Abnormal Placentation

Samuel T. Bauer, MD, and Clarissa Bonanno, MD

Abnormal placentation poses a diagnostic and treatment challenge for all providers caring
for pregnant women. As one of the leading causes of postpartum hemorrhage, abnormal
placentation involves the attachment of placental villi directly to the myometrium with
potentially deeper invasion into the uterine wall or surrounding organs. Surgical procedures that disrupt the integrity of uterus, including cesarean section, dilatation and curettage, and myomectomy, have been implicated as key risk factors for placenta accreta. The
diagnosis is typically made by gray-scale ultrasound and confirmed with magnetic resonance imaging, which may better delineate the extent of placental invasion. It is critical to
make the diagnosis before delivery because preoperative planning can significantly decrease blood loss and avoid substantial morbidity associated with placenta accreta. Aggressive management of hemorrhage through the use of uterotonics, fluid resuscitation,
blood products, planned hysterectomy, and surgical hemostatic agents can be life-saving
for these patients. Conservative management, including the use of uterine and placental
preservation and subsequent methotrexate therapy or pelvic artery embolization, may be
considered when a focal accreta is suspected; however, surgical management remains the
current standard of care.
Semin Perinatol 33:88-96 2009 Elsevier Inc. All rights reserved.
KEYWORDS abnormal placentation, hemorrhage, cesarean hysterectomy, placenta accreta,
placenta previa

ver the last century, maternal deaths from hemorrhage

in the developed world have decreased significantly.
Factors contributing to this welcome decline include the
availability of blood product replacement, improvements in
surgical techniques, and advances in critical care medicine.
However, hemorrhage remains the second most common
cause of pregnancy-related mortality in the United States,
accounting for approximately 17% of all maternal deaths.1
Abnormal placentation, comprised of placenta accreta, increta, and percreta, is a leading cause of postpartum hemorrhage and indication for gravid hysterectomy. These disorders are also associated with significant maternal morbidity.
Most concerning, the incidence of abnormal placentation appears to be increasing, likely a consequence of the rising
cesarean delivery rate over the past several decades.
This article focuses on the etiology, diagnosis, and management of abnormal placentation. Accurate diagnosis and

Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynecology, Columbia University Medical Center, New York, NY.
Address reprint requests to Samuel T. Bauer, MD, Division of Maternal-Fetal
Medicine, Department of Obstetrics and Gynecology, Columbia University Medical Center, 622 West 168th Street, PH-16, New York, NY
10032. E-mail: [email protected]

88

0146-0005/09/$-see front matter 2009 Elsevier Inc. All rights reserved.

doi:10.1053/j.semperi.2008.12.003

optimal management of these complex cases can improve

outcomes for women with this serious condition.

Abnormal Placentation
Abnormal placentation refers to patients with placenta accreta, increta, or percreta. Placenta accreta occurs when the
placenta becomes abnormally adherent to the uterine wall.
On microscopic examination, there is direct attachment of
the chorionic villi to the underlying myometrium, rather
than the uterine decidua. Placenta increta occurs when the
placenta invades into the myometrium, and placenta percreta
occurs when the placenta penetrates to the uterine serosa or
invades into surrounding organs. In the literature, the term
placenta accreta may be used to refer to any degree of placental invasion, which is why we prefer the term abnormal
placentation.
In a retrospective series of 62 cases of abnormal placentation on cesarean hysterectomy specimens, pathological analysis confirmed that 75% were placenta accreta, 18% were
placenta increta, and 7% were placenta percreta.2 Although
there are no studies directly comparing outcomes of these
conditions, it is commonly understood that surgical morbidity is related to the degree of placental invasion.

Abnormal placentation

89

The incidence of abnormal placentation appears to be increasing. In a 1977 report, the incidence in the published
literature was estimated to be 1 in 7000 deliveries.3 Miller
and colleagues reported an incidence of abnormal placentation of 1 in 2510 for a 10-year period at their center ending in
1994.2 Similarly, Wu and colleagues reported an incidence of
1 in 533 over a 20-year period ending in 2002.4 These recent
estimates are almost certainly influenced by ascertainment
bias and the different criteria used to diagnose abnormal
placentation. Miller and colleagues limited their study to histologically confirmed cases of abnormal placentation on cesarean hysterectomy specimen.2 Conversely, the increased
incidence reported by Wu and colleagues may be a reflection
of the broader definition used in the study, which included:
(1) clinical diagnosis; (2) pathological diagnosis; (3) difficult
manual piecemeal removal if no separation after 20 minutes,
despite active management of the third stage; and (4) heavy
continued bleeding from the implantation site of a well-contracted uterus after placental removal during cesarean delivery.4 Finally, there are no large-scale, population-based surveys estimating the incidence of abnormal placentation.
Instead, these numbers are garnered from referral centers
that would be expected to treat a larger number of these
cases.

Risk Factors for

Abnormal Placentation

Table 1 Risk of Abnormal Placentation by Number of Previous

Cesarean Deliveries5

None
One
Two
Three
Four
Five or More

Previous
Cesarean
Deliveries

Clark 1985
PreviaAccreta %
(n 29)

MFMU 2006
PreviaAccreta %
(n 91)

None
One
Two
Three
Four or More

5
24
47
40
67

3.3
11.0
40.0
61.0
67.0

tomy was not performed. These investigators found that the

risk of abnormal placentation increased dramatically with
each cesarean delivery, particularly after the third cesarean
(Table 1).5 The risk of abnormal placentation increased even
more dramatically with each previous cesarean in the presence of placenta previa. The results of the MFMU study were
similar to the earlier single-center study by Clark and colleagues (Table 2).9 In all likelihood, the incidence of abnormal placentation will continue to rise. Since 1996, the total
cesarean delivery rate has risen yearly, reaching 31.1% in
2006.10,11 This is the highest level ever reported and represents a remarkable 50% increase during this 10-year period.

Etiology

The most well-described risk factors for abnormal placentation are previous cesarean delivery and placenta previa in the
index pregnancy.2,4,5 In fact, nearly all invasive procedures
on the uterus and uterine cavity have been associated with
abnormal placentation, including uterine curettage, hysteroscopic surgery, myomectomy, endometrial ablation, and
uterine artery embolization, though the absolute increase in
risk after these procedures is likely to be small.6-9 Advancing
maternal age is also an independent risk factor for abnormal
placentation.2,4
In a large, prospective, observational study, the centers of
the Maternal-Fetal Medicine Units (MFMU) Network quantified the risk of abnormal placentation with increasing numbers of previous cesarean deliveries.5 Of 30,132 women who
had cesarean delivery before labor, 143 cases of abnormal
placentation were diagnosed by histologic examination of
hysterectomy specimens, or by clinical means if a hysterec-

Previous Cesarean
Deliveries

Table 2 Risk of Placenta Accreta with Placenta Previa by

Number of Cesarean Deliveries5,9

Abnormal Placentation
% (n 143)
0.2
0.3
0.6
2.3
2.3
6.7

Although the risk factors for abnormal placentation are well

established, the precise etiology of this condition is largely
unknown. In normal pregnancy, the chorionic villi implant
into the spongiosus layer of the uterine decidua. There is a
natural cleavage plane superior to the decidua basalis which
allows prompt placental separation after delivery, caused by
the shearing action between the contracting myometrium
and the placenta. Myometrial contraction after delivery constricts the vascular supply to the placental bed, and hemostasis is achieved postpartum. Aberrations at any of these steps
likely contribute to defective implantation, failure of placental separation, and subsequent hemorrhage.
Historically, abnormal placentation has been attributed to
an absence or deficiency of Nitabuchs layer. Raissa Nitabuch
was a German physician who studied the vascular supply to
the placenta. The concept of Nitabuchs layer is based on
observations from her doctoral thesis at the University of
Bern in 1887.12 Nitabuch examined a single gravid uterus of
approximately 6 months gestational age with the placenta in
situ. She described the presence of a dark line located proximal to the basal plate underlying most of the placenta, which
appeared to be a largely extracellular or fibrinoid layer.
Nitabuch postulated that this was the border that separated
the chorion from the deeper decidua. It was later implied
from her work that this border effectively limited trophoblast
invasion.13 More recently, the concept of Nitabuchs layer
having a functional role and contributing to the pathology of
abnormal placentation has been refuted. Pijnenborgs work
on placental implantation has led to the discovery that trophoblasts normally invade through the endometrium to the
inner third of the myometrium.14 Two subgroups of extravil-

S.T. Bauer and C. Bonanno

90
lous cytotrophoblast invade the uterine wall: the interstitial
trophoblast invades the myometrial tissue, and the endovascular trophoblast remodels the maternal spiral arteries. This
tightly regulated process peaks between 9 weeks and 12
weeks of pregnancy and appears to be an important event in
normal pregnancies.
A deficiency of decidualization may contribute to the development of abnormal placentation. There is an increased
incidence of abnormal placentation in pregnancies with placenta previa, even in the absence of other risk factors.5,9 In
comparison to the rest of the uterine cavity, the lower uterine
segment proximal to the cervical canal contains relatively less
decidualized tissue.15 Similarly, cesarean delivery, uterine
curettage or hysteroscopic surgery, myomectomy, endometrial ablation, and uterine artery embolization may result in
localized decidual defects and consequently abnormal placentation. The risk of abnormal placentation in patients with
previous cesarean delivery and an anterior or central placenta
previa is increased fourfold over those patients with a posterior previa, which may be related to combined effects on
decidualization in the region of the prior scar.2
Abnormal placentation may also result from abnormal or
excessive trophoblast invasion. The primary invasive trophoblastic cell type is mononuclear; these cells later fuse to form
multinuclear giant cells. It is believed that the multinucleated
giant cells represent the terminally differentiated stage of extravillous trophoblast, with low invasive potential.14 There is
a paucity of giant cells at the placentalmyometrial junction
in cases of abnormal placentation, suggesting either an intrinsic abnormality in these trophoblasts or a defect in other
regulating factors.16
In an alternative hypothesis, localized differences in oxygen tension within uterine scarring may contribute to the
development of abnormal placentation. The human embryo
develops in a relatively hypoxic environment, and in vitro
work suggests that difference in oxygen tension determines
whether cytotrophoblast cells proliferate or invade.17 Embryos may preferentially implant into areas of uterine scarring and deficient decidua because of the relative deficiency
of blood flow and oxygen tension. Abnormal vascular remodeling may also contribute to abnormal placentation. A recent
study by Tantbirojin and colleagues demonstrated that cases
of abnormal placentation had a decreased proportion of normally remodeled vessels (in which the full circumference of
the vessel is replaced with endovascular trophoblast), with
many vessels displaying partial vascular changes.18 Vascular
remodeling was also demonstrated deeper in the myometrium in cases compared with controls. However, there was
no significant difference in the maximum depth of remodeled
vessels between subtypes of placenta accreta. Although there
appears to be relatively unchecked trophoblast invasion in all
cases of abnormal placentation, the authors suggested that
increta and percreta more likely arise from scar dehiscence,
allowing the chorionic villi greater access to deeper myometrial tissue.
It is likely that there are several different pathophysiological processes leading to the development of abnormal placentation. In some cases, primary defect may be poor decidu-

Figure 1 Gray-scale ultrasound for the diagnosis of abnormal placentation: obliteration of any part of the echolucent area between
the uterus and placenta.

alization, leading to the relatively superficial invasion of

placenta accreta. In other cases, excessive trophoblast invasion due to one of many potential factors may lead to the
deeper invasion of placenta increta and percreta. Conversely,
abnormal placentation may only develop when a number of
these processes are interacting in a single patient.

Diagnostic Tools
Ultrasound
The main screening modality for abnormal placentation is
gray-scale ultrasound imaging (Fig. 1). Finberg and colleagues first described specific ultrasound criteria for the diagnosis of abnormal placentation in 1992.19 These authors
prospectively evaluated 34 women with placenta previa and
a history of cesarean delivery with three diagnostic criteria:
(1) loss of the hypoechoic retroplacental zone; (2) thinning of
the hyperechoic uterine serosa bladder interface; and (3)
presence of focal exophytic masses. In these high-risk patients, the sensitivity of ultrasound in the detection of abnormal placentation was 93%, with a specificity of 79%. The
authors also noted over the course of their study that the
presence of intraplacental vascular lacunae increased the risk
of abnormal placentation.
In the largest prospective study of gray-scale ultrasound
for the diagnosis of abnormal placentation, Comstock and
colleagues evaluated 2002 patients with a previous cesarean
delivery and a low anterior placenta or placenta previa over a
12-year period.20 Diagnostic criteria that suggested abnormal
placentation included: (1) obliteration of any part of the
echolucent area between the uterus and placenta; (2) visualization of placental lacunae, defined as multiple linear, irregular vascular spaces within the placenta; and (3) interruption
of echogenic line at the uterine bladder interface (Figs. 1-3).
An ultrasound was labeled positive if any of these criteria
were found on at least one ultrasound, regardless of the findings at any subsequent scans. Using this broad definition of a
positive scan, the sensitivity of ultrasound was 100%. Among

Abnormal placentation

91

Figure 2 Gray-scale ultrasound for the diagnosis of abnormal placentation: visualization of placental lacunae.
Figure 4 MRI: abnormal uterine bulging.

individual sonographic criteria, the presence of placental lacunae had the highest sensitivity, at 93%. Of the confirmed
cases of abnormal placentation, 86% of patients had abnormal ultrasound findings between 15 weeks and 20 weeks
gestation, suggesting that the diagnosis can be made routinely at the time of the second trimester anatomical survey.
Importantly, none of these ultrasound findings differentiated
patients with varying degrees of placental invasion (ie, placenta accreta vs. placenta percreta).
Further studies have shown that abnormal placentation in
some patients may be detected even in the first trimester.
Diagnosis of abnormal placentation by ultrasound has been
documented as early as 6 weeks gestation.21 In a separate
analysis, Comstock and colleagues reported that a gestational

sac located in the lower uterine segment before 10 weeks

gestation was associated with abnormal placentation.21 A low
implantation site suggestive of abnormal placentation must
be distinguished from an ectopic pregnancy, which can develop within a cesarean delivery scar, and an aborted sac from
a failed intrauterine pregnancy. The former is typically surrounded by myometrium without any apparent connection
to the uterine cavity, and the latter will typically demonstrate
absence of the fetal heartbeat with irregularity of the gestational sac and surrounding blood.
Power and color Doppler are often used in conjunction
with gray-scale ultrasound imaging for the diagnosis of abnormal placentation. Doppler studies can highlight areas of
increased vascularity and turbulent blood flow through placental lacunae.22 Although Doppler ultrasonography seems
to perform reasonably well in the diagnosis of abnormal placentation, it does not appear to substantially increase the
accuracy of diagnosis compared with gray-scale imaging.23

Magnetic Resonance Imaging

Figure 3 Gray-scale ultrasound for the diagnosis of abnormal placentation: interruption of echogenic line at the uterine bladder
interface.

Over the last several years, there has been increased use of
magnetic resonance imaging (MRI) for the diagnosis and
characterization of abnormal placentation. Although cost and
accessibility limit its use as a screening tool, MRI may be
helpful when the placenta is difficult to visualize on ultrasound because of increased body mass index or a posterior
placenta. MRI also provides greater soft tissue contrast and a
larger field of view than ultrasonography. Lax and colleagues
performed a retrospective review of 20 prenatal MRI studies
(10 cases with abnormal placentation and 10 controls).24
This study was the first comprehensive analysis of features
associated with placental invasion on MRI. Three MRI findings were associated with abnormal placentation: (1) abnormal uterine bulging, (2) heterogeneity of signal intensity

S.T. Bauer and C. Bonanno

92

Figure 5 MRI: heterogeneity of signal intensity within the placenta.

within the placenta, and (3) the presence of dark intraplacental bands on T2-weighted images (Figs. 4-6).
MRI may be most helpful in diagnosing cases of abnormal
placentation with equivocal ultrasound findings. Warshak
and colleagues performed a historical cohort study on 453
women with a history of cesarean delivery and placenta previa or low anterior placenta.25 Ultrasonography accurately
predicted abnormal placentation in 30 of 39 of women and
correctly ruled out placenta accreta in 398 of 414 without
abnormal placentation (sensitivity 0.77, specificity 0.96).
Forty-two women underwent MRI evaluation because of
findings suspicious or inconclusive of abnormal placentation
by ultrasound. MRI accurately predicted placenta accreta in
23 of 26 cases with placenta accreta and correctly ruled out
placenta accreta in 14 of 14 cases (sensitivity 0.88, specificity
1.0). The authors concluded that a two-stage protocol for
evaluating women at high risk for abnormal placentation,
using ultrasonography followed by MRI for cases with inconclusive ultrasound findings, is the best strategy to optimize
diagnostic accuracy. In another recent study directly comparing ultrasonography and MRI for the diagnosis of abnormal
placentation in 32 cases, the sensitivity and specificity of each
technique were comparable.26 Most importantly, in the final
analysis, the inconclusive findings with one imaging modality were clarified in the other study.
There have been no studies showing that radiological techniques can accurately determine the extent of placental invasion. Certainly, with the greater soft tissue contrast provided
by MRI, it is the hope that this technology may prove useful
in distinguishing patients with superficial placenta invasion
(placenta accreta) and those with more extensive invasion
(placenta percreta) who may be at increased risk for hemorrhage and other surgical complications.

gonadotropin have been reported in patients with abnormal

placentation, there are no prospective studies supporting
their routine use.27,28
Increased levels of maternal serum cell-free fetal DNA and
placental mRNA have also been reported in patients with
abnormal placentation. In a small pilot study, Seikazawa and
colleagues demonstrated higher amounts of fetal DNA in maternal plasma in patients with abnormal placentation, higher
than those with placenta previa and still higher than control
patients.29 In another report, the maternal serum cell-free
fetal DNA level was used to follow a patient with a large
segment of retained placenta left in situ.30 Although typically
fetal DNA is undetectable in maternal serum within several
hours postpartum, in this case, fetal DNA was detected until
10 weeks postpartum, concurrent with clinical resolution. In
a more recent study increased levels of cell-free placental
mRNA were seen in patients with placenta previa who required cesarean hysterectomy.31
It has been hypothesized that abnormal placentation
causes muscular damage within the myometrium, resulting
in the elevation of creatinine kinase. The remainder of these
markers may be elevated because of increased leakage because of the pathology at the uterineplacental interface. Further research is needed to determine the utility of these markers in the diagnosis of abnormal placentation, but these data
represent an exciting new area of investigation.

Clinical Outcomes
Abnormal placentation is associated with significant maternal morbidity. The potential for significant surgical compli-

Emerging Diagnostics
Biochemical and/or biological markers may be able to improve the accuracy of antenatal diagnosis of abnormal placentation. Although elevated levels of maternal serum creatinine kinase, alpha fetoprotein, and -human chorionic

Figure 6 MRI: presence of dark intraplacental bands on T2-weighted

images.

Abnormal placentation
cations is vividly demonstrated in a case report from the
University of Vermont.32 These authors described a case of
antenatally diagnosed placenta percreta with bladder invasion. Despite optimal preoperative preparation by a multidisciplinary care team, this patient experienced a multitude of
intraoperative and postoperative complications. The patient
had a massive intrapartum hemorrhage with an estimated
blood loss at her initial surgery totaling 21 L. She required
hysterectomy, bilateral oophorectomy, and partial cystectomy, and her surgery was further complicated by transection of the right ureter. After two reoperations and a prolonged intensive care admission, the patient was ultimately
discharged on postdelivery day 18 without apparent deficits.
The authors concluded that, without extensive antenatal preparation, the patient would likely not have survived her delivery.
Hemorrhage is the most common complication of delivery
in these cases. Patients with abnormal placentation have the
potential for massive blood loss and serious sequelae, including consumptive coagulopathy, renal failure, adult respiratory distress syndrome, reoperation, and death. In the series
by Miller and colleagues, estimated blood loss exceeded 2000
cc in 66% of cases, 5000 cc in 15% of cases, and 10,000 cc in
6.5% of cases.2 Overall, 55% of women required blood transfusion, which exceeded 5 U in 21% of cases. From these data,
it seems the spectrum of blood loss and necessary transfusion
is relatively wide in these patients, which may be related to
the degree of placental invasion, the complexity of the surgery, and operator experience.
As the incidence of abnormal placentation has increased
and management of hemorrhage due to atony has improved
with medical therapy and conservative surgical treatment,
placenta accreta has become a leading indication for peripartum hysterectomy.33,34 Other well-described complications
from hysterectomy for abnormal placentation include infection, cystotomy, ureteral injury, postoperative ventilation,
intensive care admission, and reoperation, often for hemoperitoneum.2,5

Management of
Abnormal Placentation
A preoperative management plan for a patient with suspected
abnormal placentation is critical. One of the primary goals of
this effort is to facilitate coordination of the delivery by a
multidisciplinary care team, including obstetricians, anesthesia, nursing, pediatrics, critical care physicians, and the blood
bank. Some cases may require additional surgical expertise
from gynecologic oncology, urology, and/or vascular surgery. Certainly, delivery of patients with suspected abnormal
placentation at a tertiary care facility with adequate blood
bank services and sufficient surgical support should be
strongly considered. It is also important to counsel the patient and her family extensively on the suspected diagnosis,
the anticipated surgical procedure and other potential interventions, and possible complications. The options of traditional surgical management of abnormal placentation, in-

93
cluding hysterectomy versus conservative management,
should be thoroughly discussed.
A scheduled delivery is ideal, as it is associated with less
intraoperative blood loss than emergent delivery.35 However,
patients with abnormal placentation, particularly those with
concurrent placenta previa, are at risk for antenatal bleeding.
The optimal time for delivery of these patients is unclear.
Although a scheduled, nonemergent delivery is best to optimize maternal outcomes, the risks of prematurity, even in the
late preterm period, should not be minimized. The timing of
delivery should be individualized based on the antenatal suspicion of abnormal placentation, the expected degree of placental invasion and surgical risk factors, and the overall maternal status. We advocate earlier delivery, typically by 34
weeks gestation after a course of antenatal corticosteroids, in
cases of suspected placenta percreta or in cases complicated
by recurrent antenatal bleeding. In our experience, the patients at highest risk of emergent delivery are patients with
recurrent vaginal bleeding. Patients with a lower clinical suspicion of abnormal placentation, who remain asymptomatic
or who do not have concurrent placenta previa, may be delivered closer to term or at term.
Preoperative planning will also influence decisions about
the location of delivery. In some institutions, the main operative suites may be more appropriate for complex cases than
the Labor and Delivery Unit. Whether or not to begin the case
with general anesthesia versus regional anesthesia must be
decided, as well as what additional intravenous or intra-arterial access is required. The type of abdominal incision (eg,
Pfannenstiel, Maylard, vertical midline) should be determined and discussed with the patient. Most importantly,
management of the placenta should be decided before surgery. Incisions made through the placenta and any attempts
to deliver the placenta in these cases will often incite significant hemorrhage. This decision should also be discussed at
length by the operative team and should also incorporate the
patients wishes regarding conservative management and future fertility. In our most complex cases, we typically make a
vertical midline incision which will allow delivery of the
uterus from the abdominal cavity with the fetus in situ. A
fundal or posterior vertical hysterotomy for delivery of the
neonate will typically avoid the placenta and minimize hemorrhage. Preoperative or intraoperative sonographic localization of the placental edge can also be helpful to determine the
best position for the uterine incision. Placing the patient in
lithotomy before surgery allows the surgeon to monitor vaginal bleeding during the case and provides additional access
to the maternal pelvis.
Adequate blood products should be available at the time of
delivery. For our cases, we typically prepare 20 U of packed
red blood cells (PRBCs), 20 U of fresh frozen plasma (FFP),
two 6-packs of platelets, and 10 U of cryoprecipitate. Based
on our experience with massive hemorrhage, and further
substantiated by trauma literature out of Iraq, we have been
using a 1:1 ratio of PRBCs to FFP for our cases of massive
hemorrhage. Anecdotally, we feel this strategy minimizes the
potential for coagulopathy in our patients.36 In addition, a
rapid infuser and a cell salvage device (such as Cell Saver)

94
may prove helpful. Concerns about amniotic fluid embolism
and maternal alloimmunization with cell salvage and autotransfusion at cesarean delivery have not been substantiated.
In fact, no serious complication directly related to use of this
technology in obstetrics has been reported, although there
are no large prospective trials supporting its safety.37
Uterotonics should be readily available in the operating
room. Even when the placenta delivers spontaneously, patients with a preoperative suspicion of abnormal placentation
seem to be at risk for postpartum hemorrhage and uterine
atony. A three-way Foley catheter and ureteral stents should
also be available to assess the integrity of the urinary system
intraoperatively. Whether or not preoperative cystoscopy
and placement of ureteral stents reduces the risk of injury to
the urinary tract is unclear, but evidence from the gynecologic literature would suggest that these measures are not
helpful.38,39

Additional Interventions
At the time of surgery, hemostasis can typically be achieved
with a combination of suture ligation, electrocoagulation,
and pressure. To facilitate hemostasis after hysterectomy,
topical hemostatic agents may be used.40,41 Mechanical
agents allow platelet aggregation and coagulation by providing a meshwork on which clotting can take place, and include
gelatin (Gelfoam), cellulose (Oxycel, Surgicel), and collagen
(Avitene). Active agents contain thrombin alone or in combination with other procoagulant agents. These products include FloSeal, a combination of gelatin and thrombin, and
Tisseel, a combination of thrombin and fibrinogen. None of
these products has been proven superior over the others.
Some of these agents have broad FDA approval for hemostasis during surgical procedures, whereas others would be used
off-label for obstetric surgery.
Hypogastric artery catheters may be placed preoperatively
by interventional radiology in cases of suspected abnormal
placentation. The procedure involves bilateral placement of
embolization and/or balloon catheters through the femoral
arteries under fluoroscopic guidance. Gelatin pledgets are
most commonly used for embolization. If balloon catheters
are used, they may be inflated intermittently during the procedure to decrease blood loss, improve visualization in the
operative field, and thereby improve surgical outcomes.
Complications of both embolization and balloon catheters
can occur. These include transient, relatively benign complications, such as low-grade fever or hematoma at the catheter
site. However, potential serious sequelae include inadvertent
or widespread thromboembolism and ischemia to the pelvic
organs, limbs, or buttocks.42-46 In addition, embolization
may not be possible in unstable patients with continued hemorrhage because of the time required to perform the procedure under fluoroscopy, during which the surgeons typically
exit the operating room.
The literature offers conflicting evidence on the utility of
preoperative placement of hypogastric artery catheters in decreasing blood loss and improving surgical outcomes. We
use prophylactic placement of hypogastric artery catheters

S.T. Bauer and C. Bonanno

for intraoperative embolization in cases of suspected placenta
percreta. In selecting the most difficult cases for this procedure, it is difficult to demonstrate improved outcomes compared with patients in whom we do not place catheters. Overall, the literature on prophylactic catheter placement for
abnormal placentation is mixed, and there are no randomized controlled trials to provide definitive data.42-51 Postoperative placement of catheters for embolization may also be
considered in stable patients with continued pelvic bleeding,
if the interventional radiology team is available.
Recombinant activated factor VII (rFVIIa; NovoSeven) has
also been used to treat obstetric hemorrhage refractory to
conventional treatment. rFVIIa is currently approved to promote hemostasis in patients with hemophilia and inhibitors
to factor VIII and IX as well as patients with congenital factor
VII deficiency. However, rFVIIa has been used off-label for a
number of other nonhemophilic bleeding conditions, including obstetric hemorrhage. Franchini and colleagues recently
summarized the literature on rFVIIa for postpartum hemorrhage, which included 118 patients from 31 studies.52 Abnormal placentation was the third leading cause of hemorrhage in these patients, after uterine atony and uterine/
vaginal lacerations. In approximately 90% of cases, rFVIIa
was effective, in most cases with a single dose. Although the
authors advocated that use of rFVIIa be considered before
hysterectomy in cases of severe hemorrhage, this recommendation might not be appropriate in all cases of abnormal
placentation. Potential complications of rFVIIa include arterial and venous thrombotic events. The risk-to-benefit ratio
in the current literature appears quite favorable, but this may
reflect publication bias. Further evidence, ideally from randomized controlled trials, is needed to determine the optimal
dose, effectiveness, and safety of rFVIIa for obstetric hemorrhage. rFVIIa should be used cautiously in obstetric patients,
but this may be a life-saving option in some cases.
For patients with intractable bleeding due to coagulopathy, the best option may be to stop the case and pack the
abdomen. The patient is usually transferred to the intensive
care unit at this time, where she can be stabilized with additional fluid resuscitation, and red blood cell and factor replacement. Correction of metabolic acidosis and hypothermia may also improve coagulopathy in these cases. The
patient is returned to the operating room after she has been
medically stabilized for removal of packing and closure.
Placement of a surgical drain may be helpful to monitor for
continued intraperitoneal bleeding after closure.

Conservative Management
The primary goals of conservative management are to decrease operative morbidity and preserve fertility. The literature on conservative management of suspected abnormal placentation consists of case reports and case series, thus the
evidence is limited by publication bias. Timmermans and
colleagues recently reviewed the literature on conservative
management.53 These authors summarized the outcomes of
60 cases of suspected abnormal placentation, in which at
least a portion of the placenta was left in situ after delivery.

Abnormal placentation
The outcomes were summarized by the primary method of
treatment: conservative management alone, conservative
management with methotrexate, and conservative management with embolization.
Of the 26 patients who were treated with conservative
therapy alone, 22 cases of abnormal placentation were diagnosed after delivery. In most of these cases, the placenta was
partially removed. Treatment failed in 4 patients: 3 patients
underwent immediate hysterectomy for excessive bleeding
and shock, and 1 patient had a delayed hysterectomy for
major infection. Subsequent pregnancies were reported in 3
patients: 2 required hysterectomy for abnormal placentation,
and 1 patient had an uncomplicated manual evacuation of
the placenta.
There were 22 cases treated with adjunctive methotrexate.
Antenatal diagnosis was more frequent in this subgroup, and
in most cases, the entire placenta was removed. Of this
group, 5 failed treatment: 1 patient underwent hysterectomy
for persistently vascularized placental tissue, and 4 patients
underwent hysterectomy for delayed bleeding 1 to 7 weeks
postoperatively. Two patients had subsequent pregnancies,
both uneventful.
Twelve patients underwent conservative management
with uterine or hypogastric artery embolization. The diagnosis was suspected in most of these patients; the majority (11/
12) underwent embolization immediately following delivery.
There were 3 treatment failures: 2 patients underwent hysterectomy for delayed bleeding 2 to 3 months postpartum,
and 1 patient underwent hysterectomy for infection.
Overall, treatment was considered successful in 80% of
cases (48/60). The most common cause of treatment failure
was vaginal bleeding (9/60), and the most common complication overall was fever (21/60). Endometritis was relatively
common (11/60), but led to treatment failure in only 2 cases.
In addition to the inherent publication bias, without pathological examination of the uterus, the diagnosis in these cases
cannot be verified. Because of the risk of unpredictable and
often delayed hemorrhage, as well as the risk of overwhelming infection, we do not recommend conservative management for abnormal placentation to our patients. However, for
select cases in which the patient has no comorbid medical
conditions, the blood loss at delivery is minimal, and she has
a strong desire to retain her uterus with an understanding of
the significant risks, this option may be considered.

Conclusions
The incidence of abnormal placentation is increasing with the
rise in the cesarean section rate. This diagnosis is associated
with significant peripartum complications and occurs in 11%
to 25% of women with a placenta previa and one previous
cesarean delivery. Prenatal diagnosis of placenta accreta is
based on the presence of characteristic findings on ultrasound examination, with placental lacunae being the most
sensitive predictor. MRI can be helpful as an adjunctive diagnostic tool when the diagnosis is uncertain, when the placenta is posterior, or to gauge the depth of placental invasion.
The role of interventional radiology procedures in these cases

95
needs to be further evaluated. Preoperative preparation is
likely to improve maternal outcomes. Without optimal planning during the antepartum period (including multidisciplinary staff members, vascular access, cell salvage and rapid
infuser capabilities, available blood products, and hemostatic
agents), the complications from an abnormally implanted
placenta can be catastrophic, including massive hemorrhage,
damage to internal organs, disseminated intravascular coagulopathy, pulmonary edema, prolonged intubation, and prolonged intensive care admission. Significant complications
can also occur despite optimal preparation. As diagnostic
imaging techniques and serum marker modalities continue
to evolve, the ability to predict and treat massive hemorrhage
related to abnormal placentation will improve and will hopefully decrease the morbidity and mortality related to this
serious condition.

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