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Matern Child Health J (2011) 15:670–676
DOI 10.1007/s10995-010-0615-6
Alcohol Consumption During Pregnancy and Risk of Placental
Abruption and Placenta Previa
Muktar H. Aliyu • O’Neil Lynch • Philip N. Nana •
Amina P. Alio • Ronee´ E. Wilson • Phillip J. Marty
Roger Zoorob • Hamisu M. Salihu
•
Published online: 1 May 2010
Ó Springer Science+Business Media, LLC 2010
Abstract The purpose of this study was to examine the
association between prenatal alcohol consumption and the
occurrence of placental abruption and placenta previa in a
population-based sample. We used linked birth data files to
conduct a retrospective cohort study of singleton deliveries
in the state of Missouri during the period 1989 through
2005 (n = 1,221,310). The main outcomes of interest were
placenta previa, placental abruption and a composite
M. H. Aliyu
Department of Preventive Medicine, Institute for Global Health,
Vanderbilt University, Nashville, TN, USA
O. Lynch
Department of Mathematics, Minnesota State University
Moorhead, Moorhead, MN, USA
e-mail: [email protected]
P. N. Nana
Department of Obstetrics and Gynecology, University
of Yaounde 1, Yaounde, Cameroon
A. P. Alio H. M. Salihu (&)
Department of Family and Community Health, Center for
Research and Evaluation, Lawton and Rhea Chiles Center,
For Healthy Mothers and Babies, University of South Florida,
3111 E. Fletcher Avenue, Tampa, FL 33613, USA
e-mail: [email protected]
R. E. Wilson
Department of Epidemiology and Biostatistics, University
of South Florida, Tampa, FL, USA
P. J. Marty
The Chiles Center for Healthy Mothers and Babies, University
of South Florida, Tampa, FL, USA
e-mail: [email protected]
R. Zoorob
Southeast Fetal Alcohol Research and Training Center,
Meharry Medical College, Nashville, TN, USA
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outcome defined as the occurrence of either or both lesions.
Multivariate logistic regression was used to generate
adjusted odd ratios, with non-drinking mothers as the referent category. Women who consumed alcohol during
pregnancy had a 33% greater likelihood for placental
abruption during pregnancy (adjusted odds ratio (OR), 95%
confidence interval (CI) = 1.33 [1.16–1.54]). No association was observed between prenatal alcohol use and the
risk of placenta previa. Alcohol consumption in pregnancy
was positively related to the occurrence of either or both
placental conditions (adjusted OR [95% CI] = 1.29 [1.14–
1.45]). Mothers who consumed alcohol during pregnancy
were at elevated risk of experiencing placental abruption,
but not placenta previa. Our findings underscore the need
for screening and behavioral counseling interventions to
combat alcohol use by pregnant women and women of
childbearing age.
Keywords Alcohol Placenta previa
Placental abruption Population-based study
Introduction
Maternal alcohol use during pregnancy is a leading preventable cause of fetal malformations, neurodevelopmental
abnormalities and perinatal mortality [1–3]. One of the
pathways by which alcohol is postulated to exert its
inhibitory effects on fetal development is via impaired
placentation [4]. The two important placental pathologies
include placenta previa and placental abruption, both of
which are precursors of perinatal mortality and morbidity.
Placental abruption accounts for up to a third of all perinatal deaths [5, 6], mostly due to its detrimental effects
on length of gestation and fetal growth [7, 8]. Similarly,
Matern Child Health J (2011) 15:670–676
placenta previa is a major contributor to fetal growth
restriction, preterm delivery and perinatal mortality [9, 10].
There is lack of consensus regarding the association
between maternal alcohol use and placental abruption.
Whereas some published reports suggest a positive association [11–14], others do not [15]. In the case of placenta
previa, a lack of association with maternal alcohol use has
been the usual finding [10, 16]. Few studies have analyzed
the association between prenatal alcohol use and placental
abruption and placenta previa together within the same
cohort. These two placental pathologies are believed to
have a shared etiology [14], as mothers with a prior history
of placental abruption have an increased predisposition to
developing placenta previa in subsequent pregnancies [17],
and vice versa [18, 19]. In consideration of this common
origin theory, we set out to examine the association
between prenatal alcohol consumption and the occurrence
of placental abruption and placenta previa among a large
representative sample of singleton births to mothers in the
state of Missouri during the period 1989 through 2005.
Materials and Methods
We utilized the Missouri maternally linked cohort data files
covering the period 1989 through 2005. The Missouri Vital
Record System is a central registry of all Missouri births,
infant deaths and fetal deaths. The system is a reliable one
that has been adopted as ‘‘gold standard’’ to validate US.
national datasets that involve matching and linking procedures [20]. The dataset used for this study has previously
been validated through a linkage system that we describe as
follows:
A probabilistic linkage method was used in the linking
process of the Missouri data files longitudinally using a
multi-stage algorithm. The method is dependent on the
calculation of a weighted score for every possible pair of
records that reflects the likelihood that they belong to the
same person. A computer program was employed to
compare a combination of variables from two files, giving
a separate weight to each value that matches or mismatches. The weights for a pair of records are summed up
and this represents the relative likelihood of both records
belonging to the same person. Although the summing
assumes that the weights for each field are independent,
there is usually some dependence between fields.
Initially, the linkage weights were calculated using two
training datasets. The weights for a correct match came from
the exact linkage of first and family name, month and year of
birth in a training data set of 52,683 pairs of births with a
previous live birth in 1983 or 1985. These exact links were
assumed to be correct. The weights for an incorrect match
came from a computer-generated random linkage of a
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training data set of 52,683 pairs of records. Weights of an
individual variable were calculated as follows:
Wa ¼ log2 ½j1 =N1 =j2 =N2
where Wa = weight for agreement, j1 = agreement in the
first training dataset, N1 = number in the first training
dataset, j2 = agreement in the second training dataset,
N2 = number in the second training dataset.
Wd ¼ log2 ½d1 =N1 =d2 =N2
where Wd = weight for disagreement, d1 = disagreement
in the first training dataset, N1 = number in the first
training dataset, d2 = disagreement in the second training
dataset, N2 = number in the second training dataset.
Correct and incorrect match weights were assigned to
each pair of records and then summed up. Linkages with a
score\-5 were rejected. A quality of agreement indicator,
based on the level of agreement of birth outcome, maternal
first and family name, year and month of birth and race,
was then assigned to the remaining linkages and a priority
indicator was then assigned. The highest priority was given
to records with a high linkage weight that matched exactly
on month and year of birth, maternal family and first
names. The lowest priority was given to records with no
agreement on maternal first and family names, and intermediate priority levels for linkage for those records in
between. The quality of agreement and priority indicators
were used to assess the validity of potential linkages,
especially those to multiple earlier births. For multiple
linkages, the most likely potential linkage based on the
score and quality of agreement indicator was accepted.
Paternal last name and zip code of residence could change
between pregnancies and two summary weights were calculated: one with paternal name and zip code and one
without; the higher sum was used. A family indicator
variable to define sibship groups was then assigned.
For the purpose of this study we selected singleton live
births within the gestational age range of 20–44 weeks.
Based on previously published reports [21] we assigned
women to the following drinking categories: class I drinker
(1–2 drinks per week); class 2 drinker (3–4 drinks per
week); class 3 drinker (C5 drinks per week). We used nondrinking mothers as the referent category. The exposure of
interest, namely, alcohol intake during pregnancy, was
measured at delivery through direct questioning of the
mother regarding the number of alcohol drinks consumed
per week. There was no biomarker confirmation of the
maternal self-reported number of drinks consumed.
Although the Missouri dataset has been validated in terms
of the accuracy of its linkage procedure as being highly
successful and complete [22], validation of alcohol intake
as an isolated measure has not been formally performed.
Nonetheless, previous studies on alcohol and birth
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672
outcomes using the same dataset reported results that were
consistent with the literature [3, 23].
The main outcomes of interest were placenta previa,
placental abruption and a composite outcome defined as the
occurrence of either lesion. Placenta previa is defined as an
obstetric complication in which the placenta is attached to
the uterine wall close to or covering the cervix. It can
sometimes occur in the later part of the first trimester, but
usually during the second or third. It is a leading cause of
vaginal bleeding. Placental abruption is defined as a condition where all or part of the placenta has pulled away
from the uterine wall, disrupting the flow of blood and
oxygen to the fetus. Small abruptions can heal, but larger
ones can cause fetal distress or death.
Gestational age was based on the interval between the last
menstrual period and the date of delivery of the baby (95
percent of cases). When the menstrual estimate of gestational
age was inconsistent with the birth weight (e.g., very low
birth weight at term), a clinical estimate of gestational age on
the vital records was used instead [24, 25].
Socio-demographic characteristics were captured by
maternal self-report. The distribution of the following
selected characteristics was compared between drinking
and non-drinking mothers to assess differences in baseline
characteristics: maternal age, parity, race, education, marital status and adequacy of prenatal care. Adequacy of
prenatal care was assessed using the revised graduated
index algorithm, which has been found to be more accurate
than several others, especially in describing the level of
prenatal care utilization among groups that are high-risk
[26, 27]. This index assesses the adequacy of care based on
when the trimester prenatal care begun, number of visits,
and the gestational age of the infant at birth. In this study,
inadequate prenatal care utilization refers to women who
either had missing prenatal care information, had prenatal
care but the level was considered sub-optimal, or mothers
who had no prenatal care at all. We performed crude frequency comparisons between the two groups for the presence of common obstetric complications, namely, anemia,
insulin-dependent diabetes mellitus, other types of diabetes
mellitus, chronic hypertension, preeclampsia, eclampsia,
abruption placenta and placenta previa.
Statistical Analysis
Chi-square test was used to assess differences in sociodemographic characteristics and maternal pregnancy
complications between the two groups (Drinking/Nondrinking). We used logistic regression models to generate
adjusted odd ratios and their 95 percent confidence intervals. The covariates in our models were selected a priori
based on previously published literature and biologic
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Matern Child Health J (2011) 15:670–676
plausibility. These variables included maternal age, parity,
race, smoking, education, marital status, adequacy of prenatal care, gender of the infant and year of birth. We
constructed the regression models and assessed goodnessof-fit of the regression models using the –2 log likelihood
ratio test. We estimated the significance of main effects by
means of the Wald test, and assessed dose–response using
the chi-square test for linear trend [28].
Adjusted estimates were derived in all cases by using
non-drinking gravidas as the referent category. All tests of
hypothesis were two-tailed with a type 1 error rate fixed at
5 percent. SAS version 9.1 (SAS Institute, Cary, NC) was
used to perform all analyses. This study was approved by
the Office of the Institutional Review Board at the University of South Florida.
Results
A total of 1,304,557 singleton births were available for
analysis. We excluded pregnancies before 20 weeks or
beyond 44 weeks of gestation (69,424 or 5.3 percent) and
records for which prenatal drinking (6,897), gestational age
(6,559), birth weight (216) values were missing (total =
13,823 or 1.1 percent). The final dataset comprised a total of
1,221,310 singleton records, consisting of drinking (15,911
or 1.3 percent) and non-drinking gravidas (1,205,399 or 98.7
percent; the referent group).
Overall, the prevalence of prenatal drinking was 1.3%.
Figure 1 illustrates trend of the prevalence of prenatal
drinking during pregnancy in the study population over
the course of the study while (Table 1) shows frequency
comparison between drinking and non-drinking mothers
with respect to selected socio-demographic characteristics.
Overall, alcohol consumption among pregnant women
declined considerably from 16.8% in 1989 to 2.2% in 2005.
Those gravidas who did not abstain during pregnancy were
more likely to be older, black, multiparous and to have
smoked during pregnancy. Drinking mothers were also less
likely to be married, to have received adequate prenatal care
and to have attained high school education than their nondrinking counterparts.
Table 2 displays the prevalence of common medical and
obstetric complications among mothers in the study. The
overall prevalence of pregnancy complication was 10.9%
(N = 133,652) distributed as follows: drinkers (N = 1,444
or 9.1%) and non-drinkers (132,208 or 11.0%) [P \ 0.01].
Of the obstetric complications, anemia, placenta previa and
placental abruption were more likely among drinkers while
pre-eclampsia, eclampsia, insulin dependent diabetes, other
forms of diabetes and chronic hypertension were more
common among mothers who were non-drinkers during
pregnancy.
Matern Child Health J (2011) 15:670–676
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Fig. 1 Crude rates of the
prevalence of maternal alcohol
consumption during pregnancy
by year, Missouri, 1989–2005
Table 1 Comparison of
selected socio-demographic
characteristics by prenatal
drinking status, Missouri,
1989–2005
Non-drinker
(N = 1,205,399)%
Drinker
(N = 15,911)%
P-value
9.83
18.47
\0.0001
58.80
68.66
\0.0001
Black
14.99
21.24
\0.0001
White
82.58
77.54
80.49
78.05
\0.0001
19.42
52.44
\0.0001
67.84
59.54
\0.0001
50.94
39.40
\0.0001
Maternal age
C35 years
Parity
Multiparous
Race
Education
C12 years
Smoking
Yes
Married
Yes
Adequate prenatal care
Yes
There were 4,582 (0.4%) infants born to mothers who
were diagnosed with placenta previa and 9,349 (0.8%)
diagnosed with placental abruption in the study population.
Figure 2 is an illustration of the distribution of rates of
placenta previa and placental abruption and the composite
outcome by prenatal drinking status.
The crude estimates for the association between prenatal
drinking, placenta previa, placental abruption as well as the
composite outcome measure did not differ from the
adjusted estimates therefore only the latter are summarized
in Table 3. Overall, we detected an association between
alcohol consumption during pregnancy and placental
abruption as well as the composite outcome measure.
Women who consumed alcohol during pregnancy had a
33% greater likelihood for placental abruption during
pregnancy (adjusted OR = 1.33 [95% CI: 1.16–1.54]).
When the risk of placental abruption was analyzed by
severity of drinking, a J-shaped trend was observed with a
peak among those in the most severe category (class 3) and
a trough among moderate drinkers (class 2). These observations were similar for the composite outcome measure.
By contrast, no association was seen between alcohol use
in pregnancy and the risk of placenta previa (Table 3).
Although there was an indication of increased risk for
placenta previa in drinkers, the risk estimates failed to
reach statistical significance.
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674
Table 2 Prevalence of
common medical/obstetric
complications among mothers
by prenatal drinking status,
Missouri, 1989–2005
Matern Child Health J (2011) 15:670–676
Non-drinker
(N = 1,205,399) n (%)
Drinker
(N = 15,911) n (%)
P-value
17,420(1.45)
252(1.58)
\0.0029
49(0.31)
\0.0001
27,363(2.27)
258(1.62)
\0.0001
11,421(0.95)
119(0.75)
\0.0003
55,600(4.61)
473(2.97)
\0.0001
1,194(0.10)
10(0.06)
\0.0029
9,152(0.76)
197(1.24)
\0.0001
4,496(0.37)
86(0.54)
\0.0006
Anemia
Yes
Insulin-dependent diabetes
Yes
8,862(0.74)
Other forms of diabetes
Yes
Chronic hypertension
Yes
Pre-eclampsia
Yes
Eclampsia
Yes
Placental abruption
Yes
Placenta previa
Yes
Fig. 2 Crude rates of placenta
previa, placental abruption and
composite outcome by prenatal
drinking status, Missouri,
1989–2005
Discussion
The objective of this study was to describe the association
between alcohol consumption and risk of placental abruption and/or placenta previa in a large population-based
cohort of singleton deliveries (n = 1,221,310). Our principal finding was that mothers who consumed alcohol
during pregnancy were at elevated risk of experiencing
placental abruption, but not placenta previa. This finding is
consistent with previous reports that alcohol intake during
pregnancy increases the risk of placental abruption
[11–13]. On the other hand, our result is at variance with a
cohort study from Canada, in which no significant association was observed between placental abruption and
123
alcohol use during pregnancy. This discrepancy in results is
not surprising, because unlike our population-based study
with almost complete ascertainment of alcohol use (99%
complete) and adequate sample size, the Kramer et al. [15]
report was drawn from a relatively small (n = 36,875),
hospital-based cohort with substantial missing data for
alcohol use.
The lack of association between alcohol use in pregnancy and placenta previa is fairly well-established [8, 10].
Our inability to demonstrate an association between placenta previa and prenatal alcohol use is therefore in conformity with this trend. More specifically, the dual finding
of an association between prenatal alcohol consumption
and placental abruption, but not placenta previa replicates
Matern Child Health J (2011) 15:670–676
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Table 3 Adjusted odd ratio for the association between prenatal alcohol ingestion and placenta previa and placental abruption
Placenta previa (N = 4,582)
Number of cases Adj. OR (95% CI)
Placental abruption (N = 9,349)
a
Composite outcome (N = 13,718)
Number of cases Adj. OR (95% CI) Number of cases Adj. OR (95% CI)
Non-drinker
N = 4,496
Referent
N = 9,152
Referent
N = 13,439
Referent
Drinker
N = 86
1.19 (0.95–1.47)
N = 197
1.33 (1.16–1.54)
N = 279
1.29 (1.14–1.45)
Class 1 (1–2 drinks/week) N = 64
1.11 (0.87–1.43)
N = 144
1.28 (1.08–1.51)
N = 205
1.22 (1.06–1.41)
Class 2 (3–4 drinks/week) N = 11
1.37 (0.76–2.49)
N = 19
1.09 (0.69–1.72)
N = 29
1.15 (0.80–1.67)
Class 3 (C5 drinks/week) N = 11
1.58 (0.87–2.86)
N = 34
1.98 (1.40–2.80)
N = 45
1.89 (1.40–2.56)
Adj. OR = adjusted odds ratio. Non-drinker: number of drinks per week = 0; drinker: number of drinks per week [ 0. Adjusted estimates were
generated after controlling for the effects of maternal age, parity, race, smoking, education, marital status, adequacy of prenatal care, gender of
the infant and year of birth
a
P for trend \0.01
findings from a similar large population-based cohort [14]
and others [10, 29].
The pathway by which alcohol predisposes to placental
abruption is not fully understood, but can be postulated on
the basis of what we know about the effects of alcohol on
placentation and placental development in animal models.
Alcohol impairs the physiological conversion of uterine
arteries into high-flow, low resistance placental vessels, a
crucial process for adequate placentation and placental
development [4, 30]. Alcohol also increases the production
of prostaglandins and other inflammatory cytokines [31],
which might explain the increased necrosis and thrombi
formation seen within the labyrinthine and spongiotrophoblast layers of the alcohol-exposed placenta [4, 32]. The
net effect of these changes would be the creation of an
environment that is conducive to the detachment of the
placenta before delivery.
In interpreting the findings from this study, a number of
limitations should be considered. Underreporting of alcohol intake is a recognized phenomenon in pregnant women,
especially if ascertainment of alcohol use was based on
maternal recall in the postnatal period [12, 33]. However,
misclassification of prenatal alcohol use because of retrospective data collection is uncommon [34–37]. In addition,
the net effect of underreporting would be to bias our results
toward the null. That we still report elevated risks of placental abruption strengthens the validity of our findings.
Misclassification of placental abruption and placenta previa
on the birth certificate is also possible, but not highly likely
[14]. However, as with alcohol use, any misclassification of
placental pathology is likely to be nondifferential and to
yield conservative risk estimates [38]. Another limitation is
our database did not include information on the timing of
alcohol use or pattern of consumption (e.g., binge drinking). In addition, risk factors commonly associated with
alcohol abuse, such as illicit drug use and HIV status, were
also unavailable. We are therefore, unable to comment on
the effect of these factors on risk of placental abruption or
placenta previa in our cohort.
The strengths of this study include the large sample size,
population-based design and high response rate (*99%
complete information on the exposure variable i.e., alcohol
consumption). These merits enhance the external validity of
our findings and reduce the risk of bias arising from sample
selection, a source of concern in data derived from individual
health facilities. Another strength is our adjustment for a
wide range of important confounding factors, thereby
ensuring that any associations we detect in this study represent independent relationships between the exposure variable (prenatal alcohol use) and our defined outcomes.
In summary, we found an elevated risk of placental
abruption but not placenta previa among women who
consumed alcohol during pregnancy. Although our data
show that alcohol consumption during pregnancy is
declining there are still many women who fail to abstain
during pregnancy thus this information adds to the contemporary literature on the detrimental effects of alcohol
use in pregnancy and will be useful in screening and
behavioral counseling interventions to combat alcohol use
by pregnant women and women of childbearing age.
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DOI 10.1007/s10995-010-0615-6
Alcohol Consumption During Pregnancy and Risk of Placental
Abruption and Placenta Previa
Muktar H. Aliyu • O’Neil Lynch • Philip N. Nana •
Amina P. Alio • Ronee´ E. Wilson • Phillip J. Marty
Roger Zoorob • Hamisu M. Salihu
•
Published online: 1 May 2010
Ó Springer Science+Business Media, LLC 2010
Abstract The purpose of this study was to examine the
association between prenatal alcohol consumption and the
occurrence of placental abruption and placenta previa in a
population-based sample. We used linked birth data files to
conduct a retrospective cohort study of singleton deliveries
in the state of Missouri during the period 1989 through
2005 (n = 1,221,310). The main outcomes of interest were
placenta previa, placental abruption and a composite
M. H. Aliyu
Department of Preventive Medicine, Institute for Global Health,
Vanderbilt University, Nashville, TN, USA
O. Lynch
Department of Mathematics, Minnesota State University
Moorhead, Moorhead, MN, USA
e-mail: [email protected]
P. N. Nana
Department of Obstetrics and Gynecology, University
of Yaounde 1, Yaounde, Cameroon
A. P. Alio H. M. Salihu (&)
Department of Family and Community Health, Center for
Research and Evaluation, Lawton and Rhea Chiles Center,
For Healthy Mothers and Babies, University of South Florida,
3111 E. Fletcher Avenue, Tampa, FL 33613, USA
e-mail: [email protected]
R. E. Wilson
Department of Epidemiology and Biostatistics, University
of South Florida, Tampa, FL, USA
P. J. Marty
The Chiles Center for Healthy Mothers and Babies, University
of South Florida, Tampa, FL, USA
e-mail: [email protected]
R. Zoorob
Southeast Fetal Alcohol Research and Training Center,
Meharry Medical College, Nashville, TN, USA
123
outcome defined as the occurrence of either or both lesions.
Multivariate logistic regression was used to generate
adjusted odd ratios, with non-drinking mothers as the referent category. Women who consumed alcohol during
pregnancy had a 33% greater likelihood for placental
abruption during pregnancy (adjusted odds ratio (OR), 95%
confidence interval (CI) = 1.33 [1.16–1.54]). No association was observed between prenatal alcohol use and the
risk of placenta previa. Alcohol consumption in pregnancy
was positively related to the occurrence of either or both
placental conditions (adjusted OR [95% CI] = 1.29 [1.14–
1.45]). Mothers who consumed alcohol during pregnancy
were at elevated risk of experiencing placental abruption,
but not placenta previa. Our findings underscore the need
for screening and behavioral counseling interventions to
combat alcohol use by pregnant women and women of
childbearing age.
Keywords Alcohol Placenta previa
Placental abruption Population-based study
Introduction
Maternal alcohol use during pregnancy is a leading preventable cause of fetal malformations, neurodevelopmental
abnormalities and perinatal mortality [1–3]. One of the
pathways by which alcohol is postulated to exert its
inhibitory effects on fetal development is via impaired
placentation [4]. The two important placental pathologies
include placenta previa and placental abruption, both of
which are precursors of perinatal mortality and morbidity.
Placental abruption accounts for up to a third of all perinatal deaths [5, 6], mostly due to its detrimental effects
on length of gestation and fetal growth [7, 8]. Similarly,
Matern Child Health J (2011) 15:670–676
placenta previa is a major contributor to fetal growth
restriction, preterm delivery and perinatal mortality [9, 10].
There is lack of consensus regarding the association
between maternal alcohol use and placental abruption.
Whereas some published reports suggest a positive association [11–14], others do not [15]. In the case of placenta
previa, a lack of association with maternal alcohol use has
been the usual finding [10, 16]. Few studies have analyzed
the association between prenatal alcohol use and placental
abruption and placenta previa together within the same
cohort. These two placental pathologies are believed to
have a shared etiology [14], as mothers with a prior history
of placental abruption have an increased predisposition to
developing placenta previa in subsequent pregnancies [17],
and vice versa [18, 19]. In consideration of this common
origin theory, we set out to examine the association
between prenatal alcohol consumption and the occurrence
of placental abruption and placenta previa among a large
representative sample of singleton births to mothers in the
state of Missouri during the period 1989 through 2005.
Materials and Methods
We utilized the Missouri maternally linked cohort data files
covering the period 1989 through 2005. The Missouri Vital
Record System is a central registry of all Missouri births,
infant deaths and fetal deaths. The system is a reliable one
that has been adopted as ‘‘gold standard’’ to validate US.
national datasets that involve matching and linking procedures [20]. The dataset used for this study has previously
been validated through a linkage system that we describe as
follows:
A probabilistic linkage method was used in the linking
process of the Missouri data files longitudinally using a
multi-stage algorithm. The method is dependent on the
calculation of a weighted score for every possible pair of
records that reflects the likelihood that they belong to the
same person. A computer program was employed to
compare a combination of variables from two files, giving
a separate weight to each value that matches or mismatches. The weights for a pair of records are summed up
and this represents the relative likelihood of both records
belonging to the same person. Although the summing
assumes that the weights for each field are independent,
there is usually some dependence between fields.
Initially, the linkage weights were calculated using two
training datasets. The weights for a correct match came from
the exact linkage of first and family name, month and year of
birth in a training data set of 52,683 pairs of births with a
previous live birth in 1983 or 1985. These exact links were
assumed to be correct. The weights for an incorrect match
came from a computer-generated random linkage of a
671
training data set of 52,683 pairs of records. Weights of an
individual variable were calculated as follows:
Wa ¼ log2 ½j1 =N1 =j2 =N2
where Wa = weight for agreement, j1 = agreement in the
first training dataset, N1 = number in the first training
dataset, j2 = agreement in the second training dataset,
N2 = number in the second training dataset.
Wd ¼ log2 ½d1 =N1 =d2 =N2
where Wd = weight for disagreement, d1 = disagreement
in the first training dataset, N1 = number in the first
training dataset, d2 = disagreement in the second training
dataset, N2 = number in the second training dataset.
Correct and incorrect match weights were assigned to
each pair of records and then summed up. Linkages with a
score\-5 were rejected. A quality of agreement indicator,
based on the level of agreement of birth outcome, maternal
first and family name, year and month of birth and race,
was then assigned to the remaining linkages and a priority
indicator was then assigned. The highest priority was given
to records with a high linkage weight that matched exactly
on month and year of birth, maternal family and first
names. The lowest priority was given to records with no
agreement on maternal first and family names, and intermediate priority levels for linkage for those records in
between. The quality of agreement and priority indicators
were used to assess the validity of potential linkages,
especially those to multiple earlier births. For multiple
linkages, the most likely potential linkage based on the
score and quality of agreement indicator was accepted.
Paternal last name and zip code of residence could change
between pregnancies and two summary weights were calculated: one with paternal name and zip code and one
without; the higher sum was used. A family indicator
variable to define sibship groups was then assigned.
For the purpose of this study we selected singleton live
births within the gestational age range of 20–44 weeks.
Based on previously published reports [21] we assigned
women to the following drinking categories: class I drinker
(1–2 drinks per week); class 2 drinker (3–4 drinks per
week); class 3 drinker (C5 drinks per week). We used nondrinking mothers as the referent category. The exposure of
interest, namely, alcohol intake during pregnancy, was
measured at delivery through direct questioning of the
mother regarding the number of alcohol drinks consumed
per week. There was no biomarker confirmation of the
maternal self-reported number of drinks consumed.
Although the Missouri dataset has been validated in terms
of the accuracy of its linkage procedure as being highly
successful and complete [22], validation of alcohol intake
as an isolated measure has not been formally performed.
Nonetheless, previous studies on alcohol and birth
123
672
outcomes using the same dataset reported results that were
consistent with the literature [3, 23].
The main outcomes of interest were placenta previa,
placental abruption and a composite outcome defined as the
occurrence of either lesion. Placenta previa is defined as an
obstetric complication in which the placenta is attached to
the uterine wall close to or covering the cervix. It can
sometimes occur in the later part of the first trimester, but
usually during the second or third. It is a leading cause of
vaginal bleeding. Placental abruption is defined as a condition where all or part of the placenta has pulled away
from the uterine wall, disrupting the flow of blood and
oxygen to the fetus. Small abruptions can heal, but larger
ones can cause fetal distress or death.
Gestational age was based on the interval between the last
menstrual period and the date of delivery of the baby (95
percent of cases). When the menstrual estimate of gestational
age was inconsistent with the birth weight (e.g., very low
birth weight at term), a clinical estimate of gestational age on
the vital records was used instead [24, 25].
Socio-demographic characteristics were captured by
maternal self-report. The distribution of the following
selected characteristics was compared between drinking
and non-drinking mothers to assess differences in baseline
characteristics: maternal age, parity, race, education, marital status and adequacy of prenatal care. Adequacy of
prenatal care was assessed using the revised graduated
index algorithm, which has been found to be more accurate
than several others, especially in describing the level of
prenatal care utilization among groups that are high-risk
[26, 27]. This index assesses the adequacy of care based on
when the trimester prenatal care begun, number of visits,
and the gestational age of the infant at birth. In this study,
inadequate prenatal care utilization refers to women who
either had missing prenatal care information, had prenatal
care but the level was considered sub-optimal, or mothers
who had no prenatal care at all. We performed crude frequency comparisons between the two groups for the presence of common obstetric complications, namely, anemia,
insulin-dependent diabetes mellitus, other types of diabetes
mellitus, chronic hypertension, preeclampsia, eclampsia,
abruption placenta and placenta previa.
Statistical Analysis
Chi-square test was used to assess differences in sociodemographic characteristics and maternal pregnancy
complications between the two groups (Drinking/Nondrinking). We used logistic regression models to generate
adjusted odd ratios and their 95 percent confidence intervals. The covariates in our models were selected a priori
based on previously published literature and biologic
123
Matern Child Health J (2011) 15:670–676
plausibility. These variables included maternal age, parity,
race, smoking, education, marital status, adequacy of prenatal care, gender of the infant and year of birth. We
constructed the regression models and assessed goodnessof-fit of the regression models using the –2 log likelihood
ratio test. We estimated the significance of main effects by
means of the Wald test, and assessed dose–response using
the chi-square test for linear trend [28].
Adjusted estimates were derived in all cases by using
non-drinking gravidas as the referent category. All tests of
hypothesis were two-tailed with a type 1 error rate fixed at
5 percent. SAS version 9.1 (SAS Institute, Cary, NC) was
used to perform all analyses. This study was approved by
the Office of the Institutional Review Board at the University of South Florida.
Results
A total of 1,304,557 singleton births were available for
analysis. We excluded pregnancies before 20 weeks or
beyond 44 weeks of gestation (69,424 or 5.3 percent) and
records for which prenatal drinking (6,897), gestational age
(6,559), birth weight (216) values were missing (total =
13,823 or 1.1 percent). The final dataset comprised a total of
1,221,310 singleton records, consisting of drinking (15,911
or 1.3 percent) and non-drinking gravidas (1,205,399 or 98.7
percent; the referent group).
Overall, the prevalence of prenatal drinking was 1.3%.
Figure 1 illustrates trend of the prevalence of prenatal
drinking during pregnancy in the study population over
the course of the study while (Table 1) shows frequency
comparison between drinking and non-drinking mothers
with respect to selected socio-demographic characteristics.
Overall, alcohol consumption among pregnant women
declined considerably from 16.8% in 1989 to 2.2% in 2005.
Those gravidas who did not abstain during pregnancy were
more likely to be older, black, multiparous and to have
smoked during pregnancy. Drinking mothers were also less
likely to be married, to have received adequate prenatal care
and to have attained high school education than their nondrinking counterparts.
Table 2 displays the prevalence of common medical and
obstetric complications among mothers in the study. The
overall prevalence of pregnancy complication was 10.9%
(N = 133,652) distributed as follows: drinkers (N = 1,444
or 9.1%) and non-drinkers (132,208 or 11.0%) [P \ 0.01].
Of the obstetric complications, anemia, placenta previa and
placental abruption were more likely among drinkers while
pre-eclampsia, eclampsia, insulin dependent diabetes, other
forms of diabetes and chronic hypertension were more
common among mothers who were non-drinkers during
pregnancy.
Matern Child Health J (2011) 15:670–676
673
Fig. 1 Crude rates of the
prevalence of maternal alcohol
consumption during pregnancy
by year, Missouri, 1989–2005
Table 1 Comparison of
selected socio-demographic
characteristics by prenatal
drinking status, Missouri,
1989–2005
Non-drinker
(N = 1,205,399)%
Drinker
(N = 15,911)%
P-value
9.83
18.47
\0.0001
58.80
68.66
\0.0001
Black
14.99
21.24
\0.0001
White
82.58
77.54
80.49
78.05
\0.0001
19.42
52.44
\0.0001
67.84
59.54
\0.0001
50.94
39.40
\0.0001
Maternal age
C35 years
Parity
Multiparous
Race
Education
C12 years
Smoking
Yes
Married
Yes
Adequate prenatal care
Yes
There were 4,582 (0.4%) infants born to mothers who
were diagnosed with placenta previa and 9,349 (0.8%)
diagnosed with placental abruption in the study population.
Figure 2 is an illustration of the distribution of rates of
placenta previa and placental abruption and the composite
outcome by prenatal drinking status.
The crude estimates for the association between prenatal
drinking, placenta previa, placental abruption as well as the
composite outcome measure did not differ from the
adjusted estimates therefore only the latter are summarized
in Table 3. Overall, we detected an association between
alcohol consumption during pregnancy and placental
abruption as well as the composite outcome measure.
Women who consumed alcohol during pregnancy had a
33% greater likelihood for placental abruption during
pregnancy (adjusted OR = 1.33 [95% CI: 1.16–1.54]).
When the risk of placental abruption was analyzed by
severity of drinking, a J-shaped trend was observed with a
peak among those in the most severe category (class 3) and
a trough among moderate drinkers (class 2). These observations were similar for the composite outcome measure.
By contrast, no association was seen between alcohol use
in pregnancy and the risk of placenta previa (Table 3).
Although there was an indication of increased risk for
placenta previa in drinkers, the risk estimates failed to
reach statistical significance.
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674
Table 2 Prevalence of
common medical/obstetric
complications among mothers
by prenatal drinking status,
Missouri, 1989–2005
Matern Child Health J (2011) 15:670–676
Non-drinker
(N = 1,205,399) n (%)
Drinker
(N = 15,911) n (%)
P-value
17,420(1.45)
252(1.58)
\0.0029
49(0.31)
\0.0001
27,363(2.27)
258(1.62)
\0.0001
11,421(0.95)
119(0.75)
\0.0003
55,600(4.61)
473(2.97)
\0.0001
1,194(0.10)
10(0.06)
\0.0029
9,152(0.76)
197(1.24)
\0.0001
4,496(0.37)
86(0.54)
\0.0006
Anemia
Yes
Insulin-dependent diabetes
Yes
8,862(0.74)
Other forms of diabetes
Yes
Chronic hypertension
Yes
Pre-eclampsia
Yes
Eclampsia
Yes
Placental abruption
Yes
Placenta previa
Yes
Fig. 2 Crude rates of placenta
previa, placental abruption and
composite outcome by prenatal
drinking status, Missouri,
1989–2005
Discussion
The objective of this study was to describe the association
between alcohol consumption and risk of placental abruption and/or placenta previa in a large population-based
cohort of singleton deliveries (n = 1,221,310). Our principal finding was that mothers who consumed alcohol
during pregnancy were at elevated risk of experiencing
placental abruption, but not placenta previa. This finding is
consistent with previous reports that alcohol intake during
pregnancy increases the risk of placental abruption
[11–13]. On the other hand, our result is at variance with a
cohort study from Canada, in which no significant association was observed between placental abruption and
123
alcohol use during pregnancy. This discrepancy in results is
not surprising, because unlike our population-based study
with almost complete ascertainment of alcohol use (99%
complete) and adequate sample size, the Kramer et al. [15]
report was drawn from a relatively small (n = 36,875),
hospital-based cohort with substantial missing data for
alcohol use.
The lack of association between alcohol use in pregnancy and placenta previa is fairly well-established [8, 10].
Our inability to demonstrate an association between placenta previa and prenatal alcohol use is therefore in conformity with this trend. More specifically, the dual finding
of an association between prenatal alcohol consumption
and placental abruption, but not placenta previa replicates
Matern Child Health J (2011) 15:670–676
675
Table 3 Adjusted odd ratio for the association between prenatal alcohol ingestion and placenta previa and placental abruption
Placenta previa (N = 4,582)
Number of cases Adj. OR (95% CI)
Placental abruption (N = 9,349)
a
Composite outcome (N = 13,718)
Number of cases Adj. OR (95% CI) Number of cases Adj. OR (95% CI)
Non-drinker
N = 4,496
Referent
N = 9,152
Referent
N = 13,439
Referent
Drinker
N = 86
1.19 (0.95–1.47)
N = 197
1.33 (1.16–1.54)
N = 279
1.29 (1.14–1.45)
Class 1 (1–2 drinks/week) N = 64
1.11 (0.87–1.43)
N = 144
1.28 (1.08–1.51)
N = 205
1.22 (1.06–1.41)
Class 2 (3–4 drinks/week) N = 11
1.37 (0.76–2.49)
N = 19
1.09 (0.69–1.72)
N = 29
1.15 (0.80–1.67)
Class 3 (C5 drinks/week) N = 11
1.58 (0.87–2.86)
N = 34
1.98 (1.40–2.80)
N = 45
1.89 (1.40–2.56)
Adj. OR = adjusted odds ratio. Non-drinker: number of drinks per week = 0; drinker: number of drinks per week [ 0. Adjusted estimates were
generated after controlling for the effects of maternal age, parity, race, smoking, education, marital status, adequacy of prenatal care, gender of
the infant and year of birth
a
P for trend \0.01
findings from a similar large population-based cohort [14]
and others [10, 29].
The pathway by which alcohol predisposes to placental
abruption is not fully understood, but can be postulated on
the basis of what we know about the effects of alcohol on
placentation and placental development in animal models.
Alcohol impairs the physiological conversion of uterine
arteries into high-flow, low resistance placental vessels, a
crucial process for adequate placentation and placental
development [4, 30]. Alcohol also increases the production
of prostaglandins and other inflammatory cytokines [31],
which might explain the increased necrosis and thrombi
formation seen within the labyrinthine and spongiotrophoblast layers of the alcohol-exposed placenta [4, 32]. The
net effect of these changes would be the creation of an
environment that is conducive to the detachment of the
placenta before delivery.
In interpreting the findings from this study, a number of
limitations should be considered. Underreporting of alcohol intake is a recognized phenomenon in pregnant women,
especially if ascertainment of alcohol use was based on
maternal recall in the postnatal period [12, 33]. However,
misclassification of prenatal alcohol use because of retrospective data collection is uncommon [34–37]. In addition,
the net effect of underreporting would be to bias our results
toward the null. That we still report elevated risks of placental abruption strengthens the validity of our findings.
Misclassification of placental abruption and placenta previa
on the birth certificate is also possible, but not highly likely
[14]. However, as with alcohol use, any misclassification of
placental pathology is likely to be nondifferential and to
yield conservative risk estimates [38]. Another limitation is
our database did not include information on the timing of
alcohol use or pattern of consumption (e.g., binge drinking). In addition, risk factors commonly associated with
alcohol abuse, such as illicit drug use and HIV status, were
also unavailable. We are therefore, unable to comment on
the effect of these factors on risk of placental abruption or
placenta previa in our cohort.
The strengths of this study include the large sample size,
population-based design and high response rate (*99%
complete information on the exposure variable i.e., alcohol
consumption). These merits enhance the external validity of
our findings and reduce the risk of bias arising from sample
selection, a source of concern in data derived from individual
health facilities. Another strength is our adjustment for a
wide range of important confounding factors, thereby
ensuring that any associations we detect in this study represent independent relationships between the exposure variable (prenatal alcohol use) and our defined outcomes.
In summary, we found an elevated risk of placental
abruption but not placenta previa among women who
consumed alcohol during pregnancy. Although our data
show that alcohol consumption during pregnancy is
declining there are still many women who fail to abstain
during pregnancy thus this information adds to the contemporary literature on the detrimental effects of alcohol
use in pregnancy and will be useful in screening and
behavioral counseling interventions to combat alcohol use
by pregnant women and women of childbearing age.
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