Acta Obstetricia et Gynecologica.

2010; 89: 732–740

ACTA OVERVIEW

Etiology, clinical manifestations, and prediction of placental abruption

MINNA TIKKANEN

Department of Obstetrics and Gynecology, University Central Hospital, Helsinki, Finland

Abstract
Placental abruption, defined as complete or partial detachment of the placenta before delivery, is one of the most devastating
pregnancy complications. Bleeding and pain consist the classical symptoms of placental abruption but the clinical picture varies
from asymptomatic, in which the diagnosis is made by inspection of the placenta at delivery, to massive abruption leading to
fetal death and severe maternal morbidity. The diagnosis is always clinical. The etiology of placental abruption is not fully
understood but impaired placentation, placental insufficiency, intrauterine hypoxia, and uteroplacental underperfusion are
likely the key mechanisms causing abruption. Abruption results from a rupture of maternal decidual artery causing dissection
of the decidual-placental interface. Acute vasospasm of small vessels may precede abruption. The trophoplastic invasion in the
spiral arteries and subsequent early vascularization may be defective. Moreover, placental abruption may also be a
manifestation of an inflammatory process which could affect vascular bed. Despite heightened awareness, placental abruption
still remains unpredictable and unpreventable. A clinically useful predictive test is needed to detect individuals at risk.
Although several biomarkers have been evaluated, none has so far turned out to be useful.

Key words: Placental abruption, etiology, symptoms, diagnosis, prediction

Introduction placentation, placental insufficiency, intrauterine

Placental abruption is defined as the complete or
partial premature separation of the placenta before
delivery with hemorrhage into the decidua basalis.
The diagnosis of placental abruption is clinical (1). It
should be suspected in women who present with
vaginal bleeding or abdominal pain or both, a history
of trauma, and in those who present with otherwise
unexplained preterm birth (2,3). Symptoms of abrup-
tion vary from none, in which the diagnosis is made
only on placental inspection, to massive abruption
leading to fetal death and maternal morbidity (2,3).
Classic symptoms of abruption are vaginal bleeding,
abdominal pain, uterine contraction, and tenderness
(3). Although the main symptoms are typical and have
been well described, symptoms can vary considerably
from one patient to another.
Placental abruption seems to be multifactorial. Its
etiology is not fully understood but impaired
hypoxia, and uteroplacental underperfusion are con-
sidered the key mechanisms causing abruption (4,5–
7). Abruption results from a rupture of maternal
decidual artery causing dissection of blood at the
decidual-placental interface, around placental mar-
gin, or behind the membranes (1,8). Acute vasospasm
of small vessels may be one event immediately pre-
ceding placental separation. Thrombosis of the decid-
ual vessels with associated decidual necrosis and
venous hemorrhage also are often present (8). In
some cases, blunt trauma or rapid decompression
of the over distended uterus causes abruption, but
in most cases placental abruption seems to be a
consequence of a long-standing process perhaps dat-
ing back to the first trimester (9).
Immunological defects may well play a role in the
origin of placental abruption (10,11). These defects
may lead to maternal inflammatory response with
cytokine release resulting in a chain of events such

Correspondence: Minna Tikkanen, Department of Obstetrics and Gynecology, University Central Hospital, 00029 Helsinki, Finland.
E-mail: minna.tikkanen@hus.fi

(Received 27 August 2009; accepted 5 February 2010)

ISSN 0001-6349 print/ISSN 1600-0412 online
2010 Informa UK Ltd. (Informa Healthcare, Taylor & Francis AS)
DOI: 10.3109/00016341003686081

as shallow trophoblast invasion, defective spiral artery
remodeling, placental infarctions, and thrombosis
(12). Placental abruption may also be a manifestation
of acute or chronic inflammation (4). Infection or
inflammation and tissue injury can cause a rapid
release of various bioactive mediators at the mater-
nal-fetal interface (4,13) which may predispose to
abruption. Normal placentation requires trophoblast
invasion of maternal spiral arteries, and development
of a high-flow, low-resistance uteroplacental circula-
tion (14). Vascular remodeling occurs under the
influence of several proangiogenic and antiangiogenic
factors (15–19). Proangiogenic placental growth
factor (PlGF) deficiency and antiangiogenic soluble
fms-like tyrosine kinase 1 (sFlt-1) excess may result
from placental hypoxia associated with incomplete
remodeling of maternal spiral arteries.
Since it is likely that placental abruption is a
long-standing process (9), it would be of clinical
importance if this condition could be predicted before
it manifests clinically. Placental abruption in a previ-
ous pregnancy is the most important predictor. Also,
the knowledge of family history and measurement of
uterine artery flow in early pregnancy may provide
useful information. Several biochemical markers for
placental abruption have been studied but none has so
far emerged as clinically useful (20–29).
Current knowledge of etiology, clinical manifesta-
tions, and diagnosis of placental abruption will be
presented in this overview. Family history, placental
abruption in prior pregnancy, uterine artery flow
measurement, and selected biochemical markers
will be reviewed as potential predictors of abruption.
Materials and methods
Medline database was searched using the keywords
‘placental abruption’ or ‘abruptio placentae’ in com-
bination with ‘pregnancy’, ‘etiology’, ‘symptoms’,
‘diagnosis’, and ‘prediction’. Approximately 2100
English language articles up to October 2009 were
identified. Case reports were deleted. Only studies
focusing mainly on clinical aspects of placental abrup-
tion were included. Studies selected were mainly
published during the last 10 years, but frequently
referenced and highly regarded older reports were
not excluded. Reference lists of articles identified
by this strategy were also searched and articles judged
clinically relevant were selected. Finally, 250 articles
were judged relevant and 76 were included in this
overview. There were no randomized controlled trials
which have specifically studied placental abruption,
and the overwhelming majority of studies are cohort
studies, case-control studies, or case series examining
Placental abruption 733
risk factors associated with placental abruption. Thus,
the level of evidence of most of the studies based on
the classification of Oxford Centre of Evidence-Based
Medicine is mainly II, III, or IV.
Results
Etiology
Immunological, inflammatory, or vascular factors
seem to explain a large proportion of placental
abruption.
Immunological rejection
Excessive activation of the immune system may
suggest past exposure to major antigens (30). Cell-
mediated immunity is suppressed and humoral
immune response is upregulated in normal pregnancy
but not in placental abruption (10,30). This may lead
to exaggerated maternal immune rejection of the
fetus, activation of fetal monocytes, and release of
inflammatory agents (30,31). Trophoblastic cells
interact in the decidua with natural killer cells which
express receptors that recognize combinations of
human leukocyte antigens (HLA). HLA-G is impor-
tant in avoiding rejection of the fetus. HLA-G levels
are strongly decreased in women with placental
abruption (32).
Excessive activation of the immune system in
placental abruption may also suggest past exposure to
strong and specific superantigens (30). As candidates of
such superantigens, Chlamydia pneumoniae-specific
IgG, and IgA as well as Chlamydia trachomatis-specific
IgG, IgA, and chlamydial heat shock protein 60 antibody
rates were tested in early pregnancy in women who
subsequently developed placental abruption (28).
However, antibodies to these common superantigens
failed to predict abruption (28).
Inflammation
Neutrophils and macrophages are increased in pla-
centas of women with abruption compared to controls
(9). Oxidative stress and products of vascular activa-
tion and coagulation such as thrombin may have
similar effects (4). Abruption is associated with a
thrombin-enchanced expression of interleukin (IL)-
8, a potent neutrophil chemoattractant which leads to
a marked infiltration of decidual neutrophils (33). In a
recent study, 51% of women with preterm abruption
(<37 weeks) and 44% of women with term abruption
(‡37 weeks) had acute inflammation-associated
734 M. Tikkanen
condition or chronic clinical process, compared to
37% of control women with preterm delivery and 255
of control women with term delivery (4). However,
C-reactive protein, an objective and sensitive marker
of infection and inflammation, failed to predict sub-
sequent placental abruption when tested in early
pregnancy (28).
Vascular disease
Trophoblast invasion in the spiral arteries and con-
sequent early vascularization may be defective in
placental abruption (34). Incomplete remodeling of
arteries causes high resistance to uterine artery blood
flow which may predispose to vascular rupture of a
spiral artery in the placental bed leading to placental
abruption (14,25,34). Widening hematoma then
‘peels the placenta off’ from the decidua. This mech-
anism causes ‘a classic abruption’ with severe symp-
toms (35). Placental abruption can also be caused by
venous bleeding from marginal lakes around the edge
of the placenta leading to preterm birth (35).
Of antiangiogenic factors, sFlt-1 and soluble endo-
glin (sEng) have been studied (25,27,29). sFlt-1 binds
biologically active forms of PlGF and vascular endo-
thelial growth factor (19), and sEng blocks the bind-
ing of transforming growth factor isoforms to
endothelial receptors (36). In one study, the serum
levels of PlGF were decreased and the ratios of sFlt-1/
PlGF were increased in nulliparous women several
weeks before placental abruption, but this was the
case only in women who also developed preeclampsia
(25). Also, serum levels of sEng were elevated in late
second and early third trimesters in women who later
developed both hypertension and placental abruption
(29). PlGF and sFlt-1 are the factors regulating pla-
cental angiogenesis throughout pregnancy. However,
serum sFlt-1, PlGF, and sEng measured in early
second trimester failed to identify women with sub-
sequent placental abruption (27). These results imply
that circulating proangiogenic PlGF and antiangio-
genic sFlt-1 or sEng in early or midgestation are not
useful for predicting placental abruption.
Clinical manifestations and diagnosis
Symptoms and signs. Antepartum hemorrhage in the
second half of pregnancy occurs in 2–5% of all preg-
nancies. Placental abruption accounts for approxi-
mately one quarter of such cases (37). Classic
symptoms of placental abruption are vaginal bleeding,
abdominal pain, uterine contractions, and uterine
tenderness (3). All these symptoms are not invariably
present and asymptomatic presentation does not
exclude placental abruption (3). Vaginal bleeding is
present in 70–80% of cases (3,38), but the amount
correlates poorly with the degree of abruption (2). If
the membranes are ruptured, blood stained amniotic
fluid leeks into the vagina (3). Symptoms depend on the
location of abruption, whether it is revealed or con-
cealed, and the degree of abruption (2). Abruption
may be ‘revealed’ in cases in which blood tracks between
the membranes and the decidua and escapes through the
cervix into the vagina (2,38). This occurs in 65–80% of
the cases (3). The less common ‘concealed’ abruption
occurs when blood accumulates behind the placenta
with no obvious external bleeding (2,38). This happens
in 20–35% of cases (3). Concealed type is the most
dangerous with the worst complications. Finally, abrup-
tion may be total (7%), involving the entire placenta,
leading to fetal death, or partial (93%) with only a part of
the placenta detached from the uterine wall (3).
Uterine tenderness or pain is present in 66% and
tonic uterine contractions in 34% (38). The presence
of pain probably indicates extravasation of blood into
the myometrium. Contractions are frequent with a
rate of more than five in 10 minutes (2,14). The
presence of uterine contractions may, however, be
difficult to distinguish from general abdominal pain
associated with abruption. Nearly 20% of women
have neither pain nor bleeding (3).
Four grades of placental abruption have been
described (Table 1) (37,39,40). Grade 1 placental
abruption is found in approximately 40% of cases,
grade 2 in approximately 45%, and grade 3 in approx-
imately 15% of cases (39). The clinical classification
of placental abruption is based on the site of bleeding
(Figure 1). The bleeding can be subchorionic
(between the myometrium and the placental mem-
branes), retroplacental (between the myometrium
and the placenta), or preplacental (between the pla-
centa and amniotic fluid) (41). Subchorionic hema-
tomas may be remote from the placenta and are
thought to arise from marginal abruptions.
Table 1. Grading of placental abruption.
Grade Description
0 Asymptomatic, a small retroplacental clot detected
1 Vaginal bleeding, uterine irritability, and tenderness
present; no signs of maternal or fetal distress
2 Vaginal bleeding, uterine contractions, no signs of
maternal shock; signs of fetal distress present
3 Severe bleeding present or concealed, uterine
hypertonus, ‘wooden-hard’ uterus, persistent
abdominal pain, maternal shock, and often
coagulopathy; fetal distress or death
Modified from (37,39,40).

Subamniotic
Placenta
Intraplacental
Retroplacental
Figure 1. Different sites of placental abruption.
Preplacental hemorrhage includes both subamniotic
hematoma and massive subchorionic thrombosis (41).
Intraplacentalhematomas alsooccur. Thisclassification
of placental abruption is often used by clinicians and
differs from textbooks of pathology (1,8).
Placental abruption can be confirmed by gross
examination of the placenta. In a recent abruption
a crater-like depression on the maternal surface of the
placenta covered by dark clotted blood, the so-called
‘delle’, can be found (14). In older abruptions, fibrin
deposits appear on the site of abruption (8). A totally
abrupted placenta may not differ from normal pla-
centa by maternal surface (8,14). Bleeding may occur
into the uterine myometrium, leading to a purple
colored uterus, the so-called Couvelaire uterus
(14). Such uterus contracts poorly and can result in
massive postpartum hemorrhage.
Ultrasound. If placental abruption is suspected based
on clinical symptoms and signs, ultrasound examina-
tion is often performed to visualize subchorionic or
retroplacental hematoma. In some cases, placental
abruption can be diagnosed by ultrasound even in
asymptomatic patients (2). The ultrasonographic
appearance of abruption depends on the size and
location as well as the age of the hematoma (41).
The appearance of hematoma in acute phase varies
from hyperechoic to isoechoic when compared with
placenta. When hematoma resolves it becomes more
hypoechoid within one week and sonolucent within
two weeks (41). Small or acute revealed abruptions
are difficult to detect by ultrasound. Concealed hem-
orrhage may be more easily seen (42). Despite
improvement in sonographic equipments, the test
performance has not improved (42). Ultrasound cor-
rectly diagnoses abruption only in 15–25% of cases
(3,42). When a clot is visualized by ultrasound, the
positive predictive value for abruption is 88% (42).
Although ultrasound is not accurate in the diagnosis
Placental abruption 735
Umbilical
cord
Massive Subchorionic
subchorionic
of abruption, it is useful in monitoring cases managed
expectantly and to diagnose placenta previa.
Cardiotocographic changes. In severe cases of placental
abruption, the fetus presents with heart rate abnor-
malities. A variety of fetal cardiotocographic (CTG)
patterns have been associated with placental abrup-
tion and fetal distress, including repetitive late or
variable decelerations, decreased beat-to-beat vari-
ability, bradycardia, or sinusoidal fetal heart rate
pattern (2,3). In one study, CTG was abnormal in
69% of cases (3). Not surprisingly, abnormal CTG is
a signal of poor fetal outcome (43) and prompt action
is necessary to save the fetus. On the other hand,
conservative expectant management seems to be safe
in preterm pregnancies with placental abruption and
normal CTG (43).
Placental histopathology. Histopathology of abrupted
placentas often shows evidence of acute and chronic
lesions (9). Acute lesions include neutrophil infiltra-
tion of the chorionic plate. Chronic lesions may
develop due to a lack of adequate trophoblastic inva-
sion (34) and include placental infarcts (8,9). Histo-
logical signs of chorioamnionitis and deciduitis with
neutrophil infiltration are associated with placental
abruption in one-third of the cases (44,45). Acute
atherosis in spiral arteries leads to distinctive necro-
tizing decidual lesions (9,14) and vascular thrombo-
sis, placental infarcts, and fibrin deposits (14,44,46).
Placenta shows progression areas from chronically
infarcted chorionic villous tissue in areas immediately
adjacent to the hematoma to infarcted tissue in
more distant areas (1). Focal villous edema and
hemorrhage are caused by acute hypoxic damage
or cytokine release from injured decidua (8). The
histological features are time-dependent. Acute lea-
sions may not show ischemic changes or intravillous
736 M. Tikkanen
hemorrhage (1). However, recent or less acute hema-
tomas may show hemosiderin-laden macrophages in
the maternal space. The adjacent chorionic villi then
show chronic infarction with remnants of degenerated
villi and intervillous thrombi. Decidual necrosis is
often prominent (1). The rate of abruption is clearly
higher (4%) when the diagnosis is based on placental
pathology. Most of the additional cases have unre-
markable obstetric history (1). However, it is impor-
tant to keep in mind that placental abruption is a
clinical diagnosis, not histopathological.
Prediction of placental abruption
Family history. There is some evidence that placental
abruption occurs in families (47–49). According to one
study, placental abruption appears to cluster in families
of an index patient with recurrent placental abruption
(47). According to another study, 5% of women with
abruption reported first degree relatives with abruption
(48). A recent study from Norway showed that severe
abruption was associated with a two-fold risk in sisters
(OR 1.7–2.1) whereas less severe abruption was not
(49). The heritability of severe abruption between
sisters was estimated as 16% (49).
High recurrence rate of placental abruption and
high prevalence of thrombophilia among women with
placental abruption support genetic background (49–
51). In one study, 20% of women with placental
abruption reported first degree relatives with venous
thrombosis compared to only 6.7% of controls (52).
Genetic studies involving the use of candidate gene
approach have shown positive association between
placental abruption and polymorphisms of nitric
oxide synthase gene (53,54), although this was not
confirmed in a study from Finland (55). Also, it has
been shown that low-activity haplotype of the micro-
somal epoxide hydrolase gene protects against pla-
cental abruption (56).
History of placental abruption. The best predictor of
placental abruption is history of abruption in prior
pregnancy (3,49). Women with a history of abruption
have 7- to 20-fold risk of abruption in subsequent
pregnancy (3,57–59) and these pregnancies should be
referred as high risk pregnancies. This risk increase is
independent of smoking (60). Placental abruption
recurs in 3–17% after one episode and in 19–25%
after two episodes (3,49,57–59,61,62). Risk of recur-
rence is higher after severe abruption compared to
mild abruption (49). It is not known why placental
abruption recurs in some women. Recurrence cannot
be explained solely by common risk factors (60).
Women with a history of placental abruption are at
high risk and could benefit from the use of predictive
tests.
Uterine artery flow measurement. Data suggest that
high uterine artery pulsatility index at 11–14 weeks
or notching of the uterine artery waveform at 20–24
gestational weeks predicts subsequent abruption
(62–65), but these uterine artery flow markers
have not yet been properly validated for clinical
practice. More research effort is needed to clarify
if routine use of uterine artery Doppler measure-
ment in early pregnancy is useful and cost-effective
in the follow-up of pregnant women with a history
of placental abruption.
Biochemical markers. Approximately 1% of patients
have an elevated maternal serum alpha-fetoprotein
(AFP) level not explained by incorrect dates, struc-
tural or chromosomal abnormalities, or multiple ges-
tation (22). This unexplained second-trimester
elevation of AFP may be associated with subsequent
adverse obstetric outcome including placental abrup-
tion (22,24,66–68). In one study, elevated AFP levels
(> 2 MoM) were detected in 17% of pregnancies with
subsequent placental abruption (69). In another study
of women with preterm labor and placental abruption,
AFP levels were higher than in other groups with
preterm labor (21). Although second-trimester mater-
nal serum AFP levels are higher in women with
subsequent abruption, clinical usefulness of this test
is limited due to low sensitivity and high false-positive
rate (26).
In cases with normal chromosomes, maternal
serum free beta human chorionic gonadotrophin
(b-hCG) may be elevated in pregnancy complica-
tions, such as in early fetal loss, preterm birth, preg-
nancy induced hypertension, preeclampsia, and
intrauterine growth restriction (22,24,67,70,71).
Abnormal increased levels of b-hCG may be due to
decreased placental perfusion (22). Data linking high
b-hCG levels to placental abruption are conflicting
(26,71).
Pregnancy-associated plasma protein A (PAPP-A)
is a protease for insulin-like growth factor binding
protein-4 (68). A recent cohort study of 34,271
women indicated that women with first-trimester
PAPP-A levels at the lowest fifth centile had an
increased risk of placental abruption (68). In another
study, low PAPP-A was detected in 29% at the lowest
fifth centile and 43% at the lowest tenth centile of
women with placental abruption (64).
Maternal serum activin A is a glycoprotein (72)
produced primarily by the placental trophoblast. It

has many biological effects including tissue remodeling
and regulation of trophoblast differentiation and inva-
sion (72,73). One study reported two cases with pla-
cental abruption with high activin A levels weeks before
placental abruption (23). This calls for further studies of
this test in the prediction of placental abruption.
Fibronectin is a glycoprotein synthesized in endo-
thelial cells (73). Fibronectin seals trophoblast to
uterine decidua at implantation site (14). Fibronectin
levels are higher in women with placental abruption
(74), but more research is needed.
Thrombomodulin is a vascular endothelial cell
receptor for thrombin which neutralizes thrombin
clotting activity (75). Thrombomodulin is a marker
of endothelial cell damage and has been localized to
placental syncytiotrophoblast (75). The levels of
trombomodulin may be elevated in women with pla-
cental abruption (75).
Kleihauer-Betke test is not sensitive enough to
diagnose placental abruption (75,76). D-dimer, a fibrin
degradation fragment and a byproduct of clot lysis, has a
high negative predictive value for thromboembolic
events (20,77) and can be used in early diagnosis of
placental abruption (20). Also coagulation profile
(platelet count, prothrombin time, partial thrombo-
plastin time, and fibrinogen level) has been used in
the prediction of placental abruption (20,75), but test
performance is not good enough for clinical use.
Risk factor analysis. Risk score analyses and mathe-
matical modeling have been developed in order to
predict placental abruption (47,78). An analysis of 52
obstetric risk factors related to placental abruption
was used to create a mathematical model (78). After
multivariate analysis, seven correlates overlapping
between primiparous and multiparous women
remained in the model. These were uterine bleeding
at < 28 and > 28 gestational weeks, placenta previa,
male fetal gender, preterm labor, breech position, and
cigarette smoking. The strongest predictors of pla-
cental abruption were concomitant uterine bleeding
at > 28 gestational weeks and placenta previa (78).
The cumulative risk could be calculated mathemati-
cally. In another study, each risk factor was given a
score from 1 to 3 depending of the odds ratio and a
total score was calculated (47). The investigators
concluded that the easily available information on
risk factors might be used to derive a risk score for
placental abruption.
Discussion
The etiology of placental abruption is poorly
understood, but defective trophoblastic invasion of
Placental abruption 737
the spiral arteries and consequent uteroplacental
underperfusion may play a role (34). Thus, placental
abruption, preeclampsia, and intrauterine growth
restriction often share similar histopathology (30).
High level of soluble HLA-G is needed to switch
cytokine profile towards Th-2 response. In women
with placental abruption HLA-G levels are strongly
decreased (32) which may lead to dysfunctional pla-
centa. Generalized inflammation or acute or chronic
inflammatory process may cause increased produc-
tion of proinflammatory cytokines. These cytokines,
such as tumor necrosis factor-a and IL-b1, can stim-
ulate the production of matrix metalloproteinase
(MMP) by trophoblasts and other cell types (4).
Increased premature production of MMPs may result
in the destruction of the extracellular matrix and cell
to cell interactions that lead to premature detachment
(4). MMPs seem to play important roles in normal
placental detachment (4).
One plausible hypothesis is an imbalance between
placental proangiogenic and antiangiogenic factors
preceding placental abruption. However, recent stud-
ies have not been able to link angiogenic factors and
placental abruption (25,27,29).
Abruption often happens unexpectedly. The
management depends on the extent of abruption,
gestational age, and maternal and fetal conditions.
However, it is likely that in most cases placental
abruption is a long-standing process dating back to
early pregnancy. Therefore, a predictive test would be
most useful in clinical practice. A lot of research effort
has been used to develop such a test. Several bio-
chemical markers, uterine artery flow measurement,
and risk factor analysis have been tested but no test yet
has emerged as clinically useful (20–29,47,62–65,78).
One limitation of the risk factor score analyses is that
such analyses are retrospective. However, potential
models based on risk factors of placental abruption
might be useful in the management of high risk
pregnancies if validated in prospective studies
(47,78).
Although the genetic research is currently very
active, the results of genetic association studies in
placental abruption are still premature and inconsis-
tent (51). The complex nature of the disease implies
that associations with individual polymorphisms are
only modest (51).
The most accurate predictor of abruption is a
placental abruption in prior pregnancy which should
alert clinicians to closer follow-up. Placental abrup-
tion may simply cause permanent damage to the
endometrium which then increases the risk of inap-
propriate placentation in subsequent pregnancy (57).
Thus, a history of placental abruption should always
alert subsequent placental abruption. Since patients
738 M. Tikkanen
with abruption have an increased risk of impaired
uteroplacental perfusion and recurrent abruption in
subsequent pregnancies, serial scans should be con-
sidered during the second half of pregnancy
(2,61,79). Testing placental function and assessment
of fetal growth six weeks before the time of previous
placental abruption has been advocated in order to
lower the risk for recurrent abruption (79). In women
with two or more prior abruptions, amniocentesis for
lung maturity and delivery at 37 weeks of gestation
might be recommended (2).
This overview is a clinically oriented summary of
the most relevant literature related to the etiology,
clinical manifestations, and predictors of placental
abruption. However, no randomized controlled trials
which had specifically studied placental abruption
were identified. This has a major impact on the
strength of evidence which is mainly II, III, or IV.
Clearly many unanswered questions still remain.
Acknowledgements
This study was supported by Helsinki University
Hospital Research Grants. Professors Jorma Paavo-
nen and Olavi Ylikorkala are thanked for valuable
comments on the manuscript.
Declaration of interest: The author reports no
conflicts of interest. The author alone is responsible
for the content and writing of the paper.
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