PEDIATRICS Vol. 99 No. 4 April 1997,
p. e2
Copyright ©1997 by the American Academy of Pediatrics
ELECTRONIC ARTICLE:
Maternal Receipt of Magnesium Sulfate Does Not Seem to Reduce the
Risk of Neonatal White Matter Damage
Alan Leviton*, 
,
Nigel Paneth§,
Mervyn Susser
,
M. Lynn Reuss,
Elizabeth N. Allred*,
Karl Kuban*, ,
Ulana Sanocka, ¶,
Thomas Hegyi#, **,
Mark Hiatt#, **,
Farrokh Shahrivar, , and
Linda J. Van Marter, §§
From * Children's Hospital and Harvard Medical School,
Boston, Massachusetts; § Michigan State University, East Lansing,
Michigan; Columbia University, New York, New York; ¶ Babies'
Hospital, New York, New York; # St Peter's Medical Center, New
Brunswick, New Jersey; ** Robert Wood Johnson Medical School, New
Brunswick, New Jersey; St Luke's-Roosevelt Medical Center,
New York, New York; and §§ Brigham and Women's Hospital, Boston,
Massachusetts.
ABSTRACT
- INTRODUCTION
- METHODS
- RESULTS
- DISCUSSION
- ADDENDUM
- ACKNOWLEDGMENTS
- ABBREVIATIONS
- REFERENCES
ABSTRACT 
Objective. To investigate whether in
utero exposure to magnesium sulfate is associated with a lower
incidence of cranial ultrasonographic abnormalities that predict
cerebral palsy in infants who weigh less than 1501 g at birth.
Design. For a prospective study of the antecedents of
cranial ultrasonographic abnormalities, we enrolled infants who weighed 500 to 1500 g when born at five institutions. Data were collected by interview of the mothers and review of medical records. Protocol cranial ultrasonograms were obtained as close as possible to postnatal days 1, 7, and 21. Abnormality on cranial ultrasound scans was determined by a consensus committee of three sonologists.
Results. Of the 1518 infants for whom we knew whether the
mothers received magnesium sulfate, the first protocol cranial
ultrasound scan was available for 1409 infants, the second for 1274 infants, and the third for 1050 infants. Forty-five percent of infants were exposed to magnesium sulfate before delivery. The major correlates of magnesium sulfate exposure were receipt of antenatal corticosteriods and a diagnosis of preeclampsia and/or pregnancy-induced hypertension. Maternal magnesium receipt was not associated with a reduced incidence of hypoechoic or hyperechoic images of white matter parenchyma, intraventricular hemorrhage, or ventriculomegaly, even when the sample
was stratified by each of six potential confounders. When adjustment
was made for gestational age, a measure of birth weight for gestational
age, antenatal corticosteroid exposure, preeclampsia and
pregnancy-induced hypertension, route of delivery, and the occurrence
of any labor, the risk ratios for each cranial ultrasonographic abnormality associated with magnesium sulfate exposure hovered close to
1.
Conclusion. Maternal receipt of magnesium sulfate does not
seem to be associated with an appreciably reduced risk of cranial ultrasonographically defined neonatal white matter damage,
intraventricular hemorrhage, or ventriculomegaly. low birth
weight, magnesium sulfate, periventricular leukomalacia, antenatal
corticosteriods, intraventricular hemorrhage, pregnancy-induced
hypertension.
INTRODUCTION
Based on their recently published case-control study, Nelson and
Grether1 concluded that maternal receipt of magnesium sulfate was associated with a greatly reduced risk of cerebral palsy in
very low birth weight infants. They characterized magnesium sulfate as
an inexpensive intervention that seems to be relatively safe. One
additional study has also found a reduced incidence of cerebral palsy
in those born before term who were exposed antenatally to magnesium
sulfate,2 but another has not.3
Hypoechoic images (ie, echolucencies or what some consider cysts) in
the cerebral white matter parenchyma, some of which are referred to as
"periventricular leukomalacia," are the cranial ultrasonographic
abnormalities that best predict cerebral palsy in premature
infants.4 Hyperechoic images (ie, echodensities), sometimes interpreted as infarction or grade IV hemorrhage, also predict an increased risk of cerebral palsy.
In one sample, 54% of prematurely born infants in whom disabling
cerebral palsy developed had parenchymal echodensity and lucency or
ventricular enlargement seen on cranial ultrasound scans obtained
between 1 and 5 weeks after birth.9 This has led to the
inferences that cerebral palsy in those born before term probably
represents two disorders; only one of these disorders is characterized
by a cranial ultrasound signature, and as much as half of disabling
cerebral palsy in preterm infants is a consequence of this disorder.
The study of the antecedents of etiologically heterogeneous disorders
such as cerebral palsy should be enhanced by study of more homogeneous
subgroups, such as those with early sonographic expression.
If maternal receipt of magnesium sulfate reduces the risk of cerebral
palsy in the prematurely born, then magnesium sulfate exposure in utero
could be expected to reduce the risk of hyperechoic and hypoechoic
images. This report explores the relationships between magnesium
sulfate and hyperechoic and hypoechoic images of parenchymal white
matter (which we refer to jointly as ultrasonographic expressions of
white matter damage) and other cranial ultrasound abnormalities, both
before and after adjustment for potential confounders.
METHODS
Sample
The mothers of 1665 infants were recruited for this study. To be
eligible, infants had to weigh 500 to 1500 g when born at five
participating hospitals between January 1991 and December 1993. A total
of 60 infants died before cranial ultrasound scans could be obtained or
had scans that, despite intensive efforts, could not be found months to
years later. Information about receipt of magnesium sulfate and
potential confounders was available from maternal medical records for
1518 of the 1605 infants for whom scans were available (Table
1). These infants and their 1331 mothers constitute the
sample for this set of analyses. The distributions of maternal,
obstetric, and newborn characteristics are presented in Table 1. The
gestational age estimate was based on the following hierarchy: fetal
ultrasound scan estimate obtained before the end of the 13th week of
gestation (32% of the sample), dates in the prenatal record (62%),
maternal interview (4%), and the admission log book of the neonatal
intensive care unit (2%).
|
Table 1.
Characteristics of Very Low Birth Weight Infants and Their Mothers Who
Were or Were Not Exposed to Magnesium Sulfate and Whether the Mothers
Were Given a Diagnosis of Pregnancy-induced Hypertension
[View Table]
|
We divided gestational age into three groups, younger than 26 weeks, 26 to 28 weeks, and older than 28 weeks. The group of infants younger than
26 weeks represents infants near the borderline of viability. Because
we excluded infants weighing more than 1500 g, fetal growth
retardation is overrepresented in the group of infants older than 28 weeks.11
Cranial Ultrasound Scans
Manuals were created to standardize the scanning procedure and
the interpretation of scans. The six standard coronal views were those
advised by Teele and Share.12 Protocol scans were obtained
once during the first 4 postnatal days (median, day 1), once between
postnatal days 5 and 14 (median, day 7), and once between days 15 and
60 (median, day 22). The first protocol cranial ultrasound scans were
available for 1409 infants. The 109 infants who were not scanned during
the first protocol scan interval tended to be gestationally older and
more stable physiologically than their peers. All infants who died and
some who were clinically well or who were transferred to other
institutions did not have later scans. As a consequence, the second
protocol set of scans was available for 1274 infants, and the third set
was available for 1050 infants.
Each set of scans was read independently by two sonologists. Scans were
brought to a consensus committee if either reader identified: (1) a
hyperechoic or hypoechoic lesion anywhere in the cerebral white matter,
(2) moderate or severe ventriculomegaly (visually assessed against a
template), or (3) intraventricular hemorrhage (IVH; ie, hyperechoic
material in the lateral ventricles). Nine of the 10 study sonologists
constituted the consensus committees. All consensus committees
consisted of a minimum of three sonologists (each from a different
institution) reading together. After every 2-hour session, a break was
taken, and one member of the committee was rotated. All members of each
consensus committee had to agree about the presence, size, and location
of all white matter lesions and about the presence of at least moderate
ventricular dilation or IVH. If they could not agree, then the scans
were brought to a larger consensus group (consisting of the three or
four readers who could not achieve consensus plus the three or four
readers from another consensus committee). The majority decision,
needed in approximately 8% of all sets of scans presented to a
consensus committee, was accepted as the consensus reading for these
scans.
For the purposes of this study, the five major sonographic entities are
IVH, early parenchymal echo abnormality (PEA; defined as a parenchymal
hyperechoic or hypoechoic image evident on the first protocol scan),
late PEA (defined as PEA not seen on the first protocol scan and first
evident on the second or third protocol scan), any PEA (defined as
either early or late PEA), and ventriculomegaly (defined as moderate or
severe ventricular dilation on any of the three protocol scans).
Hypoechoic images of the white matter parenchyma, which probably
reflect a number of different disorders13,14 that are not
readily distinguished sonographically,15 are also included
in Table 4 as sonographic disorders of major interest.
|
Table 4.
Risk Ratios of Cranial Ultrasound Abnormalities Associated With
Maternal Receipt of Magnesium Sulfate
[View Table]
|
Pregnancy-induced Hypertension and Magnesium Sulfate
A woman was considered to have pregnancy-induced hypertension or
preeclampsia if the diagnosis of either was found in the prenatal or
delivery charts, if during an interview shortly after delivery, the
mother acknowledged that she was told she had preeclampsia, toxemia, or
pregnancy-induced hypertension, or if the diastolic blood pressure
during pregnancy was 90 or higher, but prepregnancy hypertension was
not cited in the medical records and was denied during the interview.
Classification of magnesium sulfate receipt (ie, yes or no) was based
on information in the mother's medical record. Details about dose and
duration of magnesium sulfate were not collected.
Confounders and Correlates
For the purposes of this report, the main potential confounders
of assessments of the relationship between magnesium sulfate receipt
and intracranial sonographic abnormalities of the newborns were deemed
a priori to be preeclampsia and pregnancy-induced hypertension, receipt
of any antenatal corticosteroids, multiple gestations (ie, singletons
versus twins and triplets), the occurrence of any labor, route of
delivery, gestational age (ie, <26, 26 to 28, and >28 weeks), and
birth weight z score (ie, 
1 or greater, less than 1 to
2, and less than 2). The birth weight z score is the
number of SDs the infant's birth weight is from the median for
gestational age. Infants whose birth weight z scores are
less than 2 are in the lower 2.5% of all infants classified by birth weight for gestational age. Subsequent examinations of our data did not
identify other potential confounders.
Analysis
The null hypothesis evaluated is that infants born to women who
received magnesium sulfate shortly before delivery have the same risk
of IVH, early PEA, late PEA, any PEA, a hypoechoic image in white
matter parenchyma, and ventriculomegaly as do infants born to women who
did not receive magnesium sulfate. The relationships among variables
were evaluated in univariate analyses and in different strata defined
by the presence or absence, or level, of each potential confounder. We
created logistic regression models to adjust for all the potential
confounders at the same time. The separate analyses of singletons and
multifetal gestations provided such similar results that only findings
of the entire sample are presented. Given a sample size of 1050 infants
who had third protocol scans, a magnesium sulfate exposure prevalence
of 44% and a prevalence of any PEA of 12%, this study has a power of
0.998 to perceive an odds ratio of 0.5 and a power of 0.75 to perceive
an odds ratio of 0.67.
RESULTS
The mothers of 45% (678 of 1518) of infants were given magnesium
sulfate before delivery. These infants were more likely than their
peers to be exposed antenatally to corticosteroids (60% vs 46%), and
their mothers were more likely to carry a diagnosis of
pregnancy-induced hypertension or preeclampsia (37% vs 18%). Women
with pregnancy-induced hypertension were more likely than their peers
to give birth to gestationally older infants who had evidence of fetal
growth retardation (ie, birth weight z score less than 2)
(Table 1).
The risks of IVH, PEA, and ventriculomegaly were reduced in infants
born to women who received antenatal corticosteroids or were given a
diagnosis of preeclampsia or pregnancy-induced hypertension. Receipt of
magnesium sulfate was not associated with a reduced risk of these
cranial ultrasonographically defined disorders (Table 2).
|
Table 2.
Characteristics of Infants and Their Mothers Among Groups of Infants
Classified by the Presence of Any Cranial Ultrasonographic Abnormality
[View Table]
|
When infants were stratified according to the presence or absence of a
potential confounder, receipt of magnesium sulfate was not associated
with appreciable reductions of any cranial ultrasound abnormality among
the infants of mothers with pregnancy-induced hypertension or among the
infants of mothers who had labor (Table 3). The risk of
IVH was slightly reduced among those exposed to magnesium sulfate in
strata defined by the absence of labor, abdominal delivery, and
maternal receipt of corticosteroids, as well as in the gestationally
oldest infants and those who were growth retarded. Magnesium sulfate
receipt was not associated with a reduced risk of the other cranial
ultrasonographic abnormalities in any of the strata.
|
Table 3.
Incidence (per 100 Infants) of Cranial Ultrasound Abnormalities Among
Those Exposed Antenatally to Magnesium Sulfate Compared With the
Incidence in Those Not Exposed, Evaluated Separately in Strata of Very
Low Birth Weight Infants With or Without a Potentially Confounding
Characteristic
[View Table]
|
When logistic regression adjustment was made for the six potential
confounders (ie, gestational age divided into three groups, birth
weight z score divided into three groups, antenatal
corticosteroids, preeclampsia and/or pregnancy-induced hypertension,
route of delivery, and labor) magnesium sulfate was not associated with
a reduced risk of IVH, PEA of any form, or ventriculomegaly (Table
4).
DISCUSSION
We did not find evidence that magnesium sulfate reduces the
incidence of those cranial ultrasound abnormalities that predict cerebral palsy in preterm infants. Our analyses, stratified by the
presence or absence of preeclampsia and pregnancy-induced hypertension,
as well as by other potential correlates of magnesium receipt and
cranial ultrasound abnormalities, indicate that our findings are
unlikely to be attributable to confounding.
Because the cranial ultrasonographic expression of neonatal white
matter disorders predicts cerebral palsy in very low birth weight
infants, we assumed that if magnesium sulfate reduced the risk of
cerebral palsy, then it might do so by reducing the risk of neonatal
white matter disorders. Our failure to find a protective effect of
magnesium sulfate on the risk of neonatal white matter disorders
suggests that if magnesium sulfate does prevent cerebral palsy in those
born before term, it does so by a mechanism not associated with
preventing sonographically evident neonatal white matter damage. The
alternative inference is that magnesium sulfate does not reduce the
risk of cerebral palsy in very low birth weight infants.
Explanations for a reduced risk of cerebral palsy without a
reduced risk of neonatal white matter damage might be plausible if some
cerebral palsy in those born before term is caused by gray matter
damage. Indeed, in laboratory animal studies, magnesium does seem to
reduce the frequency and severity of neuronal damage caused by
excitotoxic amino acids.16
IVH and ventriculomegaly are correlates of white matter
damage.21 For this reason we sought, but did not find,
an inverse relationship between maternal magnesium sulfate receipt and
risk of IVH and ventriculomegaly in the newborn. Our failure to find a
reduced risk of IVH in association with maternal receipt of magnesium
sulfate is in keeping with the observation of some
investigators28,29 but not of others.30,31
Our study has a number of potential limitations. First, approximately
one third (468 of 1518) of the infants did not have third protocol
cranial ultrasound scans. This might have limited our ability to
identify hypoechoic images in some infants. On the other hand, infants
who did not have third protocol scans were the most mature and
physiologically stable, precisely those least likely to have had
hypoechoic images.4
Second, half of the infants had their third protocol cranial
ultrasound scans obtained by postnatal day 22. In our sample, however,
the proportion of third protocol scans with new hypoechoic images
remained constant during each 10-day interval, between days 22 and 60. Thus, it is unlikely that we would have had a sizable increase in the
number of infants with hypoechoic images had more of the third protocol
scans been obtained closer to postnatal day 60.
The third limitation of our study is our failure to collect
information about the amount and timing of magnesium sulfate
administration. The fourth limitation is the relatively modest power to
perceive modest reductions in the odds ratios for white matter echo
abnormality. The fifth limitation is that this is an observational
study and not a randomized clinical trial.
On the other hand, our study has a number of strengths, including
consensus reading of every set of scans deemed abnormal by either of
two readers, data collected prospectively about magnesium sulfate and
correlates, and as large a sample studied in such detail as is likely
to be available. Our findings need to be assessed in light of the
strengths and potential limitations of this study, as well as in light
of the findings, strengths, and potential limitations of other studies
of magnesium sulfate. The ideal study, a randomized clinical trial, is
unlikely to be published soon.
ADDENDUM
Since this paper was accepted for publication, two relevant
articles have been published:
Schendel DE, Berg CJ, Yeargin-Alsopp M, Boyle CA, Decoufle P. Prenatal
magnesium sulfate exposure and the risk for cerebral palsy or mental
retardation among very low-birth-weight children aged 3 to 5 years.
JAMA. 1996;276:1805-1810
Rouse DJ, Hauth JC, Nelson KG, Goldenberg RL. The feasibility of a
randomized clinical perinatal trial: maternal magnesium sulfate for the prevention of cerebral palsy. Am J Obstet
Gynecol. 1996;175:701-705
FOOTNOTES
Received for publication Apr 1, 1996; accepted Aug 20, 1996.
Reprint requests to (A.L.) Carnegie 207, Children's Hospital,
300 Longwood Ave, Boston, MA 02115.
ACKNOWLEDGMENTS
Funds for this project were provided by grant NS 27306 from the
National Institute of Neurological Disorders and Stroke.
We are grateful to the women who not only agreed to be interviewed for
this study, but also allowed data to be collected from their infants'
charts. We also express appreciation to our colleagues who contributed
to the success of this project.
ABBREVIATIONS
IVH, intraventricular hemorrhage.
PEA, parenchymal
echo abnormality.
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