American Journal of Epidemiology Vol. 153, No.

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Copyright © 2001 by The Johns Hopkins University School of Hygiene and Public Health Printed in U.S.A.
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Placental Abruption and Perinatal Mortality Ananth and Wilcox

Placental Abruption and Perinatal Mortality in the United States

Cande V. Ananth1 and Allen J. Wilcox2

Placental abruption is an uncommon obstetric complication associated with high perinatal mortality rates. The
authors explored the associations of abruption with fetal growth restriction, preterm delivery, and perinatal
survival. The study was based on 7,508,655 singleton births delivered in 1995 and 1996 in the United States.
Abruption was recorded in 6.5 per 1,000 births. Perinatal mortality was 119 per 1,000 births with abruption
compared with 8.2 per 1,000 among all other births. The high mortality with abruption was due, in part, to its
strong association with preterm delivery; 55% of the excess perinatal deaths with abruption were due to early
delivery. Furthermore, babies in the lowest centile of weight (<1% adjusted for gestational age) were almost nine
times as likely to be born with abruption than those in the heaviest (≥90%) birth weight centiles. This relative risk

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progressively declined with higher birth weight centiles. After controlling for fetal growth restriction and early
delivery, the high risk of perinatal death associated with abruption persisted. Even babies born at 40 weeks of
gestation and birth weight of 3,500–3,999 g (where mortality was lowest) had a 25-fold higher mortality with
abruption. The link between fetal growth restriction and abruption suggests that the origins of abruption lie at
least in midpregnancy and perhaps even earlier. Am J Epidemiol 2001;153:332–7.

abruptio placentae; birth weight; fetal growth retardation; infant mortality

In normal pregnancies, placental separation occurs imme-
diately after birth, while in pregnancies complicated by
abruption, the placenta begins to detach before birth (1).
This premature detachment commonly produces pain and
vaginal bleeding, the clinical hallmarks of placental abrup-
tion, and occurs in about 0.6–1.0 percent of pregnancies (2).
Maternal risks associated with abruption include massive
blood loss, disseminated intravascular coagulopathy, renal
failure, and, less commonly, maternal death (1, 3).
Abruption is potentially disastrous to the fetus as well, with
perinatal mortality as high as 60 percent (4–7). Surprisingly
little is known about the underlying etiology of abruption.
We present recent data from the United States to explore the
associations of abruption with fetal growth restriction,
preterm delivery, and perinatal survival.
MATERIALS AND METHODS
Analysis was based on 7,508,655 singleton US births for
1995 and 1996 assembled by the National Center for Health
Received for publication January 18, 2000, and accepted for pub-
lication June 12, 2000.
1
Division of Epidemiology and Biostatistics, Department of
Obstetrics, Gynecology, and Reproductive Sciences, University of
Medicine and Dentistry of New Jersey, Robert Wood Johnson
Medical School, New Brunswick, NJ.
2
Epidemiology Branch, National Institute of Environmental Health
Sciences, Research Triangle Park, NC.
Correspondence to Dr. Cande V. Ananth, Division of Epidemiology
and Biostatistics, Department of Obstetrics, Gynecology, and
Reproductive Sciences, University of Medicine and Dentistry of New
Jersey, Robert Wood Johnson Medical School, 125 Paterson Street,
New Brunswick, NJ 08901-1977 (e-mail: ananthcv@EPI.UMDNJ.
EDU).
Statistics and derived from the linked birth/infant death data
sets. Perinatal mortality was defined to include stillbirths
(occurring after 20 weeks of gestation) and neonatal deaths
(occurring up to 28 days after birth). Abruption was defined
as the complete or partial separation of the placenta prior to
the delivery of the fetus. The diagnosis of abruption is based
on clinical presentation and examination of the delivered
placenta by the attendant at delivery. It is recorded on cur-
rent US birth certificates using a check-box (yes or no) (8),
but grades and severity of abruption are not documented.
The diagnosis of abruption on vital statistics is subject to
potential underascertainment (9), and information on some
important risk factors and confounders of abruption is
poorly recorded or unavailable on vital statistics data.
For 95 percent of births, the gestational age assignment
on vital records was based on the date of the last menstrual
period. A clinical estimate was used when the date of the last
menstrual period was missing or when the reported birth
weight was inconsistent with last menstrual period-based
gestational age (10). Missing data on the month of the last
menstrual period were imputed (11). Growth restriction was
assessed in centiles of weight (<1, 1–2, 3–4, 5–9, and there-
after in 10-centile increments derived from the complete US
data set) within strata of gestational age. Babies at or above
the 90th centile (who had the lowest risk of abruption)
served as the comparison group.
One reason that babies born with abruption are at higher
risk of mortality is that they are delivered prematurely. In
order to estimate the portion of abruption mortality that
might be explained by early delivery, we performed direct
standardization by gestational age. Specifically, we applied
the gestational age-specific mortality rates of nonabruption
births to the gestational age distribution of abruption births.

332
 Placental Abruption and Perinatal Mortality 333

This provided an estimate of total mortality for nonabruption
births had they had the same gestational age distribution of
abruption births. The increase in mortality due to the change
in the gestational age distribution was divided by the total
excess mortality observed among abruption births to esti-
mate the fraction of deaths attributable to the excess of
preterm births among women with abruption. In the same
fashion, we assessed the contribution of growth restriction to
abruption mortality by applying weight-specific mortality
rates to the birth weight distributions of abruption and
nonabruption births. In the case of birth weight, the analysis
was further stratified by gestational age to remove the effects
of early delivery from the effects of growth restriction.
RESULTS
Placental abruption was recorded in 46,731 pregnancies,
an incidence of 6.2 per 1,000 pregnancies (table 1).
Pregnancies diagnosed with abruption were far more likely
deaths per 1,000 births) (table 1). At the optimal gestational
age of 40 weeks (when overall mortality was lowest), peri-
natal mortality was 19-fold greater for abruption than for
nonabruption births (34.6 vs. 1.8 per 1,000 births, respec-
tively) (figure 3). Mortality with abruption was more likely
to occur before delivery than after (relative risk for stillbirth
was 18 compared with 10 for neonatal death).
In order to separate fetal growth restriction from early
delivery, we examined term babies alone (≥37 weeks). Both
weight distributions were strikingly Gaussian (figure 4) but
with a downward shift of the abruption births by about 250
g. (This shift was also seen at preterm gestational ages down
to 28 weeks.) Given this generalized growth restriction with
abruption, there was nonetheless a high risk of mortality
among babies of normal fetal size (figure 5). The best sur-
vival (with or without abruption) was among babies weigh-
ing 3,500–3,999 g. Even among term babies with this opti-
mal weight, abruption was associated with a 25-fold
mortality risk.

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to end in preterm delivery; 51 percent ended before 37 com-
pleted weeks compared with 10.1 percent of all other births
(figure 1). This substantial increase in early delivery
resulted in more small babies. Among babies born with
abruption, 46 percent weighed less than 2,500 g compared
with 6.4 percent among all other pregnancies.
The smaller size of babies born with abruption, however,
was not due simply to preterm delivery. Babies born with
abruption were also smaller at most gestational ages (figure
2). Since fetal growth restriction precedes delivery, the risk
of abruption at delivery can be expressed as a function of
fetal size. The relative risk for abruption was highest among
babies in the lowest 1 percent of weight at each gestational
age and progressively declined with increasing weight cen-
tiles (table 2).
The perinatal mortality rate associated with abruption was
119.2 per 1,000 births or nearly 12 percent. This rate was
nearly 15 times the mortality among other pregnancies (8.2
The strong association of abruption with preterm delivery
implies that some of the mortality associated with abruption
may simply be due to the delivery of an immature fetus.
Fifty-five percent of the excess perinatal deaths linked with
an abruption delivery were due to early gestational age
alone. In contrast, the small fetal size at birth contributed
only 9 percent to the perinatal mortality associated with
abruption (despite the strong predictive value of poor fetal
growth as a risk factor for abruption).
DISCUSSION
Placental abruption is an obstetric complication that poses
severe hazards to the pregnant woman and her fetus.
Although uncommon, abruption accounts for 12 percent of
all perinatal deaths. Several studies have reported increased
frequency of this condition among older women, multi-
parous women, smokers, illicit substance users, and those

TABLE 1. Weight-specific perinatal mortality rates in relation to placental abruption, United States,
1995 and 1996

Birth Nonabruption Abruption

Relative
weight Total Total 95% CI†
PMR† PMR risk*
(g) births births

<500 22,817 702.0 1,497 692.1 1.0 0.9, 1.1

500–999 45,299 352.9 4,384 367.7 1.0 1.0, 1.1
1,000–1,499 41,304 122.7 3,795 178.4 1.5 1.4, 1.6
1,500–1,999 80,152 58.6 4,861 128.4 2.2 2.0, 2.4
2,000–2,499 286,461 16.8 6,936 83.6 5.0 4.6, 5.4
2,500–2,999 1,191,673 4.4 9,013 55.3 12.6 11.5, 13.7
3,000–3,499 2,794,679 1.8 9,419 32.4 18.0 16.0, 20.0
3,500–3,999 2,213,070 1.3 5,222 32.6 25.1 21.6, 29.3
4,000–4,499 663,893 1.4 1,382 41.2 28.7 22.1, 37.3
4,500–4,999 109,984 2.7 199 45.2 16.9 8.8, 32.3
≥5,000 12,592 12.2 23 87.0 7.2 1.9, 27.2

Total 7,461,924 8.2 46,731 119.2 14.5 14.2, 14.9

* Relative risk for perinatal mortality.
† CI, confidence interval; PMR, perinatal mortality rate (per 1,000 births).

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FIGURE 1. Distribution of gestational age at delivery for pregnancies with and without placental abruption, United States, 1995 and 1996.

FIGURE 2. Distributions of mean birth weight for pregnancies with and without placental abruption, United States, 1995 and 1996.

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TABLE 2. Relative risk for placental abruption in relation to The incidence of abruption may be increasing with time.
centiles* of birth weight, United States, 1995 and 1996 Recorded abruptions in the United States increased 29 per-
cent between 1979 and 1987 (8.2–11.5 per 1,000 births)
Birth weight All births Term births (≥37 weeks) (12). Similar data from Norway (13) indicated a 31 percent
centile Relative Relative
(%) 95% CI† 95% CI increase in the incidence between 1967–1971 and
risk risk
1987–1991 (5.7–8.3 per 1,000 births). At least some of this
<1 8.8 8.2, 9.5 9.8 9.0, 10.5 increase may reflect improvements in ultrasound tech-
1–2 5.1 4.8, 5.4 4.6 4.3, 5.0 niques to detect mild or partial abruption. The prevalence of
3–4 4.2 4.0, 4.5 3.5 3.2, 3.8 some risk factors for abruption including cocaine and drug
5–9 3.6 3.4, 3.8 2.7 2.5, 2.9
use (7, 14) increased between 1980 and 1987 (15), which
10–19 3.1 3.0, 3.3 2.0 1.9, 2.1
20–29 2.8 2.7, 2.9 1.7 1.6, 1.8
may also have contributed to an increased incidence.
30–39 2.5 2.4, 2.7 1.5 1.4, 1.6 Multiple births due to assisted reproductive methods have
40–49 2.3 2.2, 2.5 1.4 1.3, 1.5 been increasing over time, with multiple fetuses raising the
50–59 2.1 2.0, 2.3 1.4 1.3, 1.5 risk for abruption (1, 5).
60–69 1.8 1.7, 1.9 1.2 1.1, 1.3 In searching for the causes of abruption, clinical studies
70–79 1.5 1.4, 1.6 1.2 1.2, 1.3 have sometimes focused on events near the time of delivery,
80–89 1.3 1.2, 1.3 1.1 1.0, 1.2 such as trauma (1). While abruption often appears to be an
≥90 1.0 Referent 1.0 Referent acute event, its association with poor fetal growth suggests
* Birth weight centiles were adjusted for gestational age. that the origins of abruption may lie at least in midpreg-

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† CI, confidence interval. nancy, perhaps extending back to the earliest stages of preg-
nancy. The association with fetal growth restriction is so
strong that growth restriction in itself can serve as a marker
with hypertensive disorders. However, most cases of abrup- for abruption risk (table 2). The chronic processes underly-
tion occur with no known cause. ing abruption may also contribute to the risk of preterm

FIGURE 3. Gestational age-specific perinatal mortality rates (plotted on a logarithmic scale) for pregnancies with and without placental abrup-
tion, United States, 1995 and 1996.

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FIGURE 4. Distribution of birth weight for term pregnancies (≥37 weeks) with and without placental abruption, United States, 1995 and 1996.

FIGURE 5. Birth weight-specific perinatal mortality rates (plotted on a logarithmic scale) in term pregnancies (≥37 weeks) with and without
placental abruption, United States, 1995 and 1996.

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delivery, which accounts for the majority of excess mortal-
ity that accompanies abruption.
The diagnosis of abruption on vital statistics data is sub-
ject to misclassification (9) and is recorded with knowledge
of the outcome of pregnancy. A pregnancy with severe hem-
orrhage may be more likely to be recorded as an abruption
if the baby dies. The present analysis also does not take into
account some known or suspected risk factors for abruption
including smoking, crack use, chronic hypertension,
preeclampsia, chorioamnionitis, and prolonged rupture of
membranes. These factors are reported poorly or not at all
on vital statistics. Some of these factors might contribute to
the results noted here, but it is unlikely that these factors
could explain more than a small portion of the powerful
associations with fetal growth and preterm delivery.
Pathologic studies suggest that abruption is associated
with abnormal placental vasculature, thrombosis, and
reduced placental perfusion. Genetic variations may predis-
pose to these problems. A high prevalence of mutations in
the genes that encode or regulate factor V Leiden, pro-
thrombin, methylenetetrahydrofolate reductase, and homo-
cysteine has been seen among women with abruption com-
pared with other uncomplicated pregnancies (16, 17). These
genetic factors may also be contributing to the fetal growth
restriction and preterm delivery associated with abruption,
perhaps through compromise of placental function.
Since abruption is apparently a disease of the placenta,
aspects of placental development (even preconception fac-
tors) merit attention. Placental growth is primarily under the
control of fetal genes inherited from the father (18).
Imprinted paternal alleles regulate the formation of the pla-
centa and membranes surrounding the embryo, whereas the
development of the embryo itself requires contribution from
the maternally derived alleles. A search for genetic suscepti-
bility to abruption should include a consideration for pater-
nally imprinted genes.
ACKNOWLEDGMENTS
At the time of this study, Dr. Ananth was supported, in
part, through grant 029553 from the Robert Wood Johnson
Foundation, New Jersey, awarded to the Center for Perinatal
Health Initiatives.
The authors are indebted to Drs. Kitaw Demissie, Lorentz
Irgens, Robert Knuppel, Dawn Misra, George Rhoads,
Andrew Rowland, Amy Sayle, John Smulian, John Thorp,
Am J Epidemiol Vol. 153, No. 4, 2001
Placental Abruption and Perinatal Mortality 337
Anthony Vintzileos, and Jun Zhang for their comments, crit-
icisms, and insightful discussions. They are also grateful to
Susan Fosbre for secretarial assistance.
This paper was presented at the Society for Pediatric and
Perinatal Epidemiologic Research meeting in Baltimore,
Maryland, June 1999.
REFERENCES
1. Cunningham GF, MacDonald PC, Gant NF, et al, eds. Chap 37.
Obstetrical hemorrhage. In: Williams obstetrics. 19th ed.
Norwalk, CT: Appleton & Lange, 1993:819–51.
2. Ananth CV, Savitz DA, Williams MA. Placental abruption and
its association with hypertension and prolonged rupture of
membranes: a methodologic review and meta-analysis. Obstet
Gynecol 1996;88:309–18.
3. Brame RG, Harbert GM Jr, McGaughey HS, et al. Maternal
risk in abruption. Obstet Gynecol 1968;31:224–7.
Downloaded from http://aje.oxfordjournals.org/ by guest on January 5, 2012
4. Hibbard BM, Jeffcoate TNA. Abruptio placentae. Obstet
Gynecol 1966;27:155–67.
5. Williams MA, Lieberman E, Mittendorf R, et al. Risk factors
for abruptio placentae. Am J Epidemiol 1991;134:965–72.
6. Karegard M, Gennser G. Incidence and recurrence rate of
abruptio placentae in Sweden. Obstet Gynecol 1986;67:523–8.
7. Ananth CV, Berkowitz TS, Savitz DA, et al. Placental abruption
and adverse perinatal outcomes. JAMA 1999;282:1646–51.
8. Taffel SM, Ventura SJ, Gay GA. Revised US certificate of
birth—new opportunities for research on birth outcome. Birth
1989;16:188–93.
9. Buescher PA, Taylor KP, Davis MH, et al. The quality of the
new birth certificate data: a validation study in North Carolina.
Am J Public Health 1993;83:1163–5.
10. MacDorman MF, Atkinson JO. Infant mortality statistics from
the linked birth/infant death data set—1995 period data. Mon
Vital Stat 1998;46(suppl 2):1–22.
11. Taffel S, Johnson D, Heuser R. A method of imputing length of
gestation on birth certificates. Vital Health Stat 2 1982;93:1–11.
12. Saftlas AF, Olson DR, Atrash HK, et al. National trends in the
incidence of abruptio placentae, 1979–1987. Obstet Gynecol
1991;78:1081–6.
13. Rasmussen S, Irgens LM, Bergsjo P, et al. The occurrence of
placental abruption in Norway 1967–1991. Acta Obstet Gynecol
Scand 1996;75:222–8.
14. Shiono PH, Klebanoff MA, Nugent RP, et al. The impact of
cocaine and marijuana use on low birth weight and preterm birth:
a multicenter study. Am J Obstet Gynecol 1995;172:19–27.
15. Abelson HI, Miller JD. A decade of trends in cocaine use in the
household population. NIDA Res Monogr 1985;61:35–49.
16. Kupferminc MJ, Eldor A, Steinman N, et al. Increased fre-
quency of genetic thrombophilia in women with complications
of pregnancy. N Engl J Med 1999;340:9–13.
17. de Vries JIP, Dekker GA, Huijgens PC, et al. Hyperhomo-
cysteinaemia and protein S deficiency in complicated pregnan-
cies. Br J Obstet Gynaecol 1997;104:1248–54.
18. Bartolomei MS, Tilghman SM. Genomic imprinting in mam-
mals. Annu Rev Genet 1997;31:493–525.