Overview of postpartum hemorrhage

Author: Michael A Belfort, MBBCH, MD, PhD, FRCSC, FRCOG

Section Editor: Charles J Lockwood, MD, MHCM
Deputy Editor: Vanessa A Barss, MD, FACOG

Contributor Disclosures

All topics are updated as new evidence becomes available and our peer review process is
complete.

Literature review current through: Feb 2019. | This topic last updated: Jan 02, 2019.

INTRODUCTION

Postpartum hemorrhage (PPH) is an obstetric emergency. It is one of the top five

causes of maternal mortality in both high and low per capita income countries,
although the absolute risk of death from PPH is much lower in high-income
countries. Timely diagnosis, appropriate resources, and appropriate management
are critical for preventing death.

This topic will present an overview of major issues relating to PPH. Clinical use of
specific medical and minimally invasive interventions, and surgical interventions at
laparotomy, for management of PPH are discussed separately (See "Postpartum
hemorrhage: Medical and minimally invasive management" and "Postpartum
hemorrhage: Management approaches requiring laparotomy".)

TERMINOLOGY

PPH occurring in the first 24 hours after delivery may be called primary or early
PPH, and is the subject of this topic. PPH occurring from 24 hours to 12 weeks
after delivery is usually called secondary, late, or delayed PPH, and is discussed
separately. (See "Secondary (late) postpartum hemorrhage".)
DEFINITION/DIAGNOSIS

We make the diagnosis of PPH in postpartum women with bleeding that is greater
than expected and results in signs and/or symptoms of hypovolemia (table 1).
Diagnosis may be delayed in symptomatic women when bleeding is not observed,
such as intra-abdominal bleeding after a vaginal delivery or after closure of the
abdomen in a cesarean delivery.

Multiple other criteria for diagnosis of PPH are in use worldwide (table 2).
Although PPH is classically defined by the volume of blood loss (ie, estimated
blood loss ≥500 mL after vaginal birth or ≥1000 mL after cesarean delivery), this
diagnosis is problematic because the mean blood loss reported after vaginal and
cesarean deliveries is approximately 400 to 600 mL and 1000 mL, respectively [1-
3], bleeding may not be visible externally, or blood in collection devices may be
mixed with amniotic fluid.

In 2017, the American College of Obstetricians and Gynecologists revised their

definition of PPH from the classic one (≥500 mL after vaginal birth or ≥1000 mL
after cesarean delivery) to (1) cumulative blood loss ≥1000 mL or (2) bleeding
associated with signs/symptoms of hypovolemia within 24 hours of the birth
process regardless of delivery route in order to reduce the number of women
inappropriately labeled with this diagnosis [4].

INCIDENCE

The incidence of PPH varies widely, depending upon the criteria used to diagnose
the disorder. A reasonable estimate is 1 to 5 percent of deliveries [5,6]. In an
analysis of population-based data from the United States National Inpatient
Sample, the incidence was between 2 and 3 percent during the years 1994 to 2006
[7] and 3 percent in 2012 to 2013 [8].
PHYSIOLOGIC MECHANISMS THAT LIMIT POSTPARTUM BLOOD
LOSS

The potential for massive hemorrhage after delivery is high because, in late
pregnancy, uterine artery blood flow is 500 to 700 mL/min and accounts for
approximately 15 percent of cardiac output. Normally, hemostasis occurs upon
placental separation because uterine bleeding is controlled by a combination of
two mechanisms:

● Contraction of the myometrium, which compresses the blood vessels

supplying the placental bed and causes mechanical hemostasis.

● Local decidual hemostatic factors (tissue factor [9,10], type-1 plasminogen

activator inhibitor [11,12], systemic coagulation factors [eg, platelets,
circulating clotting factors]), which cause clotting.

The pathogenesis of most cases of PPH is a disturbance in one or both of these

mechanisms. The pathogenesis for most of the remaining PPH cases is loss of
intact vasculature (ie, trauma).

PATHOGENESIS

Focal or diffuse atony — The most common cause of PPH is uterine atony (ie, lack
of effective contraction of the uterus after delivery), which complicates 1 in 40
births in the United States and is responsible for at least 75 percent of cases of
PPH [8]. The diagnosis of atony is generally made when the uterus does not
become firm after routine management of the third stage of labor (ie, uterine
massage and oxytocin). Atony may or may not be associated with retained tissue.
Placental disorders (eg, morbidly adherent placenta, placenta previa, abruptio
placentae), retained products of conception, and uterine inversion result in PPH
because they inhibit effective uterine contraction, either focally or diffusely.
With diffuse atony, blood loss can be much greater than observed because a
flaccid and dilated uterus may contain a significant amount of blood. With focal
localized atony, the fundal region may be well contracted while the lower uterine
segment is dilated (ballooning) and atonic, which is difficult to appreciate on
abdominal examination, but may be detected on vaginal examination.

Although diffuse uterine atony is the most common cause of PPH, it is often
responsive to administration of additional uterotonic drugs; thus, it is not the most
common reason for massive transfusion at delivery [13].

Trauma — Trauma-related bleeding can be due to lacerations (including uterine

rupture) or surgical incisions.

Cervical and vaginal lacerations may develop as a result of the natural processes
of delivery or may be related to provider interventions. They may not be noted until
excessive postpartum vaginal bleeding prompts lower genital tract examination,
including examination for vaginal and vulvar hematomas.

Corpus lacerations may be complete transmyometrial ruptures or incomplete

lacerations of the inner myometrium [14]. (See "Uterine rupture: Unscarred uterus"
and "Uterine rupture: After previous cesarean delivery".)

At cesarean delivery, hemorrhage from the uterine incision is generally caused by

lateral extension of the incision, which can result from spontaneous tearing of an
edematous lower segment during an otherwise uneventful cesarean delivery after
prolonged labor, from an incision made too low or not sufficiently curved on the
lower segment, or from delivery of the fetus through an incision that is too small.
Bleeding from lateral extension of the uterine incision is readily ascertained by
inspection of the incision, lateral pelvic sidewalls, and broad ligament.
Retroperitoneal enlargement and bulging of the broad ligament at cesarean
delivery can be signs of retroperitoneal hemorrhage.
Coagulopathy — Coagulopathy is a cause of PPH in women with an inherited or
acquired bleeding diathesis, and a result of PPH when there is a severe reduction
of clotting factors due to persistent heavy bleeding and hemodilution of the
remaining clotting factors. Acute coagulopathies can be caused by amniotic fluid
embolism, placental abruption, preeclampsia with severe features, or HELLP
syndrome.

RISK FACTORS AND SPECIFIC ETIOLOGIES

Many risk factors for PPH have been reported and are often interdependent. The
types and frequencies are illustrated by the following large series:

● In a study including over 154,000 deliveries that compared 666 cases of PPH
to controls without hemorrhage, factors significantly associated with
hemorrhage were, in decreasing order of frequency [15]:

• Retained placenta/membranes (odds ratio [OR] 3.5, 95% CI 2.1-5.8)

• Failure to progress during the second stage of labor (OR 3.4, 95% CI 2.4-
4.7)

• Morbidly adherent placenta (OR 3.3, 95% CI 1.7-6.4)

• Lacerations (OR 2.4, 95% CI 2.0-2.8)

• Instrumental delivery (OR 2.3, 95% CI 1.6-3.4)

• Large for gestational age newborn (eg, >4000 g) (OR 1.9, 95% CI 1.6-2.4)

• Hypertensive disorders (preeclampsia, eclampsia, HELLP [Hemolysis,

Elevated Liver enzymes, Low Platelets]) (OR 1.7, 95% CI 1.2-2.1)

• Induction of labor (OR 1.4, 95% CI 1.1-1.7)

Prolonged first or second stage of labor (OR 1.4, 95% CI 1.2-1.7)

 ● In a• study including over 690,000 deliveries, the four risk factors associated
with the highest odds for predicting the need for massive transfusion (n =
406) during hospitalization for delivery were [16]:

• Abnormal placentation (placenta accreta or previa) (1.6/10,000

deliveries, adjusted OR [aOR] 18.5, 95% CI 14.7-23.3)

• Placental abruption (1.0/10,000 deliveries, aOR 14.6, 95% CI 11.2-19.0)

• Severe preeclampsia (0.8/10,000 deliveries, aOR 10.4, 95% CI 7.7-14.2)

• Intrauterine fetal demise (0.7/10,000 deliveries, aOR 5.5, 95% CI 3.9-7.8)

Other purported risk factors include: personal or family history of previous PPH
(see 'Recurrence' below), obesity, high parity, Asian or Hispanic race, precipitous
labor, uterine overdistention (eg, multiple gestation, polyhydramnios, macrosomia),
chorioamnionitis, uterine inversion, leiomyoma, Couvelaire uterus, inherited
bleeding diathesis, acquired bleeding diathesis (eg, amniotic fluid embolism,
abruptio placentae, sepsis, fetal demise), assisted reproductive technology, and
use of some drugs (uterine relaxants, antithrombotic drugs, possibly
antidepressants) [13,17-27].

Although there are many known risk factors for PPH, knowledge of these risk
factors is not always clinically useful for prevention of hemorrhage.

ASSESSMENT OF SEVERITY OF HEMORRHAGE

Significant drops in blood pressure are generally not manifested until substantial
bleeding has occurred, and up to 25 percent of a patient's blood volume (≥1500
mL in pregnancy) can be lost before blood pressure falls and heart rate rises [28].
Hemoglobin and hematocrit values are poor indicators of acute blood loss since
they may not decline immediately after an acute bleed. However, a low fibrinogen
level (less than 200 mg/dL) is predictive of severe PPH defined as need for
transfusion of multiple units of blood and blood products, need for angiographic
embolization or surgical management of hemorrhage, or maternal death. (See
"Postpartum hemorrhage: Medical and minimally invasive management", section
on 'Laboratory evaluation'.)

California maternal quality care collaborative staging system — The California

Maternal Quality Care Collaborative OB Hemorrhage Protocol describes the
following stages of PPH [29]:

● Stage 0: Blood loss <500 mL with vaginal delivery or <1000 mL with cesarean
delivery. Stable vital signs.

● Stage 1: Blood loss >500 mL vaginal delivery or >1000 mL cesarean delivery

or change in vital signs (by >15 percent or heart rate ≥110 beats/minute,
blood pressure ≤85/45 mmHg, O2 saturation <95%)

● Stage 2: Continued bleeding with total blood loss <1500 mL

● Stage 3: Continued bleeding with total blood loss >1500 mL or transfusion of

more than 2 units packed red blood cells or unstable vital signs or suspicion
of disseminated intravascular coagulation

Advanced trauma life support classification — The Advanced Trauma Life Support

manual describes four classes of hemorrhage to emphasize the progressive signs
and symptoms leading to the shock state [30]. The following classes were derived
from nonpregnant populations and may be somewhat different in postpartum
women:

● Class I hemorrhage involves a blood volume loss of up to 15 percent. The

heart rate is minimally elevated or normal, and there is no change in blood
pressure, pulse pressure, or respiratory rate.

● Class II hemorrhage occurs when there is a 15 to 30 percent blood volume

loss and is manifested clinically as tachycardia (heart rate of 100 to 120),
 tachypnea (respiratory rate of 20 to 24), and a decreased pulse pressure,
although systolic blood pressure changes minimally if at all. The skin may be
cool and clammy, and capillary refill may be delayed. An increasing maternal
heart rate and tachypnea with stable systolic blood pressure should be
regarded as evidence of compensated shock and should prompt investigation
and institution of a PPH protocol, even if only light vaginal bleeding is
observed.

● Class III hemorrhage involves a 30 to 40 percent blood volume loss, resulting

in a significant drop in blood pressure and changes in mental status. Any
hypotension (systolic blood pressure less than 90 mmHg) or drop in blood
pressure greater than 20 to 30 percent of the measurement at presentation is
cause for concern. While diminished anxiety or pain may contribute to such a
drop, the clinician must assume it is due to hemorrhage until proven
otherwise. Heart rate (≥120 and "thready") and respiratory rate are markedly
elevated, while urine output is diminished. Capillary refill is delayed.

● Class IV hemorrhage involves more than 40 percent blood volume loss

leading to significant depression in blood pressure and mental status. Most
patients in class IV shock are hypotensive (systolic blood pressure less than
90 mmHg). Pulse pressure is narrowed (≤25 mmHg), and tachycardia is
marked (>120). Urine output is minimal or absent. The skin is cold and pale,
and capillary refill is delayed.

Differential diagnosis of mild hemodynamic instability — Although vasodilatation

due to neuraxial anesthesia and vasovagal reactions may result in
lightheadedness/syncope, tachycardia, and hypotension, these entities are less
likely postpartum than PPH, and they are readily reversible and generally not
dangerous. Lightheadedness, tachycardia, or hypotension is unlikely to be due to
neuraxial anesthesia if the woman was hemodynamically stable prior to delivery,
the level of the block did not become significantly higher immediately following
delivery, and symptoms did not abruptly follow systemic administration of a drug
known to cause hypotension. (See "Adverse effects of neuraxial analgesia and
anesthesia for obstetrics", section on 'Hypotension'.)

PLANNING

Management of risk — Women with risk factors for PPH should be identified and
counseled as appropriate for their level of risk and gestational age (see 'Risk
factors and specific etiologies' above).

Planning for these patients involves ensuring availability of resources that might
be needed, including personnel, medication, equipment, adequate intravenous
access, and blood products. For example, the American College of Obstetricians
recommends that women identified prenatally as high risk for PPH (eg, placenta
accreta spectrum, prepregnancy body mass index >50, clinically significant
bleeding disorder, or other surgical/medical high risk factor) should plan to be
delivered in a facility that has an appropriate level of care for their needs [31].

Intrapartum, blood should be typed and screened for women with a medium risk
factor for PPH (eg, prior uterine surgery, multiple gestation, grand multiparity, prior
PPH, large fibroids, macrosomia, body mass index >40, anemia, chorioamnionitis,
prolonged second stage, oxytocin >24 hours, magnesium sulfate administration)
and typed and crossmatched for those at high risk of PPH (eg, placental previa or
accreta, bleeding diathesis, two or more medium risk factors for PPH). Use of a
cell saver (blood salvage) should be considered for women at increased risk of
PPH, but is not cost-effective as a routine in all cesarean deliveries [32]. (See
"Postpartum hemorrhage: Management approaches requiring laparotomy", section
on 'Role of intraoperative cell salvage'.)

Routine prophylactic use of uterotonic drugs, such as oxytocin, reduces the risk of
PPH by 50 percent in the overall obstetric population [33]. Prophylactic
administration of tranexamic acid is under investigation [34]. (See "Management
of the third stage of labor: Drug therapy to minimize hemorrhage" and "Postpartum
hemorrhage: Medical and minimally invasive management", section on 'Administer
tranexamic acid'.)

Specific interventions are available for managing risk in women when the
following conditions are identified antenatally:

● Abnormal placentation (see "Management of the placenta accreta spectrum

(placenta accreta, increta, and percreta)" and "Placenta previa: Management").

● Bleeding diatheses (see "Treatment of von Willebrand disease", section on

'Pregnancy and delivery' and "Clinical manifestations and diagnosis of
hemophilia", section on 'Obstetrical issues' and "Use of anticoagulants during
pregnancy and postpartum", section on 'Labor and delivery' and
"Thrombocytopenia in pregnancy" and "Thrombocytopenia in pregnancy",
section on 'Management decisions').

However, for most patients, knowledge of risk factors for PPH is not useful
clinically because only a small proportion of at-risk women develop PPH
(abnormal placentation is an exception) and many women without risk factors
experience PPH [25,35]. As an example, the California quality improvement toolkit
classifies patients as low, medium, or high risk for PPH:

● Low risk

• Singleton pregnancy

• Fewer than four previous deliveries

• No previous uterine surgery

• No history of PPH

● Medium risk
 • Prior uterine surgery

• More than four previous deliveries

• Multiple gestation

• Large fibroids

• Chorioamnionitis

• Magnesium sulfate or prolonged oxytocin infusion

● High risk

• Morbidly adherent placenta

• Hematocrit <30 percent

• Bleeding at admission

• Bleeding diathesis/coagulation defect

• History of PPH

• Tachycardia, hypotension

In a validation study, the incidence of severe PPH (ie, necessitating transfusion) in

the three groups was 0.8, 2.0, and 7.3 percent, respectively, and only 22 percent of
severe PPH cases occurred in the high-risk group [35].

PPH protocols and algorithms — Ideally, each hospital labor and delivery unit
should have a PPH protocol. The protocol should provide a standardized approach
to evaluating and monitoring the patient with PPH, notifying a multidisciplinary
team, and treatment. Development and consistent application of a comprehensive
protocol for management of PPH appears to result in improved outcomes for
these women [36-38]. In an observational study, the initiation of a PPH protocol
was associated with resolution of maternal bleeding at an earlier stage, use of
fewer blood products, and a 64 percent reduction in the rate of disseminated
intravascular coagulation [39].

Some graphic examples of PPH protocols are provided below:

● Texas Children’s Hospital flowchart (algorithm 1A).

● American College of Obstetricians and Gynecologists four-stage system for

classifying PPH, and checklist of appropriate interventions at each stage.

● The California Maternal Quality Care Collaborative provides comprehensive

information in several formats for management of PPH.

Massive transfusion is often required with severe PPH, and can be facilitated by
use of an algorithm (algorithm 1B)

PPH kits — In addition to a protocol, it is useful for labor and delivery units to
assemble kits that contain medications and instruments that may be needed to
manage PPH so that these resources are readily available when needed (similar to
a "code cart") (table 3).

Training and simulation — The Joint Commission recommends that obstetrical

staff [40]:

● Undergo team training to teach staff to work together and communicate more
effectively when PPH occurs

● Conduct clinical drills to help staff prepare for PPH, and

● Conduct debriefings after PPH to evaluate team performance and identify

areas for improvement

Simulation team training can help to identify areas that need practice, and regular
unannounced simulated PPH scenarios in a real-life setting, such as the labor and
delivery unit or post-anesthesia care unit, may also increase comfort with the
protocols and teamwork required in such emergencies. (See "Reducing adverse
obstetrical outcomes through safety sciences", section on 'Postpartum
hemorrhage'.)

GENERAL PRINCIPLES OF MANAGEMENT

Objective measurement of blood loss — Once PPH is suspected, or in those cases

where there is a high probability that PPH will occur, objective quantitative
measurement of blood loss should be initiated. This is an important factor for
early recognition of excessive blood loss and timely initiation of life-saving
interventions [41-43]:

● Collect blood in graduated measurement containers, including drapes with

calibrated pockets.

● Use visual aids (eg, posters) that correlate the size and appearance of blood
on specific surfaces (eg, maternity pad, bed sheet, lap sponge) with the
volume of blood absorbed by that surface (picture 1). Regularly scheduling
standardized training in the use of these charts can be helpful for this
assessment.

● Measure the total weight of bloody materials and subtract the known weight
of the same materials when dry. The difference in weight between wet and dry
in grams approximates the volume of blood in milliliters.

A systematic review concluded evidence was insufficient to support the use of

one method over another for estimating blood loss after vaginal birth [44]. For all
of these methods, the clinician should attempt to account for fluids other than
blood (eg, amniotic fluid, irrigation fluid, urine) that are collected or absorbed.
Timely diagnosis and early intervention — Timeliness in recognition of PPH,
determining the cause, and initiating treatment is critical, as almost 90 percent of
deaths due to PPH occur within four hours of giving birth [45,46]. It is important to
not allow the patient to become moribund before initiating life-saving measures.
Early intervention may prevent shock (inadequate perfusion and oxygenation of
tissues) and the development of the potentially lethal triad of hypothermia,
acidosis, and coagulopathy. These interventions are described separately. (See
"Postpartum hemorrhage: Medical and minimally invasive management".)

Teamwork — In the author's opinion, clinical training programs that encourage a

team approach for early recognition of PPH can improve outcomes by engaging
the necessary providers before hypovolemia and uncompensated shock occur.
Obstetricians, midwives, nurses, anesthesiologists, hematologists/blood bank
personnel, laboratory medicine, surgical subspecialists (eg, vascular, urology), and
interventional radiologists may be involved in managing PPH [47]. These
individuals are often summoned and required to work together under conditions of
great stress and time pressures. Coordination is essential and can be facilitated
by protocols and flow diagrams that anticipate how the team will communicate
and function together.

Monitor bleeding, vital signs, and laboratory results — Close maternal monitoring

is critical to assess the best approach to and aggressiveness of intervention, and
requires bedside evaluation by the provider. Laboratory evaluation includes
complete blood count, coagulation studies, potassium and ionized calcium levels.
(See "Postpartum hemorrhage: Medical and minimally invasive management",
section on 'Laboratory evaluation'.)

Treatment goals — Treatment goals are to:

● Restore or maintain adequate circulatory volume to prevent hypoperfusion of

vital organs
 ● Restore or maintain adequate tissue oxygenation

● Reverse or prevent coagulopathy

● Eliminate the obstetric cause of PPH

Treatment approach — Potential interventions for management of PPH are listed

in the table (table 4) and discussed below.

Consider the cause and severity of bleeding, and need for laparotomy — The
treatment approach is based on a combination of factors, including the cause and
severity of bleeding and whether the abdomen is already open for cesarean
delivery. The four most common causes can be considered using the Four T’s
mnemonic: Tone: uterine atony; Trauma: laceration, hematoma, inversion, rupture;
Tissue: retained tissue or invasive placenta; and Thrombin: coagulopathy [48].

● Treatment of atony, the most common cause of PPH, is influenced by both the
route of delivery and severity of bleeding (table 5). After a vaginal birth,
treatment of atony begins with uterotonic drugs and minimally invasive
procedures (eg, intrauterine balloon tamponade) and progresses to more
invasive procedures (eg, uterine artery embolization) until hemorrhage is
controlled. It is usually possible and desirable to avoid laparotomy and its
associated morbidity. (See "Postpartum hemorrhage: Medical and minimally
invasive management", section on 'Manage atony'.)

Uterotonic drugs are also used to treat atony at cesarean delivery, but since
the abdomen is already open, surgical procedures to control bleeding
requiring laparotomy (eg, uterine artery and utero-ovarian artery ligation,
uterine compression sutures) are employed much sooner than after a vaginal
delivery, and uterine artery embolization is considered if these procedure fail.
(See "Postpartum hemorrhage: Management approaches requiring
laparotomy".)
 The obstetrical provider should initiate a sequence of nonoperative and
operative interventions for control of PPH and promptly assess the success
or failure of each measure. If an intervention does not succeed, the next
treatment in the sequence must be swiftly instituted. Indecisiveness delays
therapy and results in excessive hemorrhage, which eventually causes
dilutional coagulopathy and severe hypovolemia, tissue hypoxia, hypothermia,
and acidosis. This will make control of hemorrhage much more difficult and
will increase the likelihood of hysterectomy, major morbidity from
hemorrhagic shock, and death.

● Traumatic, hemorrhaging lacerations need to be controlled surgically, either

transvaginally or transabdominally.

● Retained placental tissue needs to be identified and removed. Placenta

accreta spectrum generally requires hysterectomy. (See "Retained placenta
after vaginal birth" and "Management of the placenta accreta spectrum
(placenta accreta, increta, and percreta)".)

● Coagulopathy is treated medically, with transfusion of blood and blood

products.

● Early administration of tranexamic acid, an anti-fibrinolytic drug, can reduce

death due to bleeding in women with postpartum hemorrhage related to atony
or trauma. (See "Postpartum hemorrhage: Medical and minimally invasive
management", section on 'Administer tranexamic acid'.)

Approach to hemodynamically unstable patients — When hemorrhage is

suspected as the cause of hemodynamic instability, initial (and expedited)
management with blood and blood products is advised (as opposed to large
volume crystalloid infusion). Hypovolemic hemorrhagic shock is treated with
aggressive volume resuscitation with packed red cells and other appropriate blood
products. Transfusion should keep up with blood loss, with early activation of a
protocol for large volume transfusion in those patients with heavy bleeding.
Development of a standardized institutional approach to massive transfusion
improves outcome (algorithm 1B). There are no data from clinical trials of PPH to
help guide management of transfusion specifically in PPH [49] (see "Postpartum
hemorrhage: Medical and minimally invasive management", section on 'Transfuse
red blood cells, platelets, plasma'). Management of patients who refuse to accept
blood transfusion is addressed separately. (See "The approach to the patient who
declines blood transfusion".)

In addition, the author believes early recourse to intrauterine balloon tamponade

can be useful to decrease ongoing uterine blood loss following vaginal delivery or
after the abdomen is closed following cesarean delivery, and that this measure will
allow additional time for assessment and evaluation, stabilization, and institution
of resuscitative procedures. In those women who continue to bleed at the time of
cesarean and the abdomen is still open, compression sutures and
devascularization are more easily accomplished than placing a tamponade
balloon, and if all else fails hysterectomy remains the definitive treatment. (See
"Postpartum hemorrhage: Management approaches requiring laparotomy", section
on 'Intrauterine balloon tamponade' and "Postpartum hemorrhage: Medical and
minimally invasive management", section on 'Perform uterine tamponade in
patients with atony or lower segment bleeding'.)

If the patient is coagulopathic with an extremely low fibrinogen level (50 to 100
mg/dL), cryoprecipitate and other high-concentration fibrinogen products (eg,
fibrinogen concentrate) are indicated since fresh frozen plasma alone will not
increase the fibrinogen level to the normal range without requiring excessive
volume infusion. (See "Postpartum hemorrhage: Medical and minimally invasive
management", section on 'Correct clotting factory deficiencies' and "Plasma
derivatives and recombinant DNA-produced coagulation factors" and "Postpartum
hemorrhage: Management approaches requiring laparotomy", section on
'Evaluation of the abdomen'.)
Under most circumstances, an acutely unstable and/or coagulopathic patient
should receive temporizing measures such as bimanual uterine compression,
balloon tamponade, aortic compression, transfusion of blood products, and
possibly a high coagulation factor concentrate (eg, fibrinogen concentrate,
prothrombin complex concentrate) to allow resuscitation to a point where general
anesthesia and surgery are better tolerated. Unless absolutely necessary,
emergency hysterectomy should be avoided in a coagulopathic patient with
inadequate intravenous access for massive transfusion/correction of electrolyte
imbalances, as major surgery in this setting may cause further deterioration in
maternal status as a result of uncontrolled retroperitoneal hemorrhage and
myocardial depression. (See "Postpartum hemorrhage: Management approaches
requiring laparotomy", section on 'Temporary measures for stabilizing
hemodynamically unstable patients' and "Postpartum hemorrhage: Management
approaches requiring laparotomy".)

Early resort to hysterectomy is appropriate in women with severe bleeding due to

diffuse placenta accreta/increta/percreta or a large uterine rupture. In contrast,
hysterectomy is generally a last resort in patients with atony, as these patients can
often be managed successfully with medical therapy and less aggressive surgical
interventions. However, hysterectomy should not be delayed in those who have
depleted their clotting factors and require prompt control of uterine hemorrhage to
prevent death. (See "Postpartum hemorrhage: Management approaches requiring
laparotomy", section on 'Role of hysterectomy'.)

Approach to hemodynamically stable patients — For hemodynamically stable

patients in whom the capacity for blood replacement exceeds that of the ongoing
hemorrhage, arterial embolization is an effective treatment for persistent bleeding.
In a systematic review of 20 observational studies, a single procedure completely
arrested bleeding in 89 percent of cases, re-embolization was necessary in 4
percent, and hysterectomy was required in 7 percent, primarily after embolization
failure [50]. Sixty-two percent of the patients in these studies were post cesarean
delivery.

Generally, arterial embolization should not be attempted in unstable patients who

have to be transferred to a radiology suite for the procedure and should not be
considered an emergency procedure for managing uncontrolled PPH of
indeterminate cause. (See "Postpartum hemorrhage: Management approaches
requiring laparotomy" and "Postpartum hemorrhage: Medical and minimally
invasive management", section on 'Consider uterine or hypogastric artery
embolization'.)

MORBIDITY AND MORTALITY

Maternal mortality — Maternal mortality after PPH averages approximately 2

percent, with wide variations worldwide depending on both the overall health of
pregnant women in the population and the resources for treatment of PPH [51].
Death rates vary from 0.6 percent in the United Kingdom to 20 percent in parts of
Africa, and from 1 in 100,000 deliveries in the United Kingdom versus 1 in 1000
deliveries in parts of the developing world. Women who are anemic at delivery due
to poor nutrition or malaria are particularly vulnerable to severe sequelae of PPH.

Transfusion — In a trial including over 20,000 women worldwide with PPH

(WOMAN), 54 percent received a blood transfusion [52]. By comparison, the rate
of transfusion in the overall obstetric population of the United States is 4 to 7 per
1000 deliveries [8,53] and the frequency of transfusion in PPH deliveries was 16
percent in 2012-2013 [8]. Risks of transfusion include infection, electrolyte
abnormalities, allergic reactions, alloimmunization, and volume overload. (See
"Indications and hemoglobin thresholds for red blood cell transfusion in the adult",
section on 'Risks and complications of transfusion'.)
Hysterectomy — In the WOMAN trial described above, 3.5 percent of women
underwent peripartum hysterectomy because of PPH [52]. In the United States, 2.5
percent of women with PPH underwent hysterectomy in 2012-2013 [8].
Hysterectomy was more common in PPH without atony than with atony (6.6
versus 1.0 percent).

Thromboembolism — In the WOMAN trial described above, 0.3 percent of women

with PPH had thromboembolic event (deep vein thrombosis, pulmonary embolus,
stroke, myocardial infarction) within 42 days of delivery [52].

Thromboembolism prophylaxis — In trauma patients, transfusion is an

independent risk factor for development of thromboembolism [54]. For this
reason, all women who have been transfused for PPH should receive mechanical
thromboprophylaxis (graduated compression stockings or pneumatic
compression device) as soon as feasible and continue thromboprophylaxis until
discharge [55]. Twelve to 24 hours after bleeding has been controlled,
pharmacologic thromboprophylaxis should be added, providing coagulation tests
are normal or close to normal. (See "Use of anticoagulants during pregnancy and
postpartum".)

Hemodynamic instability and organ failure — In the WOMAN trial described above,
60 percent of women with PPH had clinical signs of hemodynamic instability at
diagnosis of PPH and almost 4 percent developed renal failure, heart failure,
respiratory failure, or hepatic failure [52]. Treatment of hemodynamic instability
with fluids and blood can lead to volume overload, resulting in pulmonary edema
and dilutional coagulopathy.

Sheehan syndrome — Sheehan syndrome (ie, postpartum hypopituitarism) is a

rare but potentially life-threatening complication. The pituitary gland is enlarged in
pregnancy and prone to infarction from hypovolemic shock. Damage to the
pituitary can be mild or severe, and can affect the secretion of one, several, or all
of its hormones. A common presentation is a combination of failure to lactate
postdelivery and amenorrhea or oligomenorrhea, but any of the manifestations of
hypopituitarism (eg, hypotension, hyponatremia, hypothyroidism) can occur any
time from the immediate postpartum period to years after delivery. If the patient
remains hypotensive after control of hemorrhage and volume replacement, she
should be evaluated and treated for adrenal insufficiency immediately; evaluation
of other hormonal deficiencies can be deferred until four to six weeks postpartum.
This evaluation is described in detail separately. (See "Clinical manifestations of
hypopituitarism" and "Diagnostic testing for hypopituitarism".)

Treatment is also reviewed separately. (See "Treatment of hypopituitarism".)

Abdominal compartment syndrome — Abdominal compartment syndrome (organ

dysfunction caused by intraabdominal hypertension) is a rare but life-threatening
complication of PPH with intraabdominal bleeding. The diagnosis should be
considered in patients with a tensely distended abdomen and progressive oliguria
who are developing multiorgan failure. Of note, the normal postpartum patient
after cesarean delivery has been reported to have an intraabdominal pressure that
approaches that seen in abdominal compartment syndrome in nonpregnant
individuals [56].

Clinical presentation, diagnosis, and management are discussed in detail

separately. (See "Abdominal compartment syndrome in adults".)

Asherman syndrome — Development of intrauterine adhesions (termed Asherman

syndrome) can lead to menstrual abnormalities and infertility. Approximately 90
percent of cases of severe intrauterine adhesive disease are related to uterine
curettage for pregnancy complications, such as PPH [57,58]. Uterine compression
sutures used to treat PPH have also been associated with the development of
intrauterine adhesions [59-62].

Treatment is discussed separately. (See "Intrauterine adhesions: Clinical

manifestation and diagnosis".)
Severe postpartum anemia — Postpartum anemia is common: One classic criteria
for PPH was a 10-point decline in postpartum hematocrit concentration from
antepartum levels. Postpartum anemia can also be defined as a hemoglobin level
of <11 g/dL at 1 week postpartum and <12 g/dL at 8 weeks postpartum [63].

● Treatment – Severe anemia due to PPH may require red cell transfusions,
depending on the severity of anemia and the degree of symptomatology
attributable to anemia. A common practice is to offer a transfusion to
symptomatic women with a hemoglobin value <7 g/dL [4]. (See "Indications
and hemoglobin thresholds for red blood cell transfusion in the adult".)

In most cases of PPH, the amount of iron lost is not fully replaced by the
transfused blood. Oral iron should lead to a modest reticulocytosis beginning
in approximately seven days and a rise in the hemoglobin concentration of
approximately 2 g/dL over the ensuing three weeks. Single dose parenteral
iron therapy is another option; advantages are that hemoglobin levels rise
faster, symptoms of anemia improve sooner, and less gastric upset occurs
compared with oral therapy [64]. Nevertheless, most women with mild to
moderate anemia resolve the anemia sufficiently rapidly with oral iron and it is
cheap and convenient [65-67]. A ferritin level at approximately six weeks
postpartum helps to guide iron therapy. Treatment of iron deficiency anemia
is discussed in detail separately. (See "Treatment of iron deficiency anemia in
adults".)

Although erythropoietin can increase the rate of recovery to normal

hemoglobin levels, it does not have an immediate effect and has not been
proven to reduce transfusion requirements after PPH [68]. It is no more
effective than iron therapy in this setting [69], and it is expensive. However, for
the few women with severe anemia who do not respond to iron therapy
because of blunted erythropoiesis due to infection and/or inflammation, some
 hematologists consider recombinant human erythropoietin an alternative to
transfusion [63].

RECURRENCE

Women with a prior PPH have as much as a 15 percent risk of recurrence in a

subsequent pregnancy [70,71]. The risk of recurrence depends, in part, on the
underlying cause (eg, the risk of recurrent abruption is 5 to 15 percent).

PPH alone is not a strong indication for screening for inherited bleeding diatheses,
given that undiagnosed bleeding disorders are rarely the cause of PPH. As an
example, one study of 50 women with PPH who underwent postpartum screening
identified a bleeding diathesis in only one woman [72]. However, unexplained PPH
that does not respond to general measures should alert clinicians to the possibility
of a bleeding disorder as a causative factor [73], especially in women with a
history of menorrhagia, excessive bleeding after minor trauma, or a family history
of a bleeding disorder. (See "Approach to the adult with a suspected bleeding
disorder".)

PREVENTION

Active management of the third stage of labor can reduce the incidence of PPH
due to atony. (See "Management of the third stage of labor: Drug therapy to
minimize hemorrhage".)

SOCIETY GUIDELINE LINKS

Links to society and government-sponsored guidelines from selected countries

and regions around the world are provided separately. (See "Society guideline
links: Obstetric hemorrhage".)
INFORMATION FOR PATIENTS

UpToDate offers two types of patient education materials, "The Basics" and
"Beyond the Basics." The Basics patient education pieces are written in plain
language, at the 5th to 6th grade reading level, and they answer the four or five key
questions a patient might have about a given condition. These articles are best for
patients who want a general overview and who prefer short, easy-to-read
materials. Beyond the Basics patient education pieces are longer, more
sophisticated, and more detailed. These articles are written at the 10th to 12th
grade reading level and are best for patients who want in-depth information and
are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We
encourage you to print or e-mail these topics to your patients. (You can also locate
patient education articles on a variety of subjects by searching on "patient info"
and the keyword(s) of interest.)

● Basics topic (see "Patient education: Postpartum hemorrhage (The Basics)")

SUMMARY AND RECOMMENDATIONS

● Primary PPH occurs in the first 24 hours after delivery (also called early PPH),
and secondary PPH occurs 24 hours to 12 weeks after delivery (also called
late or delayed PPH). (See 'Terminology' above.)

● The most common causes of PPH are atony (which may be related to
placental disorders), trauma, and acquired or congenital coagulation defects.

● We make the diagnosis of PPH in postpartum women with bleeding that is

greater than expected and results in signs and/or symptoms of hypovolemia
(table 1). Diagnosis may be delayed in symptomatic women when bleeding is
not observed, such as intra-abdominal bleeding after a vaginal delivery or
 after closure of the abdomen in a cesarean delivery. (See
'Definition/diagnosis' above.)

● Significant drops in blood pressure are generally not manifested until

substantial bleeding has occurred, and up to 25 percent of a patient's blood
volume (≥1500 mL in pregnancy) can be lost before blood pressure falls and
heart rate rises. Hemoglobin and hematocrit values are poor indicators of
acute blood loss, but a low fibrinogen level (less than 200 mg/dL) is predictive
of severe PPH defined as need for transfusion of multiple units of blood and
blood products, need for angiographic embolization or surgical management
of hemorrhage, or maternal death. (See 'Assessment of severity of
hemorrhage' above.)

● Women with risk factors for PPH should be identified when possible, and
counseled as appropriate for their level of risk and gestational age (see 'Risk
factors and specific etiologies' above). Planning for these patients involves
ensuring availability of resources that might be needed, including personnel,
medications, equipment, adequate intravenous access, and blood products.
Coordination is essential and can be facilitated by use of graphic protocols
(eg, (algorithm 1A-B)), availability of PPH kits (table 3), and
training/simulation. (See 'Planning' above.)

● Routine prophylactic use of uterotonic drugs, such as oxytocin, reduces the

risk of PPH by 50 percent in the overall obstetric population. Specific
interventions are available for managing risk in women with abnormal
placentation or bleeding diatheses. For most patients, knowledge of risk
factors for PPH is not useful clinically because only a small proportion of at-
risk women develop PPH (abnormal placentation is an exception) and many
women without risk factors experience PPH. (See 'Management of risk'
above.)
 ● Many interventions are available for management of PPH (table 4). The
approach to management of PPH varies depending on the cause and severity
of bleeding (table 5) and whether the patient has had a vaginal birth or
cesarean delivery. Traumatic, hemorrhaging lesions are managed surgically
and coagulopathy is managed medically, with replacement of blood products.
The treatment of atony depends on the route of delivery, as there is less
concern about the morbidity of open operative interventions when the
patient's abdomen is already open. (See 'General principles of management'
above.)

● We treat patients with mild to moderate postpartum anemia with an oral

rather than a parenteral iron preparation. Oral treatment is more convenient,
cheaper, and not associated with severe side effects. Severe anemia may
require transfusion. (See 'Severe postpartum anemia' above.)

● Women with a prior PPH have as much as a 15 percent risk of recurrence in a

subsequent pregnancy. PPH alone is not a strong indication for screening for
inherited bleeding diatheses, given that undiagnosed bleeding disorders are
rarely the cause of PPH. However, unexplained PPH that does not respond to
general measures should alert clinicians to the possibility of a bleeding
disorder as a causative factor, especially in women with a history of
menorrhagia, excessive bleeding after minor trauma, or a family history of a
bleeding disorder. (See 'Recurrence' above.)

ACKNOWLEDGMENT

The author and UpToDate would like to acknowledge Dr. Allan J Jacobs, who
contributed to earlier versions of this topic review.

REFERENCES
 1. Andolina K, Daly S, Roberts N, et al. Objective measurement of blood loss at
delivery: is it more than a guess. Am J Obstet Gynecol 1999; 180:S69.

2. Ueland K. Maternal cardiovascular dynamics. VII. Intrapartum blood volume

changes. Am J Obstet Gynecol 1976; 126:671.

3. Stafford I, Dildy GA, Clark SL, Belfort MA. Visually estimated and calculated
blood loss in vaginal and cesarean delivery. Am J Obstet Gynecol 2008;
199:519.e1.

4. Committee on Practice Bulletins-Obstetrics. Practice Bulletin No. 183:

Postpartum Hemorrhage. Obstet Gynecol 2017; 130:e168.

5. Lu MC, Fridman M, Korst LM, et al. Variations in the incidence of postpartum

hemorrhage across hospitals in California. Matern Child Health J 2005; 9:297.

6. Sheldon WR, Blum J, Vogel JP, et al. Postpartum haemorrhage management,

risks, and maternal outcomes: findings from the World Health Organization
Multicountry Survey on Maternal and Newborn Health. BJOG 2014; 121 Suppl
1:5.

7. Callaghan WM, Kuklina EV, Berg CJ. Trends in postpartum hemorrhage: United
States, 1994-2006. Am J Obstet Gynecol 2010; 202:353.e1.

8. Marshall AL, Durani U, Bartley A, et al. The impact of postpartum hemorrhage

on hospital length of stay and inpatient mortality: a National Inpatient Sample-
based analysis. Am J Obstet Gynecol 2017; 217:344.e1.

9. Lockwood CJ, Schatz F. A biological model for the regulation of peri-

implantational hemostasis and menstruation. J Soc Gynecol Investig 1996;
3:159.

10. Lockwood CJ, Nemerson Y, Krikun G, et al. Steroid-modulated stromal cell

tissue factor expression: a model for the regulation of endometrial
hemostasis and menstruation. J Clin Endocrinol Metab 1993; 77:1014.
11. Lockwood CJ. Regulation of plasminogen activator inhibitor 1 expression by
interaction of epidermal growth factor with progestin during decidualization
of human endometrial stromal cells. Am J Obstet Gynecol 2001; 184:798.

12. Lockwood CJ, Krikun G, Schatz F. The decidua regulates hemostasis in human
endometrium. Semin Reprod Endocrinol 1999; 17:45.

13. Bateman BT, Berman MF, Riley LE, Leffert LR. The epidemiology of postpartum
hemorrhage in a large, nationwide sample of deliveries. Anesth Analg 2010;
110:1368.

14. Conrad LB, Groome LJ, Black DR. Management of Persistent Postpartum
Hemorrhage Caused by Inner Myometrial Lacerations. Obstet Gynecol 2015;
126:266.

15. Sheiner E, Sarid L, Levy A, et al. Obstetric risk factors and outcome of
pregnancies complicated with early postpartum hemorrhage: a population-
based study. J Matern Fetal Neonatal Med 2005; 18:149.

16. Mhyre JM, Shilkrut A, Kuklina EV, et al. Massive blood transfusion during
hospitalization for delivery in New York State, 1998-2007. Obstet Gynecol
2013; 122:1288.

17. Rouse DJ, Leindecker S, Landon M, et al. The MFMU Cesarean Registry:
uterine atony after primary cesarean delivery. Am J Obstet Gynecol 2005;
193:1056.

18. Cheng YW, Delaney SS, Hopkins LM, Caughey AB. The association between
the length of first stage of labor, mode of delivery, and perinatal outcomes in
women undergoing induction of labor. Am J Obstet Gynecol 2009; 201:477.e1.

19. Blomberg M. Maternal obesity and risk of postpartum hemorrhage. Obstet

Gynecol 2011; 118:561.
20. Wetta LA, Szychowski JM, Seals S, et al. Risk factors for uterine
atony/postpartum hemorrhage requiring treatment after vaginal delivery. Am
J Obstet Gynecol 2013; 209:51.e1.

21. Kramer MS, Berg C, Abenhaim H, et al. Incidence, risk factors, and temporal
trends in severe postpartum hemorrhage. Am J Obstet Gynecol 2013;
209:449.e1.

22. Sharp GC, Saunders PT, Greene SA, et al. Intergenerational transmission of
postpartum hemorrhage risk: analysis of 2 Scottish birth cohorts. Am J
Obstet Gynecol 2014; 211:51.e1.

23. Bruning AH, Heller HM, Kieviet N, et al. Antidepressants during pregnancy and
postpartum hemorrhage: a systematic review. Eur J Obstet Gynecol Reprod
Biol 2015; 189:38.

24. Oberg AS, Hernandéz-Diaź S, Frisell T, et al. Genetic contribution to

postpartum haemorrhage in Swedish population: cohort study of 466,686
births. BMJ 2014; 349:g4984.

25. Giannella L, Mfuta K, Pedroni D, et al. Delays in the delivery room of a primary
maternity unit: a retrospective analysis of obstetric outcomes. J Matern Fetal
Neonatal Med 2013; 26:593.

26. Grzeskowiak LE, McBain R, Dekker GA, Clifton VL. Antidepressant use in late
gestation and risk of postpartum haemorrhage: a retrospective cohort study.
BJOG 2016; 123:1929.

27. Nyfløt LT, Sandven I, Oldereid NB, et al. Assisted reproductive technology and
severe postpartum haemorrhage: a case-control study. BJOG 2017; 124:1198.

28. Bonnar J. Massive obstetric haemorrhage. Baillieres Best Pract Res Clin
Obstet Gynaecol 2000; 14:1.
29. https://www.cmqcc.org/resource/ob-hem-emergency-management-plan-table
-chart (Accessed on September 13, 2017).

30. American College of Surgeons. Advanced Trauma Life Support (Student Manu
al). American College of Surgeons 1997.

31. American Congress of Gynecologists and Obstetricians. Obstetric hemorrhag

e bundle. www.acog.org/About-ACOG/ACOG-Districts/District-II/SMI-OB-Hem
orrhage. (Accessed on August 30, 2017).

32. Lim G, Melnyk V, Facco FL, et al. Cost-effectiveness Analysis of Intraoperative

Cell Salvage for Obstetric Hemorrhage. Anesthesiology 2018; 128:328.

33. Westhoff G, Cotter AM, Tolosa JE. Prophylactic oxytocin for the third stage of
labour to prevent postpartum haemorrhage. Cochrane Database Syst Rev
2013; :CD001808.

34. Lakshmi SD, Abraham R. Role of Prophylactic Tranexamic Acid in Reducing

Blood Loss during Elective Caesarean Section: A Randomized Controlled
Study. J Clin Diagn Res 2016; 10:QC17.

35. Dilla AJ, Waters JH, Yazer MH. Clinical validation of risk stratification criteria
for peripartum hemorrhage. Obstet Gynecol 2013; 122:120.

36. Rizvi F, Mackey R, Barrett T, et al. Successful reduction of massive postpartum

haemorrhage by use of guidelines and staff education. BJOG 2004; 111:495.

37. Shields LE, Wiesner S, Fulton J, Pelletreau B. Comprehensive maternal

hemorrhage protocols reduce the use of blood products and improve patient
safety. Am J Obstet Gynecol 2015; 212:272.

38. Skupski DW, Brady D, Lowenwirt IP, et al. Improvement in Outcomes of Major
Obstetric Hemorrhage Through Systematic Change. Obstet Gynecol 2017;
130:770.
39. Shields LE, Smalarz K, Reffigee L, et al. Comprehensive maternal hemorrhage
protocols improve patient safety and reduce utilization of blood products. Am
J Obstet Gynecol 2011; 205:368.e1.

40. http://www.jointcommission.org/Sentinel_Event_Alert__Issue_30_Preventing_i
nfant_death_and_injury_during_delivery_Additional_Resources/ (Accessed on
June 10, 2015).

41. Schorn MN. Measurement of blood loss: review of the literature. J Midwifery
Womens Health 2010; 55:20.

42. Bose P, Regan F, Paterson-Brown S. Improving the accuracy of estimated

blood loss at obstetric haemorrhage using clinical reconstructions. BJOG
2006; 113:919.

43. Lyndon A, Miller S, Huwe V, Rosen M, et al. Blood loss: Clinical techniques for
ongoing quantitative measurement. California Maternal Quality Care Collabor
ative. CMQCC Obstetric Hemorrhage Toolkit; 1/6/2010.

44. Diaz V, Abalos E, Carroli G. Methods for blood loss estimation after vaginal
birth. Cochrane Database Syst Rev 2018; 9:CD010980.

45. Prata N, Gerdts C. Measurement of postpartum blood loss. BMJ 2010;

340:c555.

46. Li XF, Fortney JA, Kotelchuck M, Glover LH. The postpartum period: the key to
maternal mortality. Int J Gynaecol Obstet 1996; 54:1.

47. Novello A, King JC. Health advisory: Prevention of maternal deaths through im
proved management of hemorrhage. www.acog.org/acog_districts/dist_notic
e.cfm?recno=1&bulletin=1517 (Accessed on May 02, 2006).

48. Evensen A, Anderson JM, Fontaine P. Postpartum Hemorrhage: Prevention

and Treatment. Am Fam Physician 2017; 95:442.
49. James AH, McLintock C, Lockhart E. Postpartum hemorrhage: when
uterotonics and sutures fail. Am J Hematol 2012; 87 Suppl 1:S16.

50. Ruiz Labarta FJ, Pintado Recarte MP, Alvarez Luque A, et al. Outcomes of
pelvic arterial embolization in the management of postpartum haemorrhage:
a case series study and systematic review. Eur J Obstet Gynecol Reprod Biol
2016; 206:12.

51. Shakur H, Elbourne D, Gülmezoglu M, et al. The WOMAN Trial (World Maternal
Antifibrinolytic Trial): tranexamic acid for the treatment of postpartum
haemorrhage: an international randomised, double blind placebo controlled
trial. Trials 2010; 11:40.

52. WOMAN Trial Collaborators. Effect of early tranexamic acid administration on

mortality, hysterectomy, and other morbidities in women with post-partum
haemorrhage (WOMAN): an international, randomised, double-blind, placebo-
controlled trial. Lancet 2017.

53. Kuklina EV, Meikle SF, Jamieson DJ, et al. Severe obstetric morbidity in the
United States: 1998-2005. Obstet Gynecol 2009; 113:293.

54. Geerts WH, Code KI, Jay RM, et al. A prospective study of venous
thromboembolism after major trauma. N Engl J Med 1994; 331:1601.

55. Pacheco LD, Saade GR, Gei AF, Hankins GD. Cutting-edge advances in the
medical management of obstetrical hemorrhage. Am J Obstet Gynecol 2011;
205:526.

56. Abdel-Razeq SS, Campbell K, Funai EF, et al. Normative postpartum

intraabdominal pressure: potential implications in the diagnosis of abdominal
compartment syndrome. Am J Obstet Gynecol 2010; 203:149.e1.

57. March CM. Intrauterine adhesions. Obstet Gynecol Clin North Am 1995;
22:491.
58. Schenker JG. Etiology of and therapeutic approach to synechia uteri. Eur J
Obstet Gynecol Reprod Biol 1996; 65:109.

59. Poujade O, Grossetti A, Mougel L, et al. Risk of synechiae following uterine

compression sutures in the management of major postpartum haemorrhage.
BJOG 2011; 118:433.

60. Rasheed SM, Amin MM, Abd Ellah AH, et al. Reproductive performance after
conservative surgical treatment of postpartum hemorrhage. Int J Gynaecol
Obstet 2014; 124:248.

61. Rathat G, Do Trinh P, Mercier G, et al. Synechia after uterine compression

sutures. Fertil Steril 2011; 95:405.

62. Ibrahim MI, Raafat TA, Ellaithy MI, Aly RT. Risk of postpartum uterine
synechiae following uterine compression suturing during postpartum
haemorrhage. Aust N Z J Obstet Gynaecol 2013; 53:37.

63. Milman N. Postpartum anemia II: prevention and treatment. Ann Hematol
2012; 91:143.

64. Holm C, Thomsen LL, Norgaard A, Langhoff-Roos J. Single-dose intravenous

iron infusion or oral iron for treatment of fatigue after postpartum
haemorrhage: a randomized controlled trial. Vox Sang 2017; 112:219.

65. Bhandal N, Russell R. Intravenous versus oral iron therapy for postpartum
anaemia. BJOG 2006; 113:1248.

66. Anemia during pregnancy and in the postpartum: intravenous iron therapy
revisited. Eur J Obstet Gynecol Reprod Biol 2005; 123 Suppl 2:S1.

67. Perelló MF, Coloma JL, Masoller N, et al. Intravenous ferrous sucrose versus
placebo in addition to oral iron therapy for the treatment of severe postpartum
anaemia: a randomised controlled trial. BJOG 2014; 121:706.
68. Kotto-Kome AC, Calhoun DA, Montenegro R, et al. Effect of administering
recombinant erythropoietin to women with postpartum anemia: a meta-
analysis. J Perinatol 2004; 24:11.

69. Wågström E, Akesson A, Van Rooijen M, et al. Erythropoietin and intravenous

iron therapy in postpartum anaemia. Acta Obstet Gynecol Scand 2007;
86:957.

70. Oberg AS, Hernandez-Diaz S, Palmsten K, et al. Patterns of recurrence of

postpartum hemorrhage in a large population-based cohort. Am J Obstet
Gynecol 2014; 210:229.e1.

71. Ford JB, Roberts CL, Bell JC, et al. Postpartum haemorrhage occurrence and
recurrence: a population-based study. Med J Aust 2007; 187:391.

72. Kadir RA, Kingman CE, Chi C, et al. Is primary postpartum haemorrhage a
good predictor of inherited bleeding disorders? Haemophilia 2007; 13:178.

73. Kadir RA, Aledort LM. Obstetrical and gynaecological bleeding: a common
presenting symptom. Clin Lab Haematol 2000; 22 Suppl 1:12.

Topic 6710 Version 105.0

© 2019 UpToDate, Inc. All rights reserved.