Expert Review
org
Placental abruption at near-term and term
gestations: pathophysiology, epidemiology,
diagnosis, and management
Justin S. Brandt, MD; Cande V. Ananth, PhD, MPH
Introduction
Placental abruption is the premature
separation of the placenta from its uter-
ine attachment before the delivery of a
fetus. Although the clinical manifesta-
tions are myriad, abruption is classically
associated with vaginal bleeding and
abdominal pain, with or without uterine
contractions, and is often accompanied
by abnormal fetal heart rate (FHR)
patterns. Clinical challenges arise when
pregnant people with this condition
present with profound vaginal bleeding,
From the Division of Maternal-Fetal Medicine,
Department of Obstetrics, Gynecology, and
Reproductive Sciences, Rutgers Robert Wood
Johnson Medical School, New Brunswick, NJ
(Dr Brandt); Division of Epidemiology and
Biostatistics, Department of Obstetrics,
Gynecology, and Reproductive Sciences,
Rutgers Robert Wood Johnson Medical School,
New Brunswick, NJ (Dr Ananth); Department of
Biostatistics and Epidemiology, Rutgers School
of Public Health, Piscataway, NJ (Dr Ananth);
Cardiovascular Institute of New Jersey and
Department of Medicine, Rutgers Robert Wood
Johnson Medical School, New Brunswick, NJ
(Dr Ananth); and Environmental and
Occupational Health Sciences Institute, Rutgers
Robert Wood Johnson Medical School,
Piscataway, NJ (Dr Ananth).
Received Dec. 26, 2021; revised June 27, 2022;
accepted June 29, 2022.
The authors report no conflict of interest.
No financial support was necessary for the
preparation of this manuscript or acquiring data.
C.V.A. is supported, in part, by the National
Heart, Lung, and Blood Institute (grant number
R01-HL150065) and the National Institute of
Environmental Health Sciences (grant number
R01-ES033190), National Institutes of Health.
Corresponding author: Justin S. Brandt, MD.
jsb288@rwjms.rutgers.edu
0002-9378/$36.00
ª 2022 Elsevier Inc. All rights reserved.
https://doi.org/10.1016/j.ajog.2022.06.059
ajog.
Placental abruption is the premature separation of the placenta from its uterine
attachment before the delivery of a fetus. The clinical manifestations of abruption typi-
cally include vaginal bleeding and abdominal pain with a wide variety of abnormal fetal
heart rate patterns. Clinical challenges arise when pregnant people with this condition
present with profound vaginal bleeding, necessitating urgent delivery, especially when
there is a concern for maternal and fetal compromise and coagulopathy. Abruption
occurs in 0.6% to 1.2% of all pregnancies, with nearly half of abruption occurring at term
gestations. An exposition of abruption at near-term (defined as the late preterm period
from 34 0/7 to 36 6/7 weeks of gestation) and term (defined as
37 weeks of gestation)
provides unique insights into its direct effects, as risks associated with preterm birth do
not impact outcomes. Here, we explore the pathophysiology, epidemiology, and diag-
nosis of abruption. We discuss the interaction of chronic processes (decidual and ute-
roplacental vasculopathy) and acute processes (shearing forces applied to the abdomen)
that underlie the pathophysiology. Risk factors for abruption and strengths of association
are summarized. Sonographic findings of abruption and fetal heart rate tracings are
presented. In addition, we propose a management algorithm for acute abruption that
incorporates blood loss, vital signs, and urine output, among other factors. Lastly, we
discuss blood component therapy, viscoelastic point-of-care testing, disseminated
intravascular coagulopathy, and management of abruption complicated by fetal death.
The review seeks to provide comprehensive, clinically focused guidance during a
gestational age range when neonatal outcomes can often be favorable if rapid and
evidence-based care is optimized.
Key words: abruptio placenta, diagnosis, epidemiology, management, near term,
pathophysiology, placental abruption, term
necessitating urgent delivery, especially from 34 0/7 to 36 6/7 weeks of gestation)
when there is a concern for and term (defined as
37 weeks of
maternal and fetal compromise and gestation) gives a unique insight into the
coagulopathy. direct effects of abruption.
The management of preterm abrup- This review focused on abruption after
tion has received significant attention in 34 weeks of gestation and sought to pro-
the obstetrical literature.1,2 This is vide clinical guidance when perinatal out-
because much of the perinatal morbidity comes can often be favorable if rapid and
and mortality associated with preterm evidence-based care is optimized. More-
abruption is impacted by gestational age over, the pathophysiology, epidemiology,
at delivery, which is a mediating variable and diagnosis of abruption were reviewed.
that features on the causal pathway be- In addition, we reviewed clinical manage-
tween abruption and adverse perinatal ment, focusing on associated challenges
outcomes.3 However, approximately half encountered by obstetricians, including
of abruption occurs at term gestations, obstetrical hemorrhage, coagulopathy, and
when preterm delivery has less impact on delivery in the setting of fetal death. Lastly,
neonatal outcomes.4e7 Therefore, the we proposed a management algorithm and
discussion of abruption at near-term other clinical pearls that are intended to
(defined as the late preterm period assist obstetrical clinicians in their daily
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clinical practices when they encounter
abruption and obstetrical hemorrhage.
Pathophysiology
The pathophysiology of abruption in-
cludes both long-standing chronic pro-
cesses and acute “triggers” and the
interaction between the 2 processes
(Figure 1).8,9 Chronic processes that
predispose to abruption include throm-
bosis, inflammation, infection, and
decidual and uteroplacental vasculop-
athy. These processes lead to placental
hypoperfusion and defective spiral artery
remodeling, placental infarction, and
shallow trophoblast invasion.10 More-
over, the relative hypoxia promotes the
expression of vascular endothelial growth
factors, which may alter the inflamma-
tory response to decidual bleeding.11
These chronic changes predispose to
abruption and other placentally medi-
ated pathologies, including fetal growth
restriction (FGR) and preeclampsia,12
FIGURE 1
Pathophysiology of placental abruption
often occurring weeks or months before
the manifestations of these complications
become clinically evident.8
Acute processes leading to abruption
are largely the consequence of mechan-
ical and shearing forces applied to the
abdomen. There may be an inciting
event that precipitates abruption, such as
abdominal trauma.13 Moreover, abrup-
tion may be precipitated by rapid
decompression of the uterine cavity after
amniotomy or after vaginal delivery of a
first twin (Figure 2).14 Rupture of
maternal decidual vessels leads to
bleeding at the decidual-placental inter-
face.10 Blood accumulates in this space,
and detachment of the placenta from the
uterus occurs, often accompanied by
vasospasm of small vessels.10
Decidual bleeding that results in
dissection and laceration along the
decidual plane may lead to retroplac-
ental, subchorionic, and subamniotic
bleeding.15 Intraplacental accumulation
of blood may also occur because of
disruption of vasculopathic decidual ar-
terioles in a setting of maternal vascular
hypoperfusion.16 Inadequate myo-
metrial contractions are unable to
constrict bleeding vessels and sinuses at
the placental bed because of uterine
distension from the fetus. Consequently,
the bleeding continues and intravascular
channels for thromboplastic materials
remain open.
The clinical sequelae of abruption are
thought to be mediated by thrombin,
which plays a crucial role in inflamma-
tion and vascular response to endothelial
injury. Decidual bleeding leads to the
release of excess thrombin, which is
generated by tissue factor expressed on
decidual cells to promote hemostasis.17,18
Higher levels of vascular endothelial
growth factor stimulate decidual endo-
thelial cells to generate more tissue factor
and more thrombin.11 This results in
degradation of extracellular matrix
and further endothelial injury from
the enhanced expression of matrix
metalloproteinases17 and the release of
proinflammatory cytokines, such as
interleukin 8.19 These factors, coupled
with the uterotonic effects of thrombin,20
may lead to rupture of membranes and
uterine contractions. When large
amounts of thrombin become intravas-
cular, consumptive coagulopathy or
disseminated intravascular coagulation
(DIC) may ensue with potential for
maternal morbidity and mortality.21

Epidemiology
Abruption complicates 0.6% to 1.2% of
pregnancies.4e7 Among singleton de-
liveries at term gestations in the US
Collaborative Perinatal Project (CPP,
1959e1966), the rate of clinical abrup-
tion was 1.4% (589 of 42,821).22 Preg-
nant people with an abruption in 1
pregnancy carry up to a 10-fold
increased risk of recurrence in a subse-
Placental abruption is the end result of an acute process (“acute pathway”), the culmination of long- quent pregnancy; the recurrence risk is
standing chronic processes (“chronic pathway”), or both. The acute pathway is driven by mechanical 25-fold higher in a third pregnancy when
and shearing forces applied to the abdomen, causing premature placental separation. The chronic 2 previous pregnancies are complicated
pathway includes thrombosis, infection, and decidual and uteroplacental vasculopathy and other by abruption.23e26 The prevalence of
inflammatory processes. Figure adapted from “Pathogenesis of abruption,” and figure created by abruption has been increasing in the
C.V.A., used with permission from UpToDate, Inc, Waltham, Massachusetts United States and Canada but declining
Brandt. Placental abruption at near term and term gestations. Am J Obstet Gynecol 2023. in other European countries, including
Finland, Denmark, Norway, Sweden,

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FIGURE 2
Electronic fetal monitoring of acute abruption with tachycardia and prolonged decelerations, preceding a terminal
bradycardia

A para 1 pregnant patient with cephalic-cephalic presenting dichorionic-diamniotic twins at 36 weeks of gestation had a vaginal delivery of the first fetus.
Immediately after delivery of the first fetus, there was a large gush of bright red blood (vaginal bleeding). The FHR of the second fetus revealed fetal
tachycardia and prolonged decelerations, which forecasted the acute abruption and preceded a terminal bradycardia. Because of the severe abruption
with FHR changes, the patient subsequently underwent urgent cesarean delivery, which was notable for bloody amniotic fluid and complete placental
separation
FHR, fetal heart rate
Brandt. Placental abruption at near term and term gestations. Am J Obstet Gynecol 2023.

and Spain.27 The reason for this diver-
gence is unclear but may be related to
different risk factor profiles of these
distinct populations. Differences in the
prevalence rates of tobacco smoking,
obesity, and multivitamin use and dif-
ferences in the implementation of uni-
versal folate fortification programs across
these countries may help explain some of
the differences in the temporal changes in
abruption rates across countries.27
The risk of abruption is 3- to 4-fold
higher among pregnant people with
chronic hypertension and 4- to 6-fold
higher among those with preeclampsia,
particularly preeclampsia with severe
features and superimposed
preeclampsia.28e31 Other clinical risk
factors for abruption include pregesta-
tional and gestational diabetes mellitus,
preterm premature rupture of mem-
branes (PROM), chorioamnionitis, and
oligohydramnios.31e33 Pregnant people
with iron deficiency anemia, infection
and other inflammatory states, folate
deficiency, and hyperhomocysteinemia
are also at increased risk.33e36 Increased
circulating folate levels in pregnancy are
associated with reduced levels of homo-
cysteine, and increased levels of homo-
cysteine are directly implicated in
methylenetetrahydrofolate reductase
gene mutation.36e38 A large population-
based study from Norway showed that
the risk of abruption was 19% lower
(odds ratio [OR], 0.81; 95% confidence
interval [CI], 0.68e0.98) among preg-
nant people who took folic acid supple-
mentation than among nonusers.
Tobacco smoking is associated with a
1.7- to 2-fold increased risk of abrup-
tion, with a strong dose-response asso-
ciation with the number of cigarettes
smoked per day.39e41 In a systematic
review and meta-analysis of observa-
tional studies that included 1,358,083
pregnancies, smoking during pregnancy
was associated with a 90% increased
odds of abruption (OR, 1.9; 95% CI,
1.8e2.0), and up to a quarter of all
abruptions were attributable to smok-
ing.42 Moreover, the risk of abruption is
increased among pregnant people who
consume illicit drugs, particularly
cocaine and marijuana.43,44
In addition, people who suffer from
mental stress or depression, especially in
the latter half of pregnancy, have an
increased risk of abruption.45,46 How-
ever, the process through which
maternal mental stress and affective
disorders are associated with the risk of
abruption is not well understood. It is
believed that altered plasma cortisol, b-
endorphin corticotrophin-releasing
hormone, and serotonin concentrations
are higher in pregnant people with mood
and/or anxiety disorders. This
abnormally elevated hormone profile, in
turn, increases the inflammation at the
maternal-fetal interface, leading to a
higher abruption risk.45
Risk factor assessments for term vs
preterm abruption reveal substantial
overlap.9 In a large retrospective cohort
study of more than 30 million births in
the United States from 1995 to 2002 that
sought to distinguish causal pathways of
abruption at term vs preterm gestations,
the authors found that chronic clinical
processes associated with oxidative
stress, vascular reactivity, and platelet
activation, such as FGR and preeclamp-
sia, were associated with increased risk of
abruption across all gestations and that
acute inflammatory conditions (eg,
chorioamnionitis and PROM) were
more important drivers of risk in pre-
term gestations.9 Moreover, this over-
lapping profile was seen by Sheiner
et al47,48 who found that pregnancy-
induced hypertension and nonvertex
presentations were associated with
abruption across all gestations and that
previous second-trimester bleeding was
strongly associated with term abruption
and polyhydramnios was strongly asso-
ciated with preterm abruption.
Clinical and nonclinical risk factors
and their strength of associations with
abruption are summarized in Table 1.
Although many factors are associated

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with abruption, the factors that have the

TABLE 1 greatest risk include previous abruption,
Risk factors and strength of associations with placental abruption chronic hypertension, preeclampsia,
Range of relative cocaine and drug use, and intimate
Variable risk or odds ratio Strength of association partner violence.
Medical or obstetrical risk factors
Chronic hypertension 1.8e5.1 þþþ Clinical presentation
Acute vs chronic abruption
Pregestational diabetes mellitus 2.5e3.0 þþ
Acute abruption is characterized by the
Gestational diabetes mellitus 0.7e0.8 þ/ sudden onset of vaginal bleeding, and
Gestational hypertension 1.5e2.5 þþ chronic abruption is characterized by
Preeclampsia 2.0e4.5 þþþ recurrent episodes of light to moderate
vaginal bleeding. The clinical manifes-
Eclampsia 3.0e5.5 þþþ
tations of abruption are influenced by
Polyhydramnios 2.0e3.0 þþ the caliber and location of maternal
Oligohydramnios 2.0e2.5 þþ decidual vessels and the chronicity of
Premature rupture of membranes 1.8e5.1 þþ bleeding. Bleeding from centrally
located, larger arteries may lead to acute
Chorioamnionitis 2.0e2.5 þþ
manifestations, including hemorrhage
Multiple pregnancy 2.0e2.5 þþ and fetal distress (and potentially
Genetic risk factors demise), necessitating urgent clinical
Thrombophilia 1.5e7.0 þþþ interventions to minimize associated
morbidity. Bleeding from peripherally
MTHFR gene mutation 1.1e1.2 þ/
located, smaller veins may not require
Hyperhomocysteinemia 1.5e4.0 þþ urgent clinical evaluation and manage-
Obstetrical history ment, even though these abruptions
Previous preeclampsia 1.5e2.0 þþ warrant additional fetal surveillance and
appropriately timed delivery to prevent
Previous FGR or SGA 1.4e2.0 þþ
fetal death.49
Previous abruption 6.0e12.0 þþþþ
Behavioral risk factors Diagnosis
Cocaine and drug use 4.0e8.0 þþþ Classic symptoms of abruption include
vaginal bleeding and abdominal pain.
Tobacco smoking during pregnancy 1.7e2.0 þþ
Uterine contractions are often present,
Alcohol use 1.5e2.5 þþ but contractions are not a specific
Infertility 1.5e2.0 þþ abruption characteristic as painful uter-
Iron deficiency anemia 2.2 þþ ine contractions are also present in
normal labor. Although there is potential
Folic acid supplementation 0.8 þþ
for bleeding from fetal sources, associ-
Multivitamin supplementation 0.7e0.8 þþ ated vaginal bleeding is typically of
Vitamin C or E supplementation 0.6e0.7 þþ maternal origin. Abruption is ultimately
Depression or anxiety 1.2e5.0 þþ a clinical diagnosis that requires the
exclusion of other causes of vaginal
Anger or outbursts 2.8 þþ
bleeding, such as placenta previa and
Intimate partner violence 5.0e6.0 þþþ cervical dilation with labor, often termed
Sociodemographic factors “bloody show.”
Advanced maternal age (
35 y) 1.5e2.5 þ Ultrasound may identify findings
concerning for abruption, especially
Parity
3 1.1e1.6 þ
when abnormal blood collections adja-
Single marital status 1.2e1.4 þ cent to and within the placenta are large
African American (Black) race and ethnicity 1.5 þ (Figures 3e5).50 Because of limitations
As the associations of risk factors near-term and term abruptions are unavailable, we presented the associations for all of third-trimester ultrasound and the
abruptions, regardless of gestational age at diagnosis or delivery. similar echotexture of hemorrhagic
FGR, fetal growth restriction; MTHFR, methylenetetrahydrofolate reductase; SGA, small for gestational age. products and placenta, sonographic
Brandt. Placental abruption at near term and term gestations. Am J Obstet Gynecol 2023. findings of abruption may not be
evident. In a study of ultrasound

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FIGURE 3
Intra-amniotic hematoma
after motor vehicle accident
at 36 weeks of gestation
A pregnant patient was a restrained passenger
in a motor vehicle accident at 35 weeks of
gestation. An ultrasound performed at 36 weeks
of gestation revealed an intra-amniotic hema-
toma with layering. The patient had an uncom-
plicated induction of labor at 37 weeks of
gestation with favorable maternal and neonatal
outcomes. Image courtesy of Susan Egan,
RDMS
Brandt. Placental abruption at near term and term gesta-
tions. Am J Obstet Gynecol 2023.
characteristics among 30 patients with
abruption, ultrasound had a sensitivity
of 57.0% (CI, 37.2e75.6), specificity of
100% (CI, 15.8e100.0), positive pre-
dictive value of 100% (CI, 79.4e100.0),
and negative predictive value of 14.0%
(CI, 1.8e42.8).51 Another prospective
study of 73 pregnant people who pre-
sented with vaginal bleeding reported a
higher sensitivity to detect abruption of
80%.14 Classic ultrasound findings were
described by Yeo et al14 and include the
following: (1) preplacental collection,
(2) “jello-like” movement of the chori-
onic plate with fetal activity, (3) retro-
placental collection, (4) marginal
collection, (5) subchorionic collection,
(6) placentomegaly or intraplacental
echogenicity, and (7) intra-amniotic
hematoma.
Concealed abruption may manifest in
pregnant people with symptoms of
abdominal pain and uterine contractions,
but without overt vaginal bleeding or with
small quantities of bleeding. Concealed
abruption can be severe and lead to fetal
death and coagulopathy.52 Clinicians
FIGURE 4
Evolution of a large subchorionic
hematoma from 32 to 35 weeks
of gestation
A pregnant patient with vaginal spotting was
observed to have a large subchorionic hema-
toma at 32 weeks of gestation (A). In this
context, she was diagnosed with a placental
abruption. After a period of inpatient surveil-
lance, she was discharged home with outpatient
fetal surveillance, including twice-weekly fetal
assessments of well-being and serial growth
ultrasounds. At 35 weeks of gestation, she had
repeat evaluation of the subchorionic hematoma
(B). The hematoma seemed slightly smaller, but
its appearance was similar to adjacent placental
tissue. Images courtesy of Susan Egan, RDMS
Brandt. Placental abruption at near term and term gesta-
tions. Am J Obstet Gynecol 2023.
should have a high index of suspicion in
cases of spontaneous tachysystole, even if
there are normal ultrasound findings,
especially with rapid labor progress.
Approximately 10% of spontaneous pre-
term labor has been attributed to con-
cealed abruption,53 but the impact of
concealed abruption on labor at near-
term and term gestations is less clear.
In some cases of abruption, there is
extravasation of blood into the myo-
metrium, known as uteroplacental
apoplexy or Couvelaire uterus
MAY 2023 American Journal of Obstetrics & Gynecology
Expert Review
FIGURE 5
Placentomegaly associated with
catastrophic acute abruption
A pregnant patient had an ultrasound at 33 4/7
weeks of gestation that was notable for pla-
centomegaly. The placenta was bulky and
contained intraplacental heterogenicities. As a
patient with gestational diabetes mellitus (class
A2), the patient was compliant with twice-
weekly fetal surveillance with alternating bio-
physical profiles and nonstress tests. In the 36th
week of gestation, she experienced heavy
vaginal bleeding at home. She was transported
by emergency medical services to a local hos-
pital in hemorrhagic shock with disseminated
intravascular coagulopathy and fetal death
Brandt. Placental abruption at near term and term gesta-
tions. Am J Obstet Gynecol 2023.
(Figure 6). This condition is typically
not evident sonographically54 but may
be ascertained through direct external
inspection of the uterus at cesarean de-
livery or hysterectomy. Uteroplacental
apoplexy is not an absolute indication
for hysterectomy.
Clinical management of abruption
Acute near-term and term abruptions,
whether mild or severe, are typically
managed by maternal stabilization fol-
lowed by delivery. Delivery is recom-
mended to minimize the risks of
ongoing vaginal bleeding and the poten-
tial for fetal compromise and maternal
injury. An algorithm for the management
of abruption is described in Figure 7.
There is a lack of evidence to guide
delivery timing for chronic abruption.55
Furthermore, there is a lack of data to
guide management strategies, such as
inpatient vs outpatient care for these
complicated pregnancies. After diag-
nosis and a period of observation in
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Expert Review
FIGURE 6
Couvelaire uterus
Image used with permission from Shashank
Parulekar, editor of the “Journal of Postgraduate
Gynecology & Obstetrics”
Brandt. Placental abruption at near term and term gesta-
tions. Am J Obstet Gynecol 2023.
inpatient settings, outpatient manage-
ment may be reasonable for preterm
patients with chronic abruption who can
comply with additional fetal surveil-
lance, including serial fetal growth as-
sessments and antenatal testing. Once or
twice-weekly fetal surveillance, such as
fetal nonstress testing and biophysical
profiles, should be initiated at the time of
diagnosis.56 Multivessel Doppler veloc-
imetry should be employed when there is
concurrent FGR57 or when fetal anemia
is suspected.58 Patients with chronic
abruption also require close monitoring
for recurrent episodes of vaginal
bleeding. In our opinion, it is reasonable
to deliver pregnant patients with chronic
abruption during the 36th and 37th
weeks of gestation. However, the deci-
sion should be individualized in situa-
tions where there are complicating
factors, such as FGR, oligohydramnios,
and ongoing vaginal bleeding. The
development of any FHR abnormalities
in chronic cases should be an indication
for delivery in all near-term or term
gestations.
At initial evaluation of new-onset
vaginal bleeding in near-term and term
gestations, abruption severity should be
ascertained through thorough history,
evaluating the inciting event (if any) and
quantifying estimated blood loss. The
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FIGURE 7
Algorithm to guide the management of obstetrical hemorrhage
associated with placental abruption with acute hemorrhage
The algorithm for the management of placental abruption with acute hemorrhage employs the
Advanced Trauma Life Support classification of hypovolemic shock, which has not been validated in
pregnancy and does not consider various factors that may impact physiological compensatory
changes. The staging system is presented here as a theoretical framework to guide the clinical
approach to resuscitation in the context of obstetrical hemorrhage because of placental abruption.
Laboratory tests include complete blood count and coagulation studies (including prothrombin time,
activated partial thromboplastin time, and fibrinogen) and/or point-of-care tests (including arterial
blood gas assessment, thromboelastography, and rotational thromboelastometry)
FFP, fresh frozen plasma; IUFD, intrauterine fetal death; IV, intravenous; MFM, maternal-fetal medicine; MTP, massive transfusion
protocol; NICU, neonatal intensive care unit; PRBC, packed red blood cells; T&S, type and screen
Brandt. Placental abruption at near term and term gestations. Am J Obstet Gynecol 2023.
amount of vaginal bleeding, which may hypertension and preeclampsia among
be difficult to quantify because of con- pregnant people with abruption at near-
cealed bleeding, does not correlate with term and term gestations, the ATLS
clinical sequelae.50 Therefore, clinical classification may underestimate the
evaluation should also incorporate the amount of intravenous (IV) fluid and
assessment of vital signs, urine output, blood products that are required for
and mental status. The Advanced resuscitation in some cases. Despite
Trauma Life Support (ATLS) classifica- these potential limitations, the ATLS
tion of stages of hemorrhagic shock in- classification is presented as a theoretical
corporates these parameters to create a framework to guide the clinical
profile of clinical findings associated approach to resuscitation (Table 2).
with various degrees of hemorrhage.59 The initial management focuses on
The staging system has not been vali- maternal stabilization, including place-
dated in pregnancy and does not ment of large-bore IV catheters (eg, 16
consider factors that may impact physi- or 18 gauge) and fluid resuscitation with
ological compensatory changes. For crystalloids.60 Stat laboratory tests to
example, given the high prevalence of evaluate hemoglobin and platelet count
ajog.org Expert Review

as well as coagulation parameters

(including prothrombin time [PT] and TABLE 2
fibrinogen), and a blood type and anti- The Advanced Trauma Life Support classification of hypovolemic shock
body screen for red blood cell cross Variable Class 1 Class 2 Class 3 Class 4
matching, should be obtained. Estimated blood loss (%) <15 15e30 30e40 >40
Kleihauer-Betke testing is indicated in
Heart rate (bpm) <100 100e120 120e140 >140
patients with vaginal bleeding who are
Rh(D) negative to guide the appropriate Blood pressure Normal Normal Decreased Greatly
decreased
administration of Rh(D) immune glob-
ulin, and it does not provide insight into Pulse pressure Normal or Decreased Decreased Decreased
abruption severity. Blood products and increased
coagulation factors may be needed with Respiratory rate (breaths per 14e20 20e30 30e40 >35
uncrossed type O-negative blood minute)
immediately available and activation of Mental status Slightly anxious Mildly Anxious, Confused,
massive transfusion protocols when anxious confused lethargic
clinically indicated.61 Urine output (mL per hour) >30 20e30 5e15 Minimal
Fetal status should be assessed after Caveat: The ATLS classification of hypovolemic shock has not been validated in pregnancy and does not consider various factors
initiating maternal stabilization efforts. that may impact physiological compensatory changes, such as maternal age, medical comorbidities, and medications (eg, beta-
blockers). The staging system is presented here as a theoretical framework to guide the clinical approach to resuscitation in the
A wide array of abnormal FHR patterns context of obstetrical hemorrhage because of placental abruption. Adapted from the American College of Surgeons.59
is possible,62e65 reflecting the underly- ALTS, Advanced Trauma Life Support.
ing pathophysiology of this condition Brandt. Placental abruption at near term and term gestations. Am J Obstet Gynecol 2023.
(Table 3). In acute and severe abrup-
tions, there is often marked fetal brady-
cardia with absent variability, which is a were abnormal.72 Moreover, the severity Intrauterine resuscitative measures,
preterminal FHR pattern. This fetal of FHR changes corresponds with the such as maternal position changes and
bradycardia can occur suddenly or can severity of abruption. In an analysis of 40 supplemental oxygen, may be of limited
be heralded by variable, late, or pro- pregnant people in Japan with abrup- benefit. Antenatal corticosteroids to
longed decelerations (Figure 8). Fetal tion, absent variability and bradycardia promote fetal maturation may be
tachycardia and minimal or absent were associated with 5-minute Apgar considered before 36 6/7 weeks of
variability may or may not be present. In scores of <7, arterial umbilical cord gestation (when delivery is anticipated in
cases of decreased fetoplacental blood blood pH of <7.1, and larger abrup- 7 days and before 37 weeks of gestation),
flow and hypoxia, sinusoidal FHR pat- tion.64 Several studies have suggested but delivery should not be deferred to
terns can be seen before the terminal that acute abruption is an important administer steroids in the late preterm
bradycardia (Figure 9).66e68 Abnormal- contributor to category III FHR patterns period (34 0/7 to 36 6/7 weeks of gesta-
ities in the uterine contraction pattern, because of terminal bradycardia and si- tion).73 Tocolytics should not be used
such as tetanic or high-frequency, low- nusoidal FHR patterns.62,64e68 during this gestational age range.
amplitude contractions, may be
present.69e71 In chronic abruption, there
may be normal FHR patterns and toco- TABLE 3
dynamometry allowing conservative Fetal heart rate patterns associated with acute and chronic placental
management initially. However, when abruption
the fetus is becoming compromised, Abruption
variable or late decelerations with or type FHR patterns Tocodynamometry
without fetal tachycardia and minimal or Acute  Variable, late, or prolonged decelerations  Increased resting tone
absent variability are frequently present.  Fetal tachycardia with minimal and/or absent  Tetanic or high-frequency,
Most abruptions will have FHR variability low-amplitude
 In cases of profound hypoxia and/or anemia, contractions
changes, although it is not clear if sinusoidal pattern before terminal bradycardia
abruption at near-term and term gesta-  Terminal bradycardia
tions have different profiles of abnormal
Chronic  Normal patterns  Normal patterns
FHR patterns compared with abruption  When a fetus is becoming compromised, vari-
at preterm gestations. In a retrospective able or late decelerations with or without fetal
cohort study of 355 patients who had tachycardia and minimal and/or absent
clinical abruption in 2009 and delivered variability
in a consortium of 94 centers in Japan, FHR, fetal heart rate.
and after excluding 89 fetal deaths on Brandt. Placental abruption at near term and term gestations. Am J Obstet Gynecol 2023.
presentation, 166 FHR tracings (62.4%)

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Expert Review ajog.org

FIGURE 8
Electronic fetal monitoring of acute abruption with recurrent variable decelerations and minimal variability

A para 2 pregnant patient presented with crampy abdominal pain for 1 day at 37 weeks of gestation. On examination, her abdomen was tender and firm,
described by the evaluating physician as “rock hard.” She denied vaginal bleeding. Electronic FHR monitoring revealed recurrent variable decelerations
and minimal variability. The patient underwent urgent cesarean delivery under general anesthesia for presumed concealed abruption with category 2 FHR
pattern. The amniotic fluid was noted to be meconium stained and blood tinged. The umbilical artery gas revealed a pH of 7.02, PCO2 of 79.0 mm Hg,
and standard base excess of 11.9 mmol/L, indicating mixed metabolic and respiratory acidosis
FHR, fetal heart rate
Brandt. Placental abruption at near term and term gestations. Am J Obstet Gynecol 2023.

Magnesium sulfate is not used during
this range for neuroprotection, although
it should be used for seizure prophylaxis
in cases of preeclampsia with severe
features.
After delivery, there may be evidence
of an adherent clot on the fetal surface
of the placenta (Figure 10).74 If an
intraplacental hematoma forms and
self-limits the amount of bleeding, the
abruption may be detected at delivery
with the observation of an organized
hematoma in an area of the infarcted
placenta. The histologic finding that
seems to be most strongly associated
with acute abruption is hemorrhage in
the decidua basalis with underlying
parenchymal indentation (Figure 11).75
In the absence of this indentation (eg, if
the abruption is acute and blood passes
vaginally or into the amniotic fluid)
and in chronic abruption, other
nonspecific histologic features may be
present on postpartum pathologic
evaluation of the placenta, including
intravillous and intervillous hemor-
rhage, early trophoblastic necrosis, and
decidual inflammation.74 A retrospec-
tive study of 305 cases of abruption that
characterized placental histopathology
found that abruption at
34 weeks of
gestation was characterized by fewer
placental maternal vascular malperfu-
sion lesions, maternal inflammatory
response lesions, and placental hemor-
rhages than abruption at <34 weeks of
gestation.76
Clinical Challenges Associated With
Abruption
Obstetrical hemorrhage
Abruption with heavy vaginal bleeding at
near-term and term gestations requires
prompt evaluation and management.
Several principles guide this care, such as
identifying the cause of bleeding, expe-
diting delivery to control bleeding,
providing supportive care, and

FIGURE 9
Example of a sinusoidal fetal heart rate pattern associated with marked fetal hypoxia because of decreased
fetoplacental blood flow

A para 1 pregnant patient was admitted to the intensive care unit with hypoxic respiratory failure, sepsis, and hypotension refractory to multiple va-
sopressors at 28 weeks of gestation. The patient was severely acidotic despite resuscitation with bicarbonate. Fetal monitoring revealed a sinusoidal
pattern (sometimes referred to as a pseudosinusoidal pattern in this context), a preterminal pattern associated with decreased fetoplacental blood flow
and severe hypoxia. The patient underwent urgent cesarean delivery, but the fetus was profoundly acidotic and died in the operating room
Brandt. Placental abruption at near term and term gestations. Am J Obstet Gynecol 2023.

S1320 American Journal of Obstetrics & Gynecology MAY 2023

ajog.org
recognizing DIC early. The administra-
tion of packed red blood cells (PRBC)
and coagulation factors, termed “blood
component therapy,” is an essential part
of this supportive care.77,78 Transfusion
of
4 units is a marker of severe obstet-
rical morbidity.79 The risk of massive
transfusion, defined as
10 units of
PRBC, is uncommon. In a large retro-
spective cohort study that included all
delivery hospitalizations for hospitals
that reported at least 1 delivery-related
transfusion per year in New York
(1998e2007), massive transfusion
occurred in 6 per 10,000 deliveries, and
abruption was a strong independent risk
factor (occurring in 1 per 10,000 de-
liveries: adjusted OR, 14.6; 95% CI,
11.2e19.0).80
Blood component therapy
The main purpose of PRBC transfusion
is to improve oxygen-carrying capacity.
If effective fluid resuscitation ensures
adequate intravascular volume, oxygen
extraction at the tissue level can
compensate for the reduction in arterial
oxygen content until anemia becomes
very severe.81,82 In stable pregnant pa-
tients with self-limited episodes of acute
vaginal bleeding (and postpartum pa-
tients), restrictive approaches to blood
transfusion may be considered. Clinical
trials suggest that a hemoglobin level of
<6 to 7 g/dL is an appropriate trans-
fusion threshold for many patients,83
but consideration of potential addi-
tional bleeding during labor and at
delivery is necessary. Transfusion in the
context of active and heavy bleeding
should not be based on specific hemo-
globin thresholds and rather should be
guided by vital signs, the amount of
current and anticipated bleeding, and
the projected length of time until de-
livery (eg, when bleeding potential is
the highest, but when active bleeding
may conclude).
Fresh frozen plasma (FFP) contains all
coagulation factors and fibrinogen. Its
use is indicated when a pregnant patient
with abruption is thought to have mul-
tiple acquired coagulation factor de-
ficiencies, such as in cases of obstetrical
hemorrhage treated with massive trans-
fusion and in cases of DIC. Although
FIGURE 10
Placenta with large adherent
retroplacental hematoma
Image courtesy of Catherine W. Chan, MD
FHR, fetal heart rate
Brandt. Placental abruption at near term and term gesta-
tions. Am J Obstet Gynecol 2023.
FFP can provide some volume expan-
sion, it should not be used for this pur-
pose. Ideally, IV fluids, such as
crystalloids and albumin and other
plasma derivatives, may restore circu-
lating blood volume without exposing
patients to the potential risks associated
with FFP. Cryoprecipitate is a plasma-
derived product that contains fibrin-
ogen and other coagulation factors,
including factor VIII, factor XIII, and
von Willebrand factor. Although its use
is declining in favor of specific coagula-
tion factor concentrates that have more
favorable risk profiles, cryoprecipitate
remains a mainstay for the treatment of
acquired hypofibrinogenemia. Cry-
oprecipitate should be administered to
ensure that the patient with abruption
has fibrinogen levels of >50 to 100 mg/
dL. In the context of active bleeding,
platelets should be transfused to a goal of
greater than 50103 per mL. Often,
platelets are transfused in the setting of
massive transfusion, accompanying
PRBC and FFP transfusions. Table 4
describes the characteristics of blood
MAY 2023 American Journal of Obstetrics & Gynecology
Expert Review
FIGURE 11
Histology of acute placental
abruption
Retroplacental hemorrhage extending into the
decidua and indenting the placental paren-
chyma, consistent with placental abruption.
Retroplacental hemorrhage is shown at the
bottom of the image, indenting the decidua and
placental parenchyma (marked by X). Chorionic
villi are above the indenting hemorrhage.
Magnification is 2. Image courtesy of Debra
Heller, MD
Brandt. Placental abruption at near term and term gesta-
tions. Am J Obstet Gynecol 2023.
components, including PRBC, FFP, cry-
oprecipitate, and platelets.
Point-of-care viscoelastic testing
Coagulation studies have limitations to
guide decision-making related to blood
transfusion in the context of abruption
with massive hemorrhage.84 These tests
were developed to monitor the degree of
coagulation conferred by exogenous an-
ticoagulants, not to ascertain the
bleeding risk of obstetrical patients.
These limitations and potential for
delayed results have driven interest in
point-of-care testing that can charac-
terize viscoelastic hemostatic proper—
ties, such as thromboelastography (TEG)
and rotational thromboelastometry
(ROTEM).85e88 These tests evaluate the
viscoelastic properties of clot, such as
time to initiate clot, time to amplify clot,
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TABLE 4
Blood component therapy to guide management of obstetrical hemorrhage because of placental abruption
ABO cross-
Time to matching
Component Volume Contents prepare Risksa Effectb required? Indications
Packed red 250e300 mL RBCs, 30 min Infection, 1 unit increases Yes, but can use O-  Hemoglobin of <6 to 7 g/
blood cells per unit; WBCs, (stored transfusion hemoglobin by 1 negative uncrossed dL (unless medical
hematocrit is plasma frozen) reactions, g/dL PRBCs in comorbidities warrant
typically 55% volume emergencies higher threshold)
overload,  Hemoglobin of <9 g/dL in
hyperkalemia active bleeding
Fresh frozen 200e250 mL All 30 min Infection, 1 unit increases Yes, but Rh(D)  Hemorrhage and/or
plasma per unit; INR of coagulation (stored transfusion factor status does not active bleeding in pa-
FFP is 1.1 factors, frozen) reactions, concentrations need to be tients with (or at risk of)
including volume overload by 30% and considered and can multiple acquired coagu-
fibrinogen increases use type AB FFP in lation factor deficiencies
fibrinogen by 10 emergencies (eg, INR of >2.0, aPTT of
e15 mg/dL >1.5 normal, or
abnormal clotting factor
activity by TEG or ROTEM)
 FFP should not be used
for volume expansion
Cryoprecipitate 10e20 mL per Fibrinogen, 30 min Infection, 1 unit increases No  Hemorrhage and/or
unit; typically factor VIII, (stored transfusion fibrinogen by 10 active bleeding in pa-
administered in factor XIII, frozen) reactions e15 mg/dL; 5- tients with acquired
5 or 10 unit pools and von unit pool hypofibrinogenemia,
Willebrand increases defined as fibrinogen of
factor fibrinogen by 50 <50 to 100 mg/dL
mg/dL
Platelets 250e300 mL Platelets, Rapidly Risks may be Increases ABO compatible  Platelets <50103/mL
per unit of plasma, available higher for whole platelets by platelets are with active bleeding and/
apheresis- small (stored at bloodederived 30103/mL to preferred, but ABO or massive transfusion
derived numbers of room platelets; 50103/mL incompatible
plateletsc or per RBCs and temperature) infection, platelets can be
5e6 units of WBCs transfusion used with minimal
pooled platelets reactions risk
Note: Prethawed PRBC and FFP may be immediately available in many high-volume centers and most level I trauma centers.
aPTT, activated partial thromboplastin time; FFP, fresh frozen plasma; INR, international normalized ratio; PRBC, packed red blood cells; RBC, red blood cell; ROTEM, rotational thromboelastometry;
TEG, thromboelastography; WBC, white blood cell.
a
Risks are greatest in those receiving massive transfusions; strategies to reduce risks include use of leukoreduced products, volume-reduced products, saline-washed products, and pathogen-
inactivated products; b Assumes no bleeding; c Apheresis: process whereby 1 or more blood components are collected, and other components are returned to the donor.
Brandt. Placental abruption at near term and term gestations. Am J Obstet Gynecol 2023.

clot strength, and the degree of fibrino-
lysis, among other properties (Table 5,
Figure 12, A). The main advantages are
rapid results and goal-directed therapy.
TEG and ROTEM results are typically
available in 15 to 20 minutes, which is
much faster than coagulation studies.88
In addition, these point-of-care tests
may direct resuscitative efforts to avoid
overtreatment.89e91 Several simplified
examples of TEG TEMograms are illus-
trated in Figure 12. In Figure 12, B, the
normal TEMogram suggests an adequate
hemostatic profile; uterotonic medica-
tions, intrauterine tamponade balloon,
and other surgical approaches may be
helpful to control bleeding. In Figure 12,
C, the TEMogram reflects prolonged
reaction (R) and kinetics (K) times,
suggesting that acquired coagulation
deficiencies are present and should be
addressed with FFP. In Figure 2, D, the
TEMogram has a slightly prolonged R
time, but the K time is prolonged, the
alpha angle is decreased, and the
maximum amplitude (MA) is decreased.
The viscoelastic properties suggest that
hypofibrinogenemia is responsible for
bleeding and cryoprecipitate is indicated.
Lastly, in the TEMogram in Figure 12, E,
the K time is prolonged and the MA is
decreased, suggesting that thrombocy-
topenia is the underlying etiology and
platelet transfusion is indicated.
An example of an obstetrical hemor-
rhage protocol that employs TEG to
guide blood component therapy is
illustrated in Figure 13. An alternative
protocol that employs ROTEM and was
used in a cohort of 521 participants who
had a moderate and severe postpartum
hemorrhage and evaluated the test
characteristics of ROTEM compared
with routine coagulation studies was
recently published.92 Cases of abruption

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TABLE 5
Thromboelastography and the viscoelastic properties of clot formation
Main Approximate
ROTEM Main corrective normal
TEG variable equivalent Derivation determinants Interpretation components values
Reaction time (R Clotting Time for clot initiation from start of Activity of Prolongation may indicate FFP 4e8 min
time) time test to the first detectable fibrin coagulation deficiency of procoagulants or
strands (amplitude of 2 mm) (min) factors presence of anticoagulants
Kinetics time (K CFT Time from clot initiation to reach Activity of Possible early indicator of clot FFP 1e4 min
time) clot width of 20 mm amplitude, coagulation deficiency or hypercoagulability
reflects amplification (min) factors
a angle CFT Thrombin burst or propagation Presence and Prolongation may suggest Cryoprecipitate 47e74
(speed at which the fibrin builds up interactions of platelet dysfunction or
and cross-linking takes place); fibrinogen deficiency, fibrinogen
slope of the line between R and K, deficiency, or both; shortening
formed by the slope of the TEG may indicate hypercoagulability
tracing from the horizontal line
(degrees)
MA Maximum Strength of the clot (stability) as Platelets Reduced MA may represent Platelets 55e73 mm
clot measured by maximum curve width (80%) and reduce platelet number and
firmness (mm) fibrin (20%) function and impaired fibrin
cross-linking
Clot lysis time at LY30, Amount of clot lysis at 30 and 60 Activity of Indicates possible need for Tranexamic 0%e8% at
30 and 60 min LY60 min after MA is achieved; fibrinolytic antifibrinolytic agents acid CL30
(CL30 and CL60) percentage decrease in amplitude factors
after maximum
clot strength
Adapted from Pavord et al123; Nelson et al.124
CFT, clot formation time; FFP, fresh frozen plasma; MA, maximum amplitude; ROTEM, rotational thromboelastometry; TEG, thromboelastography,
Brandt. Placental abruption at near term and term gestations. Am J Obstet Gynecol 2023.

with FHR changes, where urgent cesar-
ean delivery may be indicated and there
is insufficient time to wait for routine
coagulation studies, call for further
studies to ascertain whether the adop-
tion of these point-of-care tests and
incorporation into clinical management
algorithms improves outcomes.
Coagulopathy
Abruption is the most common cause
of DIC in pregnancy.93,94 Compared
with other causes of obstetrical hemor-
rhage, pregnant people with abruption
experience greater decreases in
platelets, require more platelet trans-
fusions, and have more acquired
hypofibrinogenemia.95e97 In severe
abruption, the infusion of collagen and
tissue components into maternal circu-
lation leads to the release of tissue factor
through the extrinsic clotting pathway.
Tissue factor complexes with factor VII
and activates factors IX and X.98 Sys-
temic activation of coagulation ensues,
leading to the widespread formation of
microvascular thrombi in small vessels
and endothelial injury with concomitant
fibrinolysis, a process that consumes
platelets and clotting factors.98 The
process is associated with increased
production of fibrin split products and
D-dimer and reduction in natural
anticoagulants.98
DIC may be suspected on the basis of
clinical presentation and laboratory
findings, but no single laboratory test is
sufficient to make the diagnosis.99 The
classic laboratory findings of DIC are low
platelets, prolonged PT and activated
partial thromboplastin time (PTT), and
low fibrinogen levels. There may be a
mild reduction in platelet counts or
thrombocytopenia, defined as a platelet
count of <150103 per mL.99 Clinical
DIC may have normal or mildly reduced
fibrinogen levels as it is an acute phase
reactant, which limits its sensitivity as a
test for DIC severity.99 However, early
hypofibrinogenemia is highly predictive
of severe postpartum hemorrhage.100
Prolongation of the PT and PTT may
be a relatively late finding; these tests
become prolonged when there is deple-
tion of more than 50% of clotting fac-
tors, and clinical bleeding may occur
when depletion is >50% to 75%.99
Scoring systems, such as the Interna-
tional Society of Thrombosis and He-
mostasis DIC score,101 were modified for
pregnancy93 (Table 6). Although not
widely used, a score of
26 has a sensi-
tivity of 88% and a specificity of 96% for
the diagnosis of DIC.
Observational studies have suggested
that the administration of fibrinogen
concentrate may result in reduced
blood loss in hemorrhage-associated
hypofibrinogenemia associated with

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FIGURE 12 FIGURE 13
Examples of Example of obstetrical hemorrhage protocol that employs
thromboelastography TEMogram thromboelastography
that may be encountered in
obstetrical hemorrhage

A, Normal TEMogram that illustrates the various

viscoelastic properties of clot formation. B,
Normal hemostasis: the R time, K time, a angle,
and MA are normal. C, Clotting factor deficiency:
the R and K time are prolonged, and the a angle
and MA are decreased. D, Hypofibrinogenemia:
the R time is normal or prolonged, and the K time
is prolonged, the a angle is decreased, and the
MA is decreased. E, Thrombocytopenia: the R
time is normal, but the K time is prolonged and
the MA is decreased
K time, kinetics time; MA, maximum amplitude; R time, reaction Protocol courtesy of Sue Pavord, MBChB, FRCP, FRCPath
time
Brandt. Placental abruption at near term and term gestations. Am J Obstet Gynecol 2023.
Brandt. Placental abruption at near term and term gesta-
tions. Am J Obstet Gynecol 2023.

abruption.102,103 In cases of active
bleeding, the use of fibrinogen con-
centrates as an adjunctive treatment of
obstetrical hemorrhage may reduce the
need for massive transfusion.104,105
However, a randomized, placebo-
controlled trial explored the preemp-
tive use of fibrinogen concentrates in
bleeding pregnant patients with hypo-
fibrinogenemia.106 The study, which
included 249 subjects, found that
preemptive use did not reduce the risk
of blood transfusion. Moreover, similar
results were observed in a recent
double-blind, randomized placebo-
controlled trial, which included 437
patients.107

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TABLE 6
The International Society on Thrombosis and Haemostasis scoring system, including modified pregnancy score
Modified ISTH DIC score of ‡26: DIC present ISTH DIC score of ‡5: DIC present
Variable Third-trimester values Assigned weight Assigned weight
Platelets 146103/mL to 429103/mL <50103/mL 1 <50103/mL 3
3 3 3 3
5010 /mL to 10010 /mL 2 5010 /mL to 10010 /mL 2
3
10010 /mL to 18510 /mL 1 3
>100103/mL 0
>18510 /mL 3
0
PT 9.5e13.4 s PT difference of <0.5 s 0 PT difference of >3 s 0
PT difference of 0.5e1.0 s 5 PT difference of 3e6 s 1
PT difference of 1.0e1.5 s 12 PT difference of >6 s 2
PT difference of >1.5 s 25
Fibrinogen 373e619 mg/dL <300 mg/dL 25 <100 mg/dL 1
300e400 mg/dL 6 >100 mg/dL 0
400e450 mg/dL 1
>450 mg/dL 0
D-dimer 483e2256 ng/mL <400 ng/mL 0
400e4000 ng/mL 2
>4000 ng/mL 3
PT difference: the difference between the prothrombin time result of the patient and the normal control value. Adapted form Abbassi-Ghanavati et al125; Siennicka et al126; Erez et al93; and Taylor
et al.101
DIC, disseminated intravascular coagulation; ISTH, International Society on Thrombosis and Haemostasis; PT, prothrombin time.
Brandt. Placental abruption at near term and term gestations. Am J Obstet Gynecol 2023.

Fetal death
Approximately 5% to 10% of fetal deaths
have been attributed to abruption.108
Although some of these cases may not
manifest with heavy vaginal bleeding,
abruption associated with fetal death
should be categorized as severe abrup-
tions that may also be associated with an
increased risk of maternal morbidity.
Vaginal delivery is the preferred mode
of delivery as it avoids the risks of opera-
tive bleeding that may be exacerbated by
coagulopathy and the potential sequelae
associated with multiple repeat cesarean
deliveries. In a single-center retrospective
cohort study of fetal deaths associated
with abruption (1995e2015), vaginal
delivery was successful in 14 of 15 cases
(93.3%) that underwent trial of labor.
Patients with Bishop scores of >3 had
shorter labors (3:37 hours vs 7:58 hours)
and larger blood loss (3605 mL vs 1788
mL) compared with patients with Bishop
scores of 3,109 which reflects the
observation that pregnancies complicated
by severe abruption may have rapid
labors.
The management of patients with fetal
death and previous uterine surgery and
risk factors for uterine rupture, such as
multiple cesarean deliveries, previous
classical hysterotomy, and previous
uterine rupture, should be individual-
ized.110 Induction of labor in patients
with 1 previous cesarean delivery via low
transverse hysterotomy may be consid-
ered. For some patients who are at
increased risk of uterine rupture, an in-
duction and trial of labor may be a
reasonable approach, although early
recognition of uterine rupture is imper-
ative. Some patients may require lapa-
rotomy if there is clinical concern for
uterine rupture. A repeat cesarean de-
livery may be performed for patients who
have risk factors for uterine rupture and
in whom the associated risks of trial of
labor are perceived to be prohibitive.110
Adverse Outcomes Among Pregnant
People
Short-term risks
Short-term risks of abruption are often
driven by hemorrhage. Pregnant people
who experience abruption have
increased risks of hemorrhagic shock,
DIC, need for blood transfusion, and
hysterectomy. Risks in the postpartum
period include intensive care unit
admission and maternal death.4
Long-term effects
Recent evidence has suggested that
pregnant people who experience clinical
abruption are at increased risk of mor-
tality from cardiovascular disease (CVD)
and cerebrovascular disease and nonfatal
morbidity, pointing to long-term con-
sequences of this condition. A recent
systematic review and meta-analysis of
11 studies composed of 6,325,152 preg-
nancies suggested that the risk of com-
bined CVD and stroke mortality was

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Expert Review
2.65-fold (95% CI, 1.55e4.54) higher
among pregnant people with abruption
compared with those without abrup-
tion.111 Similarly, the risk of nonfatal
CVD and stroke complications was 1.32-
fold (95% CI, 0.91e1.92) higher among
pregnant people with abruption
compared with those without abruption.
Importantly, there is evidence of
increasing risks of CVD and stroke
mortality with increasing number of
abruptions across successive pregnan-
cies. To the extent that abruption is
associated with increased risk of preterm
birth as well, it remains unknown
whether increased CVD risks are shaped
by abruption that occurs at preterm vs
term gestations.53,112e114
There are several pathways through
which abruption may confer increased
risks of CVD. It is thought that obstetrical
complications, particularly ischemic
placental disease, serve as a “stress test” that
unmasks preexisting CVD. These obstet-
rical complications induce uteroplacental
ischemia, resulting in oxidative stress,
vascular damage, and thrombosis.49
Abruption and CVD share similar path-
ways from disruption of the vascular sys-
tem and hemostatic defects, suggesting
that the factors that contribute to abrup-
tion also continue to future CVD.115
Perinatal Outcomes
Short-term effects
Pregnancies complicated by abruption
end, on average, approximately 3 to 4
weeks earlier than otherwise normal
pregnancies. Among nonabruption births,
the perinatal mortality rate is approxi-
mately 8 per 1000, which is in sharp
contrast to the mortality rate among
abruption births (15-fold greater, 120 per
1000).116 Well over half of the increased
perinatal mortality risks that accompany
abruption are attributed to preterm de-
livery and an additional 9% to FGR.116
Long-term effects
There is evidence of increased risks of
an array of neurologic complications
and neurodevelopmental deficits in
the offspring of participants that
develop abruption. Neonates exposed
to abruption, particularly those that
complicate pregnancies at preterm
S1326 American Journal of Obstetrics & Gynecology MAY 2023
gestations, are at increased risk of
cystic periventricular leukomalacia
and intraventricular hemor-
rhage.117,118 Abruption is associated
with a 6- to 10-fold increased risk of
cerebral palsy and a 2- to 4-fold
increased risk of developmental dis-
orders in infants born of abruption
pregnancies.62,118e121 Data from the
US CPP (1959e1966 with follow-up
to 1974) showed that the risk ratios
of abnormal motor and mental as-
sessments at 8 months of life were
2.35 (95% CI, 1.39e3.98) and 2.03
(95% CI, 1.13e3.64), respectively,
concerning abruption. The associa-
tions at 4 years were attenuated and
resolved fully at 7 years.22 These
findings provide compelling evidence
that some neurodevelopmental effects
of abruption may be transient.
Importantly, this study showed that
preterm birth mediated up to three-
fourths of this association at 8
months, with progressively decreasing
proportions at 4 and 7 years of the
abruption-neurodevelopmental effects
association.22 A large cohort study of
217,910 deliveries with 1003 cases of
abruption reported no increased risk
of nonfatal CVD in the offspring
(hazard ratio, 1.12; 95% CI,
0.60e2.11).122
Conclusions
Here, we focused on abruption at near-
term and term gestations, when the
impact of preterm birth is reduced and
we can glean insights into the direct ef-
fects of abruption. When pregnant peo-
ple present to labor and delivery with
symptoms of abruption e abdominal
pain, vaginal bleeding, and abnormal
FHR patterns e urgent evaluation and
management are required. Although
abnormal FHR patterns and coagulop-
athy pose clinical challenges, early
recognition of DIC, administration of
blood component therapy, and expe-
diting delivery are essential components
of abruption management. This review
sought to provide comprehensive, clini-
cally focused guidance during a gesta-
tional age range when neonatal
outcomes can often be favorable if rapid
and evidence-based care is optimized. -
ajog.org
ACKNOWLEDGMENTS
The authors thank Corrina Oxford, MD; Joshua
Marks, MD; and Anthony Vintzileos, MD, for their
reviews of the manuscript and Sue Pavord,
MBChB, FRCP, FRCPath, for sharing her
obstetrical hemorrhage protocol. Furthermore,
the authors thank Aileen Baffo, MD; Martin
Chavez, MD; Catherine W. Chan, MD; Susan
Egan, RDMS; Debra Heller, MD; and Wendy L.
Kinzler, MD, for contributing clinical images.
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