated with newer therapeutic modalities, such as HFV,
iNO, and exogenous surfactant, but the duration of ven-
tilation and oxygen therapy have not been improved as
a result. Mortality for MASINT is low, but there remains
a significant risk of pneumothorax.
ACKNOWLEDGMENTS
We thank Deborah Donoghue and Samanthi Abeywar-
dana, past and current Australian and New Zealand Neo-
natal Network Project Officers, and the Directors and
participating units of the Australian and New Zealand
Neonatal Network: Australia: Professor John Whitehall
(Women’s and Children’s Health Institute, the Towns-
ville Hospital); Professor David Tudehope (Mater Moth-
er’s Hospital, Brisbane); Dr David Cartwright (Neonatol-
ogy, Royal Women’s Hospital, Brisbane); Dr Chris Wake
(NICU, John Hunter Hospital, Newcastle); Associate Pro-
fessor Nick Evans (the John Spence Nurseries, Royal
Prince Alfred Women and Infants, Sydney); Dr Robert
Guaran (Newborn Care, Liverpool Health Service, Liv-
erpool); Dr Robert Halliday (Neonatology, Children’s
Hospital at Westmead, Sydney); Dr Kei Lui (Newborn
Care, Royal Hospital for Women, Sydney); Dr Barry
Duffy, PICU, Sydney Children’s Hospital, Sydney); Dr
Lyn Downe (NICU, Nepean Hospital); Professor William
Tarnow-Mordi (Neonatal Medicine, Westmead Hospital,
Sydney); Associate Professor Graham Reynolds (Pediat-
rics and Child Health, Canberra Hospital, Canberra); Dr
Andrew Watkins (Neonatology [Medical], Mercy Hospi-
tal for Women, Melbourne); Dr Andrew Ramsden
(NICU, Monash Medical Centre, Melbourne); Dr Peter
McDougall (Neonatal Services, Royal Children’s Hospi-
tal, Melbourne); Dr Neil Roy (Neonatal Services, Royal
Women’s Hospital, Melbourne); Dr Chris Bailey (Pedi-
atrics, Launceston General Hospital, Launceston); Asso-
ciate Professor Peter Marshall (Centre for Perinatal Med-
icine, Flinders Medical Centre, Adelaide); Dr Ross
PEDIATRICS Volume 117, Number 5, May 2006 1719
Haslam (Newborn Services, Women’s and Children’s
Hospital, Adelaide); Professor Karen Simmer (Medical
Director, Neonatology Clinical Care Unit, King Edward
Memorial Hospital, Perth); and Dr Charles Kilburn (Spe-
cial Care Nursery, Royal Darwin Hospital); New Zealand:
Dr Lindsay Mildenhall (Newborn Services, Middlemore
Hospital, Auckland); Dr Carl Kuschel (Newborn Ser-
vices, National Women’s Hospital, Auckland); Dr David
Bourchier (Newborn Care, Waikato Hospital, Hamilton);
Dr Vaughan Richardson (Neonatal Unit, Wellington
Women’s Hospital, Wellington); Dr Nicola Austin (New-
born Intensive Care, Christchurch Women’s Hospital,
Christchurch); Dr Roland Broadbent (NICU, Dunedin
Hospital); Dr Graeme Lear (Neonatal Unit, Gisborne
Hospital); Dr Jenny Corban (Pediatrics, Hawkes Bay
Hospital); Dr Ken Dawson (Newborn Unit, Wairau Hos-
pital, Nelson Marlborough District Health Board); Dr Jeff
Brown (Child Health, Mid Central Health); Dr Stephen
Bradley (Pediatrics, Rotorua Hospital, Rotorua); Dr Paul
Tomlinson (Neonatal Unit, Southland Hospital, South-
land); Dr John Doran (Child and Adolescent Commu-
nity Centre, Taranaki Base Hospital); Dr Hugh Lees (Spe-
cial Care Unit, Tauranga Hospital); Dr Philip Morrison
(Pediatrics, Timaru Hospital); Dr Chris Moyes (Child
Health, Whakatane Hospital); and Dr Peter Jankowitz
(Special Care Infant Unit, Whangarei Area Hospital).
REFERENCES
1. Cleary GM, Wiswell TE. Meconium-stained amniotic fluid and
the meconium aspiration syndrome: an update. Pediatr Clin
North Am. 1998;45:511–529
2. Wiswell TE, Bent RC. Meconium staining and the meconium
aspiration syndrome: unresolved issues. Pediatr Clin North Am.
1993;40:955–981
3. Coltart TM, Byrne DL, Bates SA. Meconium aspiration
syndrome: a 6-year retrospective study. Br J Obstet Gynaecol.
1989;96:411– 414
4. Wiswell TE, Tuggle JM, Turner BS. Meconium aspiration
syndrome: have we made a difference? Pediatrics. 1990;85:
715–721
5. Bhutani VK, Chima R, Sivieri EM. Innovative neonatal venti-
lation and meconium aspiration syndrome. Indian J Pediatr.
2003;70:421– 427
6. Wiswell TE. Advances in the treatment of the meconium aspi-
ration syndrome. Acta Paediatr. 2001;90(suppl):28 –30
7. Sriram S, Wall SN, Khoshnood B, Singh JK, Hsieh HL, Lee KS.
Racial disparity in meconium-stained amniotic fluid and meco-
nium aspiration syndrome in the United States, 1989 –2000.
Obstet Gynecol. 2003;102:1262–1268
8. Yoder BA, Kirsch EA, Barth WH, Gordon MC. Changing ob-
stetric practices associated with decreasing incidence of meco-
nium aspiration syndrome. Obstet Gynecol. 2002;99:731–739
9. Peng TC, Gutcher GR, Van Dorsten JP. A selective aggressive
approach to the neonate exposed to meconium-stained amni-
otic fluid. Am J Obstet Gynecol. 1996;175:296 –301
10. Alexander GR, Hulsey TC, Robillard PY, De Caunes F, Pa-
piernik E. Determinants of meconium-stained amniotic fluid in
term pregnancies. J Perinatol. 1994;14:259 –263
11. Karatekin G, Kesim MD, Nuhoglu A. Risk factors for meco-
nium aspiration syndrome. Int J Gynaecol Obstet. 1999;65:
295–297
1720 DARGAVILLE et al
Downloaded from pediatrics.aappublications.org at Michigan State Univ on June 14, 2015
12. Meydanli MM, Dilbaz B, Caliskan E, Dilbaz S, Haberal A. Risk
factors for meconium aspiration syndrome in infants born
through thick meconium. Int J Gynaecol Obstet. 2001;72:9 –15
13. Paz Y, Solt I, Zimmer EZ. Variables associated with meconium
aspiration syndrome in labors with thick meconium. Eur J
Obstet Gynecol Reprod Biol. 2001;94:27–30
14. Rossi EM, Philipson EH, Williams TG, Kalhan SC. Meconium
aspiration syndrome: intrapartum and neonatal attributes.
Am J Obstet Gynecol. 1989;161:1106 –1110
15. Wiswell TE, Gannon CM, Jacob J, et al. Delivery room man-
agement of the apparently vigorous meconium-stained
neonate: results of the multicenter, international collaborative
trial. Pediatrics. 2000;105:1–7
16. Hernandez C, Little BB, Dax JS, Gilstrap LC, Rosenfeld CR.
Prediction of the severity of meconium aspiration syndrome.
Am J Obstet Gynecol. 1993;169:61–70
17. Sedaghatian MR, Othman L, Hossain MM, Vidyasagar D. Risk
of meconium-stained amniotic fluid in different ethnic groups.
J Perinatol. 2000;20:257–261
18. Urbaniak KJ, McCowan LM, Townend KM. Risk factors for
meconium-aspiration syndrome. Aust NZ J Obstet Gynaecol.
1996;36:401– 406
19. Patel RR, Steer P, Doyle P, Little MP, Elliott P. Does gestation
vary by ethnic group? A London-based study of over 122,000
pregnancies with spontaneous onset of labour. Int J Epidemiol.
2004;33:107–113
20. Benny PS, Malani S, Hoby MA, Hutton JD. Meconium
aspiration: role of obstetric factors and suction. Aust NZ J Obstet
Gynaecol. 1987;27:36 –39
21. Eden RD, Seifert LS, Winegar A, Spellacy WN. Perinatal char-
acteristics of uncomplicated postdate pregnancies. Obstet Gy-
necol. 1987;69:296 –299
22. Ostrea EMJ, Naqvi M. The influence of gestational age on the
ability of the fetus to pass meconium in utero: clinical impli-
cations. Acta Obstet Gynecol Scand. 1982;61:275–277
23. Usher RH, Boyd ME, McLean FH, Kramer MS. Assessment of
fetal risk in postdate pregnancies. Am J Obstet Gynecol. 1988;
158:259 –264
24. Clausson B, Cnattingius S, Axelsson O. Outcomes of post-term
births: the role of fetal growth restriction and malformations.
Obstet Gynecol. 1999;94:758 –762
25. Sunoo CS, Kosasa TS, Nakayama RT, Hale RW. The incidence of
meconium-aspiration in Hawaii. Hawaii Med J. 1993;52:290 –293
26. Donoghue D; for the Australian and New Zealand Neonatal
Network. The Report of the Australian and New Zealand Neonatal
Network, 2002. Sydney, Australia: Australian and New Zealand
Neonatal Network; 2004
27. Liu WF, Harrington T. Delivery room risk factors for meconium
aspiration syndrome. Am J Perinatol. 2002;19:367–378
28. Agrawal V, David RJ, Harris VJ. Classification of acute respira-
tory disorders of all newborns in a tertiary care center. J Natl
Med Assoc. 2003;95:585–595
29. Roberts CL, Lancaster PA. Australian national birthweight per-
centiles by gestational age. Med J Aust. 1999;170:114 –118
30. Laws PJ, Sullivan PA. Australia’s Mothers and Babies, 2002. Sydney,
Australia: AIHW National Perinatal Statistics Unit; 2004
31. Statistics New Zealand. Births and deaths. 2005. Available at:
www.stats.govt.nz/datasets/population/births.htm. Accessed:
March 24, 2006
32. New Zealand Ministry of Health. Obstetric Procedures, 1988/
89 –1997/98. Wellington, New Zealand: New Zealand Ministry
of Health;1999
33. New Zealand Ministry of Health. Report on Maternity: Maternal
and Newborn Information, 2002. Wellington, New Zealand: New
Zealand Ministry of Health; 2004
34. Janssen PA, Lee SK, Ryan EM, et al. Outcomes of planned
 home births versus planned hospital births after regulation of
midwifery in British Columbia. CMAJ. 2002;166:315–323
35. Davis JM, Richter SE, Kendig JW, Notter RH. High-frequency
jet ventilation and surfactant treatment of newborns with se-
vere respiratory failure. Pediatr Pulmonol. 1992;13:108 –112
36. Paranka MS, Clark RH, Yoder BA, Null DM. Predictors of
failure of high-frequency oscillatory ventilation in term infants
with severe respiratory failure. Pediatrics. 1995;95:400 – 404
37. Nolent P, Hallalel F, Chevalier JY, Flamant C, Renolleau S.
Meconium aspiration syndrome requiring mechanical
ventilation: incidence and respiratory management in France
(2000 –2001) [in French]. Arch Pédiatr. 2004;11:417– 422
38. Findlay RD, Taeusch HW, Walther FJ. Surfactant replacement
therapy for meconium aspiration syndrome. Pediatrics. 1996;
97:48 –52
39. Lotze A, Mitchell BR, Bulas DI, et al. Multicenter study of
surfactant (beractant) use in the treatment of term infants with
severe respiratory failure. Survanta in Term Infants Study
Group. J Pediatr. 1998;132:40 – 47
40. Al Takroni AM, Parvathi CK, Mendis KB, Hassan S, Reddy I,
Kudair HA. Selective tracheal suctioning to prevent meconium
aspiration syndrome. Int J Gynaecol Obstet. 1998;63:259 –263
41. Blackwell SC, Carreno CA, Hassan SS, et al. Meconium stain-
ing and meconium aspiration syndrome: is there seasonal vari-
ation? Fetal Diagn Ther. 2001;16:208 –210
42. Vain NE, Szyld EG, Prudent LM, Wiswell TE, Aguilar AM,
Vivas NI. Oropharyngeal and nasopharyngeal suctioning of
meconium-stained neonates before delivery of their shoulders:
multicentre, randomised controlled trial. Lancet. 2004;364:
597– 602
43. Chinese Collaborative Study Group for Neonatal Respiratory
Diseases. Treatment of severe meconium aspiration syndrome
with porcine surfactant: a multicentre, randomized, controlled
trial. Acta Paediatr. 2005;94:896 –902

HELMET USE AND RISK OF HEAD INJURIES IN ALPINE SKIERS AND SNOWBOARDERS

“Context: Although using a helmet is assumed to reduce the risk of head

injuries in alpine sports, this effect is questioned. In contrast to bicycling or
inline skating, there is no policy of mandatory helmet use for recreational
alpine skiers and snowboarders.
Objective: To determine the effect of wearing a helmet on the risk of head
injury among skiers and snowboarders while correcting for other potential
risk factors.
Design, Setting, and Participants: Case-control study at 8 major Nor-
wegian alpine resorts during the 2002 winter season, involving 3277 injured
skiers and snowboarders reported by the ski patrol and 2992 non-injured
controls who were interviewed on Wednesdays and Saturdays. The controls
comprised every 10th person entering the bottom main ski lift at each resort
during peak hours. The number of participants interviewed corresponded
with each resort’s anticipated injury count based on earlier years. . . .
Results: Head injuries accounted for 578 injuries (17.6%). Using a helmet
was associated with a 60% reduction in the risk for head injury (odds ratio
[OR], 0.40; 95% confidence interval [CI], 0.30 – 0.55; adjusted for other risk
factors) when comparing skiers with head injuries with uninjured controls.
The effect was slightly reduced (OR, 0.45; 95% CI, 0.34 – 0.59) when skiers
with other injuries were used as controls. For the 147 potentially severe head
injuries, those who were referred to an emergency physician or for hospital
treatment, the adjusted OR was 0.43 (95% CI, 0.25– 0.77). The risk of head
injury was higher among snowboarders than for alpine skiers (adjusted OR,
1.53; 95% CI, 1.22–1.91).
Conclusion: Wearing a helmet is associated with reduced risk of head
injury among snowboarders and alpine skiers.”
Sulheim S, Holme I, Ekeland A, Bahr R. JAMA. February 22, 2006
Noted by JFL, MD

PEDIATRICS Volume 117, Number 5, May 2006 1721

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The Epidemiology of Meconium Aspiration Syndrome: Incidence, Risk Factors,
Therapies, and Outcome
Peter A. Dargaville and Beverley Copnell
Pediatrics 2006;117;1712
DOI: 10.1542/peds.2005-2215
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PEDIATRICS is the official journal of the American Academy of Pediatrics. A monthly

publication, it has been published continuously since 1948. PEDIATRICS is owned, published,
and trademarked by the American Academy of Pediatrics, 141 Northwest Point Boulevard, Elk
Grove Village, Illinois, 60007. Copyright © 2006 by the American Academy of Pediatrics. All
rights reserved. Print ISSN: 0031-4005. Online ISSN: 1098-4275.

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The Epidemiology of Meconium Aspiration Syndrome: Incidence, Risk Factors,
Therapies, and Outcome
Peter A. Dargaville and Beverley Copnell
Pediatrics 2006;117;1712
DOI: 10.1542/peds.2005-2215

The online version of this article, along with updated information and services, is
located on the World Wide Web at:
http://pediatrics.aappublications.org/content/117/5/1712.full.html

PEDIATRICS is the official journal of the American Academy of Pediatrics. A monthly

publication, it has been published continuously since 1948. PEDIATRICS is owned,
published, and trademarked by the American Academy of Pediatrics, 141 Northwest Point
Boulevard, Elk Grove Village, Illinois, 60007. Copyright © 2006 by the American Academy
of Pediatrics. All rights reserved. Print ISSN: 0031-4005. Online ISSN: 1098-4275.

Downloaded from pediatrics.aappublications.org at Michigan State Univ on June 14, 2015