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April
2007: VOLUME
4, NUMBER 8
MAGNESIUM
TOCOLYSIS
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month eNeonatal Review is unveiling our new look as well as several
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In This Issue...
In
1995, it was thought that MgSO4, in addition to being used
as a tocolytic, could function as a prophylactic to lower the prevalence
of neonatal IVH, infant mortality, and cerebral palsy. Unfortunately,
as was discovered in the Magnesium and Neurologic Endpoints Trial (MagNET),
high dose MgSO4 appears to be associated with increased IVH
and total pediatric mortality. However, because MagNET was suspended
by the Institutional Review Board at the University of Chicago, a possible
protective role for MgSO4, as it pertains to cerebral palsy,
remains unresolved.
In this issue – in a slight departure from our usual format – we present
a discussion of neuroadverse outcomes following high dose exposure to
MgSO4, possible neuroprotective effects following low dose
MgSO4 exposure, and the evidence basis for the tocolytics
that may replace MgSO4. |
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Course
Directors
Edward
E. Lawson, MD
Professor
Department of Pediatrics
- Neonatology
The Johns Hopkins
University
School of Medicine
Christoph
U. Lehmann, MD
Assistant Professor
Department of Pediatrics
- Neonatology
The Johns Hopkins
University
School of Medicine
Lawrence
M. Nogee, MD
Associate Professor
Department of Pediatrics
- Neonatology
The Johns Hopkins
University
School of Medicine
Mary
Terhaar
Assistant Professor
Undergraduate Instruction
JHU School of Nursing
Robert
J. Kopotic, MSN, RRT, FAARC
Director of Clinical
Programs
ConMed Corporation |
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GUEST
EDITORS OF THE MONTH |
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Commentary & Reviews:
Robert
Mittendorf, MD, DrPH
Professor
of Obstetrics
and Gynecology,
and Pediatrics Director, Division of General Obstetrics and Gynecology
Loyola University Medical Center
Maywood,
IL |
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Reviews:
John
G. Gianopoulos,
MD
Caestecker
Professor of Obstetrics and Gynecology Chairman, Department of
Obstetrics and Gynecology Loyola University
Medical
Center
Maywood,
IL |
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Reviews:
Jonathan
Muraskas, MD
Professor
of Pediatrics
and Neonatal-Perinatal
Medicine Chairman, Admissions Committee, Stritch School of Medicine
Loyola University
Medical
Center
Maywood,
IL |
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Guest
Faculty Disclosure
Robert
Mittendorf, MD, DrPH, has disclosed no relationship
with commercial supporters.
Jonathan
Muraskas, MD, has disclosed no relationship with commercial
supporters.
John
G. Gianopoulos, MD, has disclosed no relationship
with commercial supporters.
Unlabeled / Unapproved Uses
The authors have indicated that there will be no reference
to unlabeled/ unapproved uses of drugs or products in this presentation. |
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The
Johns Hopkins University School of Medicine and The Institute for
Johns Hopkins Nursing take responsibility for the content, quality,
and the scientific integrity of this CE activity.
At the conclusion of this activity, participants should be
able to: |
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Identify
the cranial ultrasound lesions in newborns that appear to be associated
with high dose exposures to antenatal magnesium sulfate (MgSO4) |
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Discuss
how low dose exposures to antenatal MgSO4 may be associated
with a neuroprotective effect in the developing infant and child |
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Identify
suitable tocolytics that can be used as replacements for MgSO4 |
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eNeonatal
Review is proud to continue our accredited
PODCASTS
for 2007. Listen
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An
audio interview with
Robert Mittendorf, MD, DrPH,
John G. Gianopoulos,
MD and Jonathan Muraskas,
MD from The Loyola
University Medical
Center, Maywood, IL, further exploring
the topic of Magnesium
Tocolysis.
Participants
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podcasting and how to enjoy this exciting new feature of eNeonatal
Review, please visit
this page. |
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In
1995, there was great interest, in both Chicago and Bethesda, to conduct
a randomized study to find out whether magnesium sulfate (MgSO4)
could be used during preterm labor as a preventive for cerebral palsy.
The intellectual basis for such a trial was a previously-conducted,
very persuasive, case-control study[1]. Indeed, at the time,
it seemed easy to test the ‘magnesium hypothesis’ because MgSO4 was
already being used commonly in the U.S. as a tocolytic. Moreover, it
was being used successfully, and with good evidence basis, in maternal
preeclampsia [2,3]. Indeed, despite the issues discussed
herein, MgSO4 remains the drug of choice for eclamptic seizure
prophylaxis.
Thus, based on what was thought
to be a solid epidemiologic foundation, the Magnesium and Neurologic
Endpoints Trial (MagNET) was begun at the University of Chicago. The
protocol was written by a collaborative group who convened at the National
Institutes of Health, and the study was funded by the United Cerebral
Palsy Research and Educational Foundation. Unfortunately, and to the
disappointment of all involved, the trial was suspended after 15 months.
Data analysis revealed a remarkable excess in total pediatric mortality
(fetal + neonatal + postneonatal) among babies whose mothers had been
randomized to MgSO4. Including all data - MgSO4 vs.
other tocolytics (nifedipine, indomethacin, ritodrine, or terbutaline)
or saline control - there were ten deaths in the MgSO4 arms,
whereas only one baby died in the other arms (Risk Difference, 10.7%,
95% Confidence Interval [CI] 2.9 to 18.5%; P=.02). At the request of
the CP Foundation, these adverse events were published in Lancet in
1997[4]. As an aside, it should be noted that in the years
following MagNET, it has been shown convincingly that MgSO4 is
ineffective as a tocolytic[5,6]. More importantly, in 2003,
researchers from the Cochrane Database of Systematic Reviews confirmed
the original findings from the MagNET Trial - that tocolytic MgSO4 is
associated with an increase in total pediatric mortality[7].
Moreover, in subsequent analyses
of biological data from MagNET, additional evidence was found to support
its original findings. Namely, a dose-response was found to exist between
umbilical cord serum ionized magnesium levels at delivery and subsequent
deaths in children — naturally, such a finding is important to
help establish causation[8]. In addition, because cranial
ultrasounds were done on all surviving babies, it was possible to study
relationships between magnesium and brain abnormalities such as neonatal
IVH, as well as a curious lesion in the thalami known as lenticulostriate
vasculopathy (LSV). It was found in MagNET that higher maternal serum
magnesium levels at delivery were related to neonatal IVH; IVH was found
to be associated with LSV; and, to close the triangle, LSV was found
to be associated with high exposures ( 50
g) to tocolytic MgSO4[9]. Naturally, this finding
assumed importance as the biological consequences associated with the
brain lesions could, at least partially, account for the observed increases
in pediatric mortality.
As reviewed herein, there is
evidence that is consistent with possible neuroprotective effects for
MgSO4 when used in low or modest doses, as well as reports
(from MagNET) regarding adverse neurological outcomes associated with
high dose magnesium exposures. Further, since any evidence-based plan
to abandon MgSO4 as a tocolytic requires substituting other,
more effective drugs (if, in fact, tocolytics should be used at all
in some circumstances), we discuss the efficacy of possible alternatives
- specifically, nifedipine, beta-adrenergics, indomethacin, and nitroglycerin.
References
| 1. |
Nelson
KB, Grether JK. Can
magnesium sulfate reduce the risk of cerebral palsy in very low
birthweight infants? Pediatrics 1995;95:263-9. |
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| 2. |
Lucas
MJ, Leveno KJ, Cunningham FG. A
comparison of magnesium sulfate with phenytoin for the prevention
of eclampsia. N Engl J Med 1995;333:201-5. |
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| 3. |
Eclampsia
Trial Collaborative Group. Which
anticonvulsant for women with eclampsia? Evidence from the Collaborative
Eclampsia Trial. Lancet 1995;345:1455-63. |
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| 4. |
Mittendorf
R, Covert R, Boman J, Khoshnood B, Lee KS, Siegler M Is
tocolytic magnesium sulphate associated with increased total paediatric
mortality? Lancet 1997;350:1517-8. |
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| 5. |
Gyetvai
K, Hannah ME, Hodnett ED, Ohlsson A. Tocolytics
for preterm labor: a systematic review. Obstet Gynecol 1999;94:869-77. |
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| 6. |
Higby
K, Suiter CR. A
risk-benefit assessment of therapies for premature labor. Drug
Saf 1999;21:35-56. |
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| 7. |
Crowther
CA, Hiller JE, Doyle LW. Magnesium
sulphate for preventing preterm birth in threatened preterm labour.
Cochrane Database Syst Rev, March, 2003. |
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| 8. |
Mittendorf
R, Covert R, Elin R, Pryde PG, Khoshnood B, Lee K-S. Umbilical
cord serum ionized magnesium level and total pediatric mortality.
Obstet Gynecol 2001;98:75-8. |
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| 9. |
Mittendorf
R, Dammann O, Lee K-s. Brain
lesions in newborns exposed to high dose magnesium sulfate during
preterm labor. J Perinatol 2006;26:57-63. |
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NEUROLOGICAL
EFFECTS & OUTCOMES |
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Crowther
CA, Hiller JE, Doyle LW, Haslam RR. Effect of magnesium
sulfate given for neuroprotection before preterm birth: a randomized
controlled trial. JAMA 2003; 290:2669-76.
(For non-journal subscribers, an additional fee may apply
for full text articles.) |
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Mittendorf
R, Dambrosia J, Dammann O, Pryde PG, Lee K-S, Ben-Ami TE, Yousefzadeh
D. Association between maternal serum ionized magnesium
levels at delivery and neonatal intraventricular hemorrhage. J
Pediatr 2002;140:540-6.
(For non-journal subscribers, an additional fee may apply
for full text articles.) |
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In
2003, the results of the Australasian Collaborative Trial of Magnesium
Sulphate (ACTOMgSO4), conducted by Crowther et al, was
published in JAMA. It had been a randomized study designed to find
out whether antenatal exposure to low dose (28 g or less) MgSO4 in
women at risk of preterm birth (<30 weeks gestation) could prevent
subsequent pediatric mortality and cerebral palsy in their children.
Australia and New Zealand were ideal for conducting a study such
as ACTOMgSO4 because magnesium is not used as a tocolytic
in either of those countries. Thus, there was no ethical dilemma[1]in
randomizing mothers to low dose MgSO4 as a possible neuroprophylactic
versus a saline control.
In ACTOMgSO4, data analysis included a total of 1,047
preterm newborns (PN) who had been followed up to 24 months of age.
It was found that administration of intravenous magnesium to a mother
for 24 hours prior to birth significantly reduced a secondary outcome
of the study, namely, subsequent gross motor dysfunction in her child
(3.4% vs. 6.6%, Relative Risk [RR] 0.51; 95% CI, 0.29 to 0.91); further,
it reduced death or substantial gross motor dysfunction (17.0% vs.
22.7%; RR 0.75, 95% CI 0.59 to 0.96) when considered as a secondary
composite variable (death + motor dysfunction). However, for the
prevention of cerebral palsy, the primary outcome of the study, the
difference between the MgSO4 exposed group and the placebo
group was small and not significant (6.8% vs. 8.2%, respectively,
P=0.38). Furthermore, differences between the magnesium group and
the placebo group were not significant for other neonatal outcomes
such as IVH, periventricular leukomalacia (PVL), chronic lung disease,
necrotizing enterocolitis (NEC), or length of hospital stay in the
NICU.
The important point
is that ACTOMgSO4 was a preventive trial – not a
tocolytic trial – in which relatively low doses of magnesium
were used. Indeed, although the research protocol for the study called
for a 28 g exposure to MgSO4, in practice, because of
the inherent limitations in giving drugs to actively contracting
women who might deliver at any time, including a time that preceded
the receipt of a full course of MgSO4, the actual median
exposure to MgSO4 was less than 10.5 g in the prophylactic
magnesium arm of the study[2]. Of relevance in the U.S.,
when MgSO4 is used as a tocolytic, the combined amount
of the bolus dose (usually 4 to 6 g) plus the maintenance infusions
(usually 2 or 3 g per hour) is considerably higher (the total amount
often exceeding 50 g) than the prophylactic amounts used in ACTOMgSO4.
As discussed in the
2002 article by Mittendorf et al, the unexpected and contrary reports
about certain biological and adverse cranial ultrasound data from
the Magnesium and Neurologic Endpoints Trial (MagNET) seem, on the
surface, to be at variance with the benign and somewhat encouraging
Australian findings. Originally, MagNET was designed to find out
whether IV MgSO4 given to women in preterm labor could
do the following: a) prevent neonatal IVH, b) prevent excess deaths
in PN (less than 34 weeks gestational age), and c) prevent the subsequent
development of cerebral palsy. As it turned out, opposite to one
of the primary intents of the trial, instead of decreasing the occurrence
of neonatal IVH, PN whose mothers had high blood serum ionized magnesium
levels at delivery were found to be at increased risk
for IVH (adjusted [adj] Odds Ratio [OR], 15.8; 95% CI, 1.4 to 175.0).
To add further controversy
to the role that high dose exposures to tocolytic MgSO4 (50
g or more) may play in the development of neonatal brain abnormalities,
as opposed to the possible neuroprotective benefits suggested in
ACTOMgSO4, an otherwise rare lesion of the thalami, lenticulostriate
vasculopathy (LSV), was commonly found among MagNET babies[3].
LSV is a mineralizing vasculopathy affecting the striate arteries
of the thalami (perforating branches of the middle cerebral arteries).
Previously, although LSV had been found in congenital infections
(most notably a rubella epidemic occurring in Philadelphia in the
early 1960s), it had not been reported in association with high dosage
exposures to magnesium. However, in MagNET, 14 cases of LSV were
found and confirmed by independent cranial ultrasound review (Boston
Children’s Hospital and the Floating Hospital at New England Medical
Center) in a cohort of 140 preemies. In a multivariate logistic regression
that controlled for confounding, the relationship between antenatal
exposure to high dose tocolytic MgSO4 and the outcome
of LSV was found to be significant (adj OR, 8.3; 95% CI, 1.3 to 45.0,
P=0.01). Given that white matter injuries are common in PN, but those
in the gray matter are not, it is fascinating that high dose MgSO4 could
be associated with lesions in the gray matter (thalami). Although
the importance of any neurological morbidy that may be related to
LSV remain in dispute, babies with LSV who have a readily identifiable
underlying condition appear to have a high risk for long-term neuropsychiatric
limitation[4].
In summation, a precise
and comprehensive delineation of the effects of maternal magnesium
exposure on the brain of the fetus, especially in regard to evaluating
differences between low and high dose MgSO4 exposures,
needs to be done. Indeed, the relationships among a multitude of
variables that may interact with magnesium (for example, antenatal
corticosteroids and the various inflammatory cytokines) need additional
study. Although the use of antenatal MgSO4 for neuroprotection,
even in very low doses, cannot be confidently recommended at the
moment, it is possible that such will be so in the future. The findings
of one study larger than ACTOMgSO4, the Beneficial Effects
of Antenatal Magnesium [BEAM] trial (Maternal-Fetal Medicine Network,
National Institute of Child Health and Human Development), have not
yet been reported. However, published data are consistent with an
increased occurrence of neurological injury when exposures to antenatal
MgSO4 are at high levels. Fortunately, for the sake of
children everywhere, much of this controversy is likely to be resolved
over the course of the next several years.
References
| 1. |
Muraskas
J, Marshal PA, Tomich P, Myers TF, Gianopoulos JG, Thomasma DC. Neonatal
viability in the 1990’s: held hostage by technology. Cambridge
Quarterly of Healthcare Ethics 1999;8:160-72. |
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| 2. |
Mittendorf
R, Lee K-S, Roizen NJ, Pryde PG. Magnesium
sulfate for preterm neuroprotection. (Letter to the Editor.)
JAMA 2004;291:940-1. |
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| 3. |
Mittendorf
R, Kuban K, Pryde PG, Gianopoulos J, Yousefzadeh D. Antenatal
risk factors associated with the development of lenticulostriate
vasculopathy (LSV) in neonates. J Perinatol 2005;25:101-7. |
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| 4. |
Wang
HS, Kuo MF. Sonographic
lenticulostriate vasculopathy in infancy with tic and other neuropsychiatric
disorders developed after 7 to 9 years of follow-up. Brain
Dev 2003;25 Suppl 1:S43-7. |
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Papatsonis
DNM, van Geijn HP, Adèr HJ, Lange FM, Bleker OP, Dekker GA. Nifedipine
and ritodrine in the management of preterm labor: a randomized multicenter
trial. Obstet Gynecol 1997;90:230-4.
(For non-journal subscribers, an additional fee may apply for
full text articles.) |
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Tsatsaris
V, Papatsonis D, Goffinet F, Dekker G, Carbonne B. Tocolysis
with nifedipine or beta-adrenergic agonists: a meta-analysis. Obstet
Gynecol 2001; 97:840-7.
(For non-journal subscribers, an additional fee may apply for
full text articles.) |
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Smith
GN, Walker MC, Ohlsson A, O’Brien K, Windrim R (for the Canadian
Preterm Labour Nitroglycerin Trial Group). Randomized double-blind
placebo-controlled trial of transdermal nitroglycerin for preterm
labor. Am J Obstet Gynecol 2007;196:37.e1-37.e8.
(For non-journal subscribers, an additional fee may apply for
full text articles.) |
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If
the use of magnesium sulfate (MgSO4) is to be limited, or
even eliminated, as a first-line tocolytic, then what agents are we
to substitute, and what is the evidence basis for selecting alternative
tocolytics among the drugs that are currently available for that purpose?
Among the drugs that are used
for tocolysis in the U.S., ritodrine is the only one to ever receive
approval by the Food and Drug Administration (FDA). However, despite
that approval, it has been shown that beta-adrenergics, such as ritodrine
and terbutaline (in common usage), are of limited effectiveness in prolonging
pregnancy. Moreover, as a class of tocolytics, the beta-adrenergics,
especially when used parenterally, pose a significant cardiovascular
risk for the mother. Pulmonary edema, cardiomyopathy and even maternal
death have all been shown to be associated with the use of these drugs.
In the fetus, chronic use of beta-adrenergics has also been shown to
have effects on glucose metabolism and cardiac function. Thus, when
using this class of drugs, the clinician must proceed with utmost caution;
however, in all fairness, the same warning applies to the use of any
tocolytic, even the best among them.
Of importance, another class
of tocolytics, the calcium channel blockers (potent anti-hypertensives),
have been shown to be effective for tocolysis with less maternal and
fetal toxicity than that seen with beta-adrenergics. Nifedipine, the
prime example, has been well studied. Because it does not have an FDA
approval for tocolyis, however, a relevant question would be: How favorably
does nifedipine compare to the approved drug, ritodrine (and perhaps
other beta-adrenergics) in regard to tocolytic efficacy and maternal
and fetal safety? In 1997, Papatsonis et al directly compared nifedipine
to ritodrine for tocolytic effectiveness. In a multicenter, randomized
clinical trial, nifedipine was shown to significantly lengthen the interval
from drug exposure to delivery at 24 hours (P=0.006), at 48 hours (P=0.03),
at one week (P=0.009), and at 2 weeks (P=0.005). Concerning the neonate,
there were no significant differences between nifedipine and ritodrine
in regard to Apgar scores and umbilical cord pHs. Further, the nifedipine
group had fewer admissions to the NICU (68% vs. 82%, P=0.04).
More recently (2001), Tsatsaris
et al performed a meta-analysis of randomized clinical trials comparing
nifedipine with the general class of beta-adrenergics, including ritodrine
and other drugs (mostly terbutaline and salbutamol). Eleven published
and two unpublished trials were included in the study. All were analyzed
using intent-to-treat methodology. The meta-analysis showed that nifedipine
was more effective than beta-adrenergics in delaying delivery for at
least 48 hours (OR 1.52, 95% CI 1.03 to 2.24). Moreover, nifedipine
was more effective in postponing delivery beyond 34 weeks of gestation
(OR 1.87, 95% CI 1.11 to 3.15). For the neonate, a smaller percentage
in the nifedipine group was transferred to the NICU (OR 0.65, 95% CI
0.43 to 0.97), and there were fewer cases of respiratory distress syndrome
(RDS) (OR 0.57, 95% CI 0.37 to 0.89). There were, however, no significant
differences in neonatal mortality between the two groups. In regard
to the mother, nifedipine had substantially fewer maternal side effects
than did the beta-adrenergics (OR 0.12, 95% CI 0.05 to 0.29). Of importance
in clinical practice, when considering the use of nifedipine as a tocolytic,
it is paramount to ensure there is no history of maternal cardiac disease
or diabetes, and that sufficient intravenous hydration always precedes
the administration of the drug.
Although the medical literature
will not be reviewed here because they are secondary agents, other possible
alternatives to tocolytic MgSO4 include the prostaglandin
synthetase inhibitors and non-steroidal anti-inflammatory agents (NSAIDS).
Of these, indomethacin has been shown to be effective. However, concerns
regarding premature closure in the fetus of an otherwise patent ductus
arteriosus, as well as concerns about reduction in renal arterial blood
flow leading to oligohydramnios, limit its usage in clinical practice
to short courses in women having preterm labor at less than completed
32 weeks. Also, recent analyses from observational studies have implicated
the use of indomethacin with subsequent neonatal IVH and NEC. In their
review of the subject, Macones at al(1) discussed concerns about methodological
and confounding issues in studies linking indomethacin to IVH. In their
conclusion, the authors opined that indomethacin was effective as a
tocolytic, but due to potential risks, its use should be limited. In
practical terms, indomethacin may serve as a useful adjunct tocolytic
for short courses in women who are not eligible for other drugs. However,
when using indomethacin, it is important to carefully monitor amniotic
fluid volume with follow-up antepartum ultrasound examinations.
Of interest, the recently published
Canadian trial by Smith at al has shown that transdermal nitroglycerin
may prove to be an effective tocolytic. In a double-blind, placebo-controlled
study, patients between 24 and 32 weeks gestation were randomized to
either transdermal nitroglycerin (glycerol trinitrate, GTN) by patch
or a look-alike placebo. When excluding patients who delivered at term,
GTN-exposed pregnancies gained, on average, 10.8 days in gestational
length as compared to control (P=.02). In the sub-group of women in
preterm labor who were randomized at less than 28 weeks (and excluding
those who ultimately had term deliveries), pregnancies were found to
last, on average, 23.4 days longer (P=.007). Women receiving GTN did
have more headaches. Analyzing neonatal outcomes as a composite variable
(including chronic lung disease, IVH, NEC and PVL), those exposed to
GTN had improved outcomes (RR 0.29, 95% CI 0.08 to 1.00, P=.048). It
was suggested by the authors that this improvement was based on the
substantial prolongation (23.4 days) of GTN-exposed pregnancies. Although
these initial findings are encouraging, more investigation with this
agent needs to be done in order to establish it as a superior tocolytic
having a low risk profile. Especially needed is long-term pediatric
follow-up.
In the future, it is conceivable
that tocolytics with an enhanced biochemical specificity, such as oxytocin
receptor antagonists, may be used successfully and safely. One such
drug, atosiban, is currently being used in Europe and South America
with some apparent success. However, in this country, the FDA did not
approve the one commercially available oxytocin receptor antagonist
because of an excess of unexplained neonatal deaths in its randomized
trial(2). Of interest, in a recent meta-analysis comparing atosiban
with nifedipine, Coomarasamy et al(3) found that atosiban was not superior
to the calcium channel blocker in prolonging pregnancy beyond 48 hours.
Moreover, nifedipine was found to reduce the prevalence of neonatal
RDS (OR 0.55, 95% CI 0.32 to 0.97).
In conclusion, based on this
review of the relevant evidence-based medical literature (with representative
and additional articles being especially selected), it is concluded
that nifedipine has the most support for use as a first-line tocolytic
to replace MgSO4. Although currently ongoing research may
alter any future recommendation, extant data demonstrate the superior
efficacy and improved safety profile of nifedipine as compared to other
drugs currently being used in the United States for tocolysis.
References
| 1. |
Macones
GA, Marder SJ, Clothier B, Stamilio DM. The
controversy surrounding indomethacin for tocolysis. Am J Obstet
Gynecol 2001;184:264-72. |
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| 2. |
Romero
R, Sibai BM, Sanchez-Ramos L, Valenzuela GJ, Veille JC, Tabor B,
Perry KG, Varner M, Goodwin TM, Lane R, Smith J, Shangold G, Creasy
GW. An
oxytocin receptor antagonist (atosiban) in the treatment of preterm
labor: a randomized, double-blind, placebo-controlled trial with
tocolytic rescue. Am J Obstet Gynecol 2000;182:1173-83. |
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| 3. |
Coomarasamy
A, Knox EM, Gee H, Song F, Khan KS. Effectiveness
of nifedipine versus atosiban for tocolysis in preterm labour: a
meta-analysis with an indirect comparison of randomised trials.
BJOG 2003;110:1045-9. |
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should only claim credit commensurate with the extent of their participation
in the activity.
Podcast: The Johns Hopkins University School of
Medicine designates this educational activity for a maximum of 0.5 AMA
PRA Category 1 Credit(s)TM. Physicians should only
claim credit commensurate with the extent of their participation
in the activity.
Nurses
eNewsletter: This 1.0 contact hour Educational Activity
(Provider Directed/Learner Paced) is provided by The Institute for
Johns Hopkins Nursing. Each Newsletter carries a maximum of 1.0 contact
hour or a total of 12.0 contact hours for the twelve newsletters
in this program.
Podcast: This 0.5 contact hour Educational Activity
(Provider Directed/Learner Paced) is provided by The Institute for
Johns Hopkins Nursing. Each podcast carries a maximum of 0.5 contact
hours or a total of 3.0 contact hours for the six podcasts in this
program.
Respiratory
Therapists
For United States: Visit
this page to confirm that your state will accept the CE Credits
gained through this program.
For Canada: Visit
this page to confirm that your province will accept the CE Credits
gained through this program. |
|
| Post-Test
— back
to top |
|
| To
take the post-test for eNeonatal Review you will need to visit The
Johns Hopkins University School of Medicine's CME website or The
Institute for Johns Hopkins Nursing or download a PDF of the
post-test from the issue itself for Pharmacy. If you have already
registered for another Hopkins CME program at these sites, simply
enter the requested information when prompted. Otherwise, complete
the registration form to begin the testing process. A passing grade
of 70% or higher on the post test/evaluation is required to receive
CME/CNE/CPE credit. |
|
| Statement
of Responsibility — back
to top |
|
| The
Johns Hopkins University School of Medicine and The Institute for
Johns Hopkins Nursing takes responsibility for the content, quality,
and scientific integrity of this CME/CNE/CPE activity. |
|
| Target
Audience — back
to top |
|
| This
activity has been developed for Neonatologists, NICU Nurses and
Respiratory Therapists working with Neonatal patients. There are
no fees or prerequisites for this activity. |
|
| Learning
Objectives — back
to top |
|
The
Johns Hopkins University School of Medicine and The Institute
for Johns Hopkins Nursing take responsibility for the content,
quality, and the scientific integrity of this CE activity.
At the
conclusion of this activity, participants should be able to: |
|
| | | | | |
