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OBSTETRICS

Cutting-edge advances in the medical management


of obstetrical hemorrhage
Luis D. Pacheco, MD; George R. Saade, MD; Alfredo F. Gei, MD; Gary D. V. Hankins, MD

Hemorrhagic shock is the most common form of shock encountered in obstetric practice.
Interventions that may limit transfusion requirements include normovolemic hemodilution,
use of recombinant activated factor VII, selective embolization of pelvic vessels by interventional radiology, and the use of the cell saver intraoperatively. Current understanding of
the mechanisms of acute coagulopathy calls into question the current transfusion guidelines, leading to a tendency to apply massive transfusion protocols based on hemostatic
resuscitation despite lack of prospective data.
Key words: hemorrhage, hemostatic resuscitation, pregnancy

27-year-old patient with a history


of 3 previous cesarean sections
presents for her fetal anatomy scan at 22
weeks. On ultrasound (US) examination, an anterior placenta previa is noted
with multiple lacunae and attenuation of
the retroplacental space.
Hemorrhagic shock is the most common form of shock encountered in obstetric practice. In 2005, in the United
States, hemorrhage was the third leading
cause of maternal death because of obstetric factors.1
Historically, the most frequent indication for a peripartum hysterectomy has
been uterine atony. Recent literature
suggests that this indication may be
shifting, with abnormal placentation becoming the most common reason for peripartum hysterectomy.2,3 The incidence
of placenta accreta is estimated at 1 in
From the Division of Maternal-Fetal Medicine,
Department of Obstetrics and Gynecology (Drs
Pacheco, Saade, and Hankins) and Division of
Surgical Critical Care, Department of
Anesthesiology (Dr Pacheco), The University of
Texas Medical Branch, Galveston; and the
Division of Maternal-Fetal Medicine,
Department of Obstetrics and Gynecology (Dr
Gei), Methodist Hospital, Houston, TX.
Received April 1, 2011; revised May 11, 2011;
accepted June 2, 2011.
The authors report no conflict of interest.
Reprints not available from authors.
0002-9378/$36.00
2011 Mosby, Inc. All rights reserved.
doi: 10.1016/j.ajog.2011.06.009

526

533 pregnancies.4 With the increasing


cesarean section rate as well as a decrease
in vaginal birth after cesarean section,
this number is likely to increase in the
future.
In this article, we will address some of
the new concepts in the medical management of obstetric hemorrhage. We will
focus on a theoretical case of placenta accreta; however, many of the therapeutic
recommendations apply to any cause of
massive obstetric bleeding.

Antepartum care
In the vast majority of cases, placenta accreta may be presumptively diagnosed
on the basis of US alone. Sonographic
findings suggestive of accreta include the
presence of placental lacunae giving a
Swiss cheese appearance, loss of the
normal retroplacental hypoechoic space,
and increased vascularity with uterine
wall vessel invasion as noted by the use of
color Doppler.
In recent years, there has been increased interest in the use of magnetic
resonance imaging (MRI) for the evaluation of patients with suspected placenta
accreta because it can provide information on depth of invasion and may be
particularly useful in the diagnosis of
posteriorly located placentas.5 MRI findings suggestive of placenta accreta include lower uterine bulging, heterogeneous placenta, and dark intraplacental
linear bands on T2-weighted images.6

American Journal of Obstetrics & Gynecology DECEMBER 2011

In a multicenter retrospective study,


Dwyer et al7 compared the accuracy of
both US and MRI in the diagnosis of placental accretism. The sensitivities for the
diagnosis of placenta accreta with US
and MRI were 93% and 80%, respectively. Specificities (negative study in the
absence of the condition) were 71% and
65%, respectively. Neither difference
achieved statistical significance. The accuracy for the diagnosis may be increased by complementing the abdominal US with transvaginal sonography.7
The use of paramagnetic contrast media in MRI (gadolinium) likely would
improve the diagnostic performance of
MRI; however, the agent crosses the placenta, and the effects on the fetus are
unknown.
At present, it appears that the diagnostic abilities of both US and MRI are similar. In cases where the diagnosis is unclear, MRI and US may be used as
complementary tests.8
In patients with suspected placenta
percreta, we recommend a complementary MRI to better define the extent of
invasion to adjacent organs (eg, bladder,
bowel) so that appropriate preoperative
planning may be undertaken (eg, placement of ureteral stents).
Once the diagnosis is suspected, patients should receive iron and/or folic
acid as needed to maintain normal hemoglobin values. Occasionally, patients
may require recombinant erythropoietin as adjuvant therapy. Patients should
ideally be referred to a center with a multidisciplinary team available, including
maternal fetal medicine, general surgery,
urology, vascular surgery, interventional
radiology, blood bank, and neonatology.
Maternal morbidity is reduced in women
with placental accretism who deliver in tertiary care centers.9
Recent evidence questions the need
for serial fetal growth USs in the setting
of placenta previa without accretism, as

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it does not increase the risk of intrauterine growth restriction.10 In the setting of
suspected accretism, however, we recommend sonographic follow-up every
3-4 weeks to evaluate placental location,
depth of invasion, and fetal growth.
Occasionally, patients at risk for severe
hemorrhage may benefit from preoperative autologous blood donation. Patients
donate units of their own blood during
pregnancy, and such products will be
stored in the blood bank for use on the
day of surgery. Theoretically, the hemoglobin will recover (patients will be on
iron supplements) between donations.11
In practice, however, anemia is a limiting
factor, and patients usually donate only a
limited number of units throughout
pregnancy. This technique will not prevent the risks associated with blood collection, storage, and administration and
may not be acceptable to Jehovahs Witnesses.11 Overall, the technique is not
cost effective and is recommended only
for patients with rare blood types and/or
alloimmunization to rare antibodies for
whom immediate availability of allogeneic blood products may be limited.11
Timing of delivery in women with placental accretism is a controversial subject. A recent decision analysis model
suggested that delivery at 34 weeks of
gestation may be optimal and that amniocentesis for determination of fetal
lung maturity does not improve outcomes and is not recommended.12 Advanced planning and interdisciplinary
collaboration are fundamental, and as
gestational age increases, so does the risk
of emergent bleeding. We concur with
these recommendations: patients with
suspected accretism should be delivered
between 34 and 37 weeks. Recent evidence suggests that patients with placenta previa and a cervical length less
than 30 mm have a higher risk of acute
hemorrhage.13 In deciding whether to
deliver patients closer to 34 weeks vs 37
weeks, clinicians may consider obtaining
a cervical length by transvaginal US. If
the cervix is less than 30 mm and the gestational age more than 34 weeks, we favor delivery as opposed to waiting a
few more weeks (no later than 37
weeks) to prevent bleeding and emergent
deliveries.

Intrapartum interventions
When massive blood loss is expected,
one question that comes to mind frequently is which anesthetic technique
should be used. A complete sympathectomy (eg, spinal anesthesia) could impair the patients ability to cope with
sudden hypovolemia, as the capacity to
vasoconstrict and increase systemic vascular resistances will be limited. However, regional anesthesia with a continuous epidural technique is safe and may
be appropriate for patients with placental accretism.14,15 Emergent situations,
with active bleeding, particularly if surgical access to the upper abdomen is
needed, may be better served with general anesthesia.
Acute normovolemic hemodilution (ANH)
may be undertaken in the operative
room before starting cases presumed to
be at high risk of bleeding. A central line
is placed, and blood is collected from the
patient into citrated blood bags from the
blood bank. Patients should have a hemoglobin level above 10 g/dL and no history of cardiovascular disease. On average, 500-1000 mL whole blood may be
collected and concurrently replaced with
either colloid (1:1 ratio) or crystalloid
(3:1 ratio) to maintain hemodynamic
stability. During surgery, any blood loss
will have a lower red cell content. Once
surgical bleeding is controlled, the patient is given back the blood previously
collected. The collected blood may be
stored at room temperature for up to 6
hours.11 This technique is acceptable to
some Jehovahs Witnesses as long as the
collection bag remains connected to the
central venous line at all times (avoid
circuit disconnections). Overall, there
is minimal evidence to suggest that ANH
alone has a significant effect on the need
for allogeneic blood.11
Preoperative bilateral common iliac artery balloon catheter placement with inflation after delivery of the fetus has been
reported. Theoretically, balloon inflation leads to bilateral vessel occlusion,
limiting blood loss. The efficacy of the
latter approach has been questioned.16,17
Another option involves preoperative
placement of femoral access by interventional radiology with selective emboliza-

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tion of uterine vessels at the time of delivery using polyvinyl alcohol, gel foam,
or coils.18
In our institution, the use of balloon
occlusion catheters in the pelvic circulation did not reduce transfusion requirements compared with historic controls.19 We do not use this technique.
Intraoperative cell salvage has been
successfully used in obstetric hemorrhage. Blood is aspirated from the surgical field and filtered into a collecting reservoir. Filters in the device will remove
molecules like tissue factor, alpha fetoprotein, platelets, and circulating procoagulants.20 After filtration, packed red
cells concentrated to a hematocrit of 5580% are obtained and can be readministered to the patient.
Postoperatively, patients who are Rh
negative should receive anti-D immunoglobulin as soon as possible with a dose
given according to results of a Kleihauer
Betke stain to prevent alloimmunization.11 A theoretical concern with the use
of the cell saver in obstetrics is the occurrence of iatrogenic amniotic fluid embolism (AFE) because small amounts of
amniotic fluid will bypass the filters of
the device and be present in the packed
red cells. However, more than 400 cases
of cell saver use in obstetrics have been
published, and no evidence of iatrogenic
AFE exists. This technique is safe and effective in obstetric cases where massive
blood loss is expected.21
Recombinant factor VIIa (rFVIIa) is licensed for use in patients with hemophilia and inhibitory alloantibodies.22 It
has increasingly been used for off-label
indications including trauma, heart surgery after cardiopulmonary bypass, vascular surgery, warfarin reversal, and obstetric hemorrhage. More than 75% of
level I trauma centers in the United
States recommend the use of rFVIIa in
their massive transfusion protocols. An
example of a massive transfusion protocol is provided in Figure 1.
Once endothelial injury has occurred,
subendothelial collagen and tissue factor
are exposed to the circulation. Factor VII
(endogenously and exogenously administered) will bind to tissue factor and activate the clotting cascade, leading to
local fibrin deposition. Systemically, rF-

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FIGURE 1

Example of a massive transfusion protocol


Consider activation of a MT protocol when patient actively bleeding and any of the following:
Systolic blood pressure < 90 mmHg
Ph < 7.1
Base deficit > 6 meq/L
Temperature below 34C
INR > 2.0
Platelet count < 50,000/mm

PRBC

FFP

Platelets

Cryoprecipitate

Round 1

6 units

6 units

6 units

10 units

Round 2

6 units

6 units

Round 3

20 units

Recombinant activated Factor VII (40 micrograms/kg)

Once activated, the blood bank will send 6 units of PRBC, 6 units of FFP, 6 units of platelets,
and 10 units of cryoprecipitate. After this, if the patient remains bleeding (the protocol has
not being inactivated), 6 more units of PRBC and FFP will be prepared along with 20 units of
cryoprecipitate. The latter product is given in order to elevate the fibrinogen level since the
next step of the protocol is to administer recombinant activated factor VII. At any point, if the
patients hemorrhage stops, the blood bank should be notified so that the protocol can be
terminated.

If bleeding persists, the sequence is started again.


FFP, fresh frozen plasma; INR, international normalized ratio; MT, massive transfusion; PRBC, packed red blood cells.
Pacheco. Medical management of obstetric hemorrhage. Am J Obstet Gynecol 2011.

VIIa will also bind activated platelets,


leading to fibrin formation away from
the site of injury. Despite having a very
short half-life (2-6 hours), concerns
about thromboembolism as a complication are real. A recent systematic review
of the literature showed a higher risk of
arterial thrombosis (not venous) among
patients who received rFVIIa as an adjuvant therapy for life-threatening bleeding.23 rFVIIa is not a first-line treatment
for hemorrhage and is effective only
once major sources of bleeding have
been controlled. The use of this product
should be combined with best practice
use of blood products.24 Before administration, the patient should ideally
have a platelet count 50,000/mm3, fibrinogen 50-100 mg/dL, temperature
32C, pH 7.2, and normal ionized
calcium.24 These preconditions will facilitate adequate functioning of the clotting cascade.
Seventeen randomized controlled trials in which rFVIIa was used to control
hemorrhage in different subgroups of
patients have been published. Four stud528

ies found a reduction in transfusion requirements or blood loss, but none reported a survival benefit.25 Overall, it
appears that rFVIIa is effective in limiting the amount of blood products transfused, but data on survival benefit are
lacking.
The obstetric literature has numerous
case reports and case series involving the
use of rFVIIa. Publication bias is a major
concern, and we are not aware of any
published randomized trials involving
rFVIIa in obstetric practice. The optimal
dose is still unknown. Many reports in
obstetric hemorrhage have used a dose of
90 mg/kg. If used in obstetric cases, we
recommend deep venous thrombosis
prophylaxis once the bleeding risk is
considered to be low.

Transfusion therapy
Classically, hemorrhage resuscitation
has been centered around administration of crystalloids and packed red blood
cells (PRBC). Use of other blood products like fresh frozen plasma (FFP), cryoprecipitates, and platelets is indicated if

American Journal of Obstetrics & Gynecology DECEMBER 2011

hematologic parameters are abnormal


(eg, platelet count 50,000/mm3, fibrinogen 100 mg/dL, prothrombin time
[PT], or activated partial thromboplastin time [aPTT] 1.5 normal). These
current transfusion guidelines fail to
prevent coagulopathy in massive bleedings.26 Patients with crystalloid/PRBCbased resuscitation will frequently develop dilution of clotting factors and
platelets, leading to the so called dilutional coagulopathy. The latter may be
complicated by hypothermia and acidosis, both of which lead to coagulation
dysfunction.
Massive crystalloid resuscitation may
actually worsen bleeding before achieving surgical control of hemorrhage because of increases in intravascular hydrostatic pressures and dislodgement of
fresh clots at sites of endothelial injury.27
Recent evidence has shown that early
coagulopathy may occur before hemodilution and before consumption of clotting factors takes place. This mechanism
of early coagulopathy has been studied
mainly in trauma; however, obstetric
hemorrhage may share some of the
mechanisms involved.27 Early tissue hypoperfusion leads to endothelial upregulation of the receptor thrombomodulin. This receptor interacts with
thrombin, leading to activation of the
protein C pathway. Protein C is a natural
anticoagulant that irreversibly inhibits
factors Va and VIIIa and also enhances
fibrinolysis through inhibition of plasminogen activator inhibitor 1.28 Increased
fibrinolytic activity has been described in
obstetric hemorrhage secondary to uterine atony, placental abruption, and accretism.27 These new mechanisms of coagulopathy have challenged the current
resuscitation guidelines, suggesting that
early clotting factor replacement and
early identification of excessive fibrinolysis may be associated with improved
outcomes.
Hemostatic resuscitation is a new concept that involves 3 main aspects:
1. Limiting early aggressive crystalloid
use and considering permissive hypotension.
2. Early administration of FFP and
platelets (with concomitant packed

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red blood cells), achieving a ratio of
1:1:1 without waiting for coagulation
laboratory tests.
3. Early use of rFVIIa.
Aggressive crystalloid resuscitation is
avoided to prevent hemodilution and
early clot dislodgement secondary to increases in blood pressure as a result of
volume expansion. Before surgical control of hemorrhage, permissive hypotension with systolic blood pressures between 80-100 mm Hg may be optimal to
limit ongoing blood loss.27 Permissive
hypotension may be considered in patients with postpartum hemorrhage;
however, no data is available during the
antenatal period, as uterine perfusion
pressure may be compromised.
Early administration of FFP and platelets with PRBC in a ratio of 1:1:1 prevents
early development of coagulopathy. Retrospective military and civilian data have
demonstrated absolute mortality reductions between 15-62% with the use of
higher ratios of FFP:PRBC.29,30 A significant limitation of the available, mostly
nonrandomized, studies on this topic is
the presence of survival bias. On average,
the median time to obtaining the first
unit of PRBC is 18 minutes, as opposed
to more than 1 hour for FFP (needs to be
thawed).31 Sicker patients will likely die
before availability of FFP, whereas less
sick patients will survive to the moment
when FFP is available. The latter may explain why patients with high FFP:PRBC
ratios had better survival. A limited
number of studies have specifically addressed the survivor bias in high FFP:
RBC studies. When early deaths were excluded, no survival benefit for higher
ratios was noted.32 Prospective trials are
required to validate the benefit of early
FFP administration. Despite the lack of
randomized trials, many centers in the
United States have adopted massive
transfusion protocols involving the use
of high FFP:PRBC ratios and early use of
rFVIIa.33 These massive transfusion protocols are frequently used in massive obstetric hemorrhage.
Administration of large amounts of
blood products could lead to a higher incidence of transfusion-related acute lung
injury (TRALI) and transfusion-related
immunomodulation (TRIM).34 Others

suggest the opposite, with the rationale


that early administration of FFP and
platelets achieves hemostasis earlier,
thus decreasing the total number of
blood products given.26

Hemostasis monitoring
Conventional plasma-based coagulation
analyses like the PT, aPTT, and international normalized ratio (INR) are poor
predictors for transfusion requirements
and do not identify specific coagulation
anomalies.35 The thromboelastograph
(TEG) is an easy test that provides information regarding the specific component of the coagulation process that may
be affected. A small amount of blood is
placed into a cuvette, and the blood is
stirred with an agitator connected to a
strain gauge. As the movement of the agitator is impeded by the forming clot, the
strain gauge depicts a graphic representation of the strength of the clot. Figure 2
depicts the main components of the
TEG. Both the reaction time/clotting
time and the alpha angle reflect the activity of clotting factors. Once the clot is
formed, the maximum amplitude correlates with platelet function. Lastly, the
velocity at which the amplitude decreases correlates with fibrinolytic activity.
Obstetric hemorrhage often has a significant component of enhanced fibrinolysis.36 Conventional clotting tests fail to
identify such anomaly, whereas the TEG
may easily detect it, leading to a change in
management where antifibrinolytic agents
like tranhexamic acid or epsilon aminocaproic acid should be administered.
Where available, we recommend the use of
the TEG to guide transfusion therapy.
Postpartum considerations
Patients who have had massive obstetric
hemorrhage are frequently at high risk of
developing thromboembolic complications after delivery. Immediately after
delivery, if the bleeding risk is still considered elevated, mechanical prophylaxis devices should be used. As soon as
considered safe, pharmacologic prophylaxis should be instituted.
Not infrequently, oliguria and hypotension persist after massive resuscitation. The typical approach to the latter
clinical situation is administration of

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FIGURE 2

Thromboelastogram
D

A
C

A corresponds to the reaction time. B indicates


clotting time. A, B, and the angle reflect the
function of clotting factors. In cases of clotting
factor deficiency, both times will be prolonged. C
is the maximum amplitude of the clot, and it correlates with platelet function. The amplitude is
proportional to platelet function. D indicates fibrinolysis. Cases of hyperfibrinolysis will show a
rapid resolution of the clot, giving a tear drop
appearance.
Reprinted with permission from Obstetrics and Gynecology Clinics
of North America.40
Pacheco. Medical management of obstetric hemorrhage.
Am J Obstet Gynecol 2011.

more intravenous fluids. Although in


most cases fluid therapy may be the answer, abdominal compartment syndrome must always be considered. Both
crystalloid and colloid administration
lead to third spacing of fluid (crystalloid
will third space earlier than colloid).
Consequently, bowel edema and ascitis
may ensue. Extensive surgical procedures are commonly associated with ileus, which may also favor intraabdominal hypertension. Put together, all these
factors may increase the intraabdominal
pressure to a point where compression of
the abdominal and retroperitoneal vessels will compromise preload to the
heart, leading to a drop in cardiac output
and, consequently, in blood pressure.
Another important component of this
syndrome is oliguria, as the kidney is
poorly perfused secondarily to compromised cardiac output and the kidney venous system is also compressed by increased extravascular pressure, leading
to a decrease in the gradient of perfusion.
Cephalad displacement of the diaphragm leads to bibasal atelectasies, with
more right-to-left shunt and consequent
hypoxemia. Patients on mechanical ventilators will display sudden increases in
airway pressures. Central vascular pres-

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FIGURE 3

Key aspects involved in the medical management of a patient at risk of severe obstetric hemorrhage

DVT, deep venous thrombosis; EPO, erythropoietin; Fe, iron; MRI, magnetic resonance imaging; TEG, thromboelastograph.
Pacheco. Medical management of obstetric hemorrhage. Am J Obstet Gynecol 2011.

530

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sures (central venous pressures or pulmonary pressures recorded by means of
a pulmonary artery catheter) will also be
elevated as the intrathoracic pressure
rises secondarily to the upward displacement of the diaphragm.
Obstetricians need to be familiar with
this complication, as the administration
of more fluid in an attempt to increase
blood pressure and urine output will
only worsen intraabdominal pressures
and hemodynamics. If the condition is
suspected, a bladder pressure should be
obtained at the bedside as a surrogate for
abdominal pressure.37 Bladder pressure
should be measured with the patient in
the supine position and the bladder distended with 25 mL saline after the urinary catheter has been clamped.37 Normal abdominal pressures are 0-10 mm
Hg. Abdominal hypertension is defined
as an intracavitary pressure 12 mm Hg.
Finally, abdominal compartment syndrome includes a pressure 20 mm Hg
and at least 1 organ compromised.37
Normal values of intraabdominal pressure in the postpartum period are not
known. A recent publication involving
women after a cesarean section found
mean intraabdominal pressures of 6.4
5.2 mm Hg. Interestingly, and likely because of higher risk of third spacing, patients with preeclampsia who underwent a
cesarean section had mean values of 11 9
mm Hg.38
Once the diagnosis is established, most
patients will require surgical decompression, and the open abdomen may be
managed with a vacuum-assisted closure
or a Bogota bag or silo.37 Enteral feeding
and limitation of fluid therapy are beneficial. If fluids are required, the use of colloids (eg, albumin) is recommended
over crystalloids. Limited evidence suggests that temporal use of paralytic
agents while the abdomen is open may
help achieve primary fascial closure.39
Figure 3 summarizes the key aspects involved in the medical management of the
parturient at risk of massive hemorrhage.

Summary
Obstetric hemorrhage is one of the most
common causes of maternal morbidity
and mortality worldwide. Placental accretism, just like the patient described in

the vignette, is becoming increasingly


frequent and is responsible for most
cases of peripartum hysterectomy. Interventions that may limit transfusion requirements include normovolemic hemodilution, use of rFVIIa, selective
embolization of pelvic vessels by interventional radiology, and the use of the
cell saver intraoperatively. The use of
techniques like hypotensive resuscitation and the TEG should be limited to
centers with vast experience in the management of these complex patients. Current understanding of the mechanisms
of acute coagulopathy calls into question
the current transfusion guidelines in favor of massive transfusion protocols
based on hemostatic resuscitation. Prospective trials are required to validate the
efficacy of this approach. Obstetricians
should be familiar with current transfusion protocols.
f
REFERENCES
1. Kung HC, Hoyert DL, Xu JQ, Murphy SL.
Deaths: final data for 2005. Natl Vital Stat Rep
2008;56:1-120.
2. Kwee A, Bots ML, Visser GH, Bruinse HW.
Emergency peripartum hysterectomy: a prospective study in The Netherlands. Eur J Obstet
Gynecol Reprod Biol 2006;124:187-92.
3. Smith J, Mousa HA. Peripartum hysterectomy for primary postpartum haemorrhage: incidence and maternal morbidity. J Obstet
Gynaecol 2007;27:44-7.
4. Wu S, Kocherginsky M, Hibbard JU. Abnormal placentation: twenty-year analysis. Am J
Obstet Gynecol 2005;192:1458-61.
5. Baughman WC, Corteville JE, Shah RR. Placenta accreta: spectrum of US and MR imaging
findings. Radiographics 2008;28:1905-16.
6. Teo TH, Law YM, Tay KH, Tan BS, Cheah
FK. Use of magnetic resonance imaging in evaluation of placental invasion. Clin Radiol 2009;
64:511-6.
7. Dwyer BK, Belogolovkin V, Tran L, et al. Prenatal diagnosis of placenta accreta: sonography or magnetic resonance imaging? J Ultrasound Med 2008;27:1275-81.
8. Belfort MA. Placenta accreta. Publications
Committee, Society for Maternal-Fetal Medicine. Am J Obstet Gynecol 2010;203:430-9.
9. Eller AG, Bennett MA, Sharshiner M, et al.
Maternal morbidity in cases of placenta accreta
managed by a multidisciplinary care team compared with standard obstetric care. Obstet Gynecol 2011;117:331-7.
10. Harper LM, Odibo MO, Macones GA, Crane
JP, Cahill AG. Effect of placenta previa on fetal
growth. Am J Obstet Gynecol 2010;203:
330.e1-5.

Reviews

11. Catling S. Blood conservation techniques in


obstetrics: a UK perspective. Inter J Obstet Anesthesia 2007;16:241-9.
12. Robinson BK, Grobman WA. Effectiveness
of timing strategies for delivery of individuals
with placenta previa and accreta. Obstet Gynecol 2010;116:835-42.
13. Stafford IA, Dashe JS, Shivvers SA, Alexander JM, McIntire DD, Leveno KJ. Ultrasonographic cervical length and risk of hemorrhage
in pregnancies with placenta previa. Obstet Gynecol 2010;116:595-600.
14. Parekh N, Husaini SW, Russell IF. Caesarean section for placenta previa: a retrospective
study of anaesthetic management. Br J Anaesth 2000;84:725-30.
15. Ioscovich A, Mirochnitchenko E, Halpern S,
et al. Perioperative anaesthetic management of
high order repeat caesarean section: audit of
practice in a university affiliated medical center.
Int J Obstet Anesth 2009;18:314-9.
16. Levine AB, Kuhlman K, Bonn J. Placenta
accreta: a comparison of cases managed with
and without pelvic artery balloon catheters. J
Matern Fetal Med 1999;8:173-6.
17. Mok M, Heidemann B, Dundas K, Gillespie
I, Clark V. Interventional radiology in women
with suspected placenta accreta undergoing
cesarean section. Int J Obstet Anesthesia
2008;17:255-61.
18. Angstmann T, Gard G, Harrington T, Ward
E, Thomson A, Giles W. Surgical management
of placenta accreta: a cohort series and suggested approach. Am J Obstet Gynecol
2010;202:38.e1-9.
19. Zacharias N, Gei AF, Suarez V, et al. Balloon
tip catheter occlusion of the hypogastric arteries for the management of placenta accreta.
Am J Obstet Gynecol 2003;189:S128.
20. Tawes RL Jr. Clinical applications of autotransfusion. Semin Vas Surg 1994;7:89-90.
21. Rainaldi MP, Tazzari PL, Seagliarini G,
Borghi B, Conte P. Blood salvage during cesarean section. Br J Anaesth 1998;80:196-8.
22. Stanworth SJ, Birchall J, Doree CJ, Hyde C.
Recombinant factor VIIa for the prevention and
treatment of bleeding in patients without haemophilia. Cochrane Database Syst Rev
2007;18:CD005011.
23. Levi M, Levy JH, Andersen HF, Truloff D.
Safety of recombinant activated factor VII in randomized clinical trials. N Engl J Med 2010;
363:1791-9.
24. Spahn DR, Cerny V, Coats TJ, et al. Management of bleeding following major trauma: a
European guideline. Crit Care 2007;11:R17.
25. Johansson PI, Ostrowski SR, Secher NH.
Management of major blood loss: an update.
Acta Anaesthesiol Scand 2010;54:1039-49.
26. Nascimento B, Callum J, Rubenfeld G,
Neto JB, Lin Y, Rizoli S. Clinical review: fresh
frozen plasma in massive bleedings-more
questions than answers. Crit Care 2010;14:
2002.
27. Ickx BE. Fluid and blood transfusion management in obstetrics. Eur J Anaesthesiol
2010;27:1031-5.

DECEMBER 2011 American Journal of Obstetrics & Gynecology

531

Reviews

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28. Brohi K, Cohen MJ, Davenport RA. Acute


coagulopathy of trauma: mechanism, identification, and effect. Curr Opin Crit Care 2007;
13:680-5.
29. Cotton BA, Gunter OL, Isbell J, et al.
Damage control hematology: the impact of a
trauma exsanguination protocol on survival and
blood product utilization. J Trauma 2008;64:
1177-82.
30. Wafaisade A, Maegele M, Lefering R, et al.
High plasma to red blood cell ratios are associated with lower mortality rates in patients receiving multiple transfusion (4 red blood cell units
10) during acute trauma resuscitation.
J Trauma 2011;70:81-9.
31. Snyder CW, Weinberg JA, McGwin G, et al.
The relationship of blood product ratio to mortality: survival benefit or survival bias? J Trauma
2009;66:358-62.

532

www.AJOG.org
32. Scalea TM, Bochicchio KM, Lumpkins K, et
al. Early aggressive use of fresh frozen plasma
does not improve outcome in critically injured
trauma patients. Ann Surg 2008;248:578-84.
33. Rajasekhar A, Gowing R, Zarychanski R, et
al. Survival of trauma patients after massive red
blood cell transfusion using a high or low red
blood cell to plasma transfusion ratio. Crit Care
Med 2011;39:1507-13.
34. Gonzalez EA, Moore FA, Halcomb JB, et al.
Fresh frozen plasma should be given earlier to
patients requiring massive transfusion. J Trauma
2007;62:112-9.
35. Reikvam H, Steien E, Hauge B, et al.
Thromboelastography. Transfus Apher Sci
2009;40:119-23.
36. Brigitte EI. Fluid and blood transfusion management in obstetrics. Eur J Anaesthesiol
2010;27:1031-5.

American Journal of Obstetrics & Gynecology DECEMBER 2011

37. Cheatham ML. Abdominal compartment


syndrome. Curr Opin Crit Care 2009;15:
154-62.
38. Abdel-Razeq SS, Campbell K, Funai EF,
Kaplan LJ, Bahtiyar MO. Normative postpartum
intraabdominal pressure: potential implications
in the diagnosis of abdominal compartment
syndrome. Am J Obstet Gynecol 2010;203:
149.e1-4.
39. Abouassaly CT, Dutton WD, Zaydfudim V,
et al. Post operative neuromuscular blocker use
is associated with higher primary fascial closure
rates after damage control laparotomy.
J Trauma 2010;69:557-61.
40. Pacheco LD, Gei AF. Controversies in the
management of placenta accreta. Obstet Gynecol Clin North Am 2011 [in press].

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