Overview of Postpartum Hemorrhage

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Overview of postpartum hemorrhage

Author: Michael A Belfort, MBBCH, MD, PhD, D.A. (SA), FRCSC, FRCOG, FACOG
Section Editor: Charles J Lockwood, MD, MHCM
Deputy Editor: Vanessa A Barss, MD, FACOG
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: May 2020. | This topic last updated: May 11, 2020.
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 recognition, appropriate resources, and appropriate response 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). The 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 bleeding may not be visible externally or blood in collection devices may be mixed
with amniotic fluid. In addition, postpartum morbidity is relatively infrequent among women with blood loss 500 to 999
mL [1].
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In 2017, the American College of Obstetricians and Gynecologists revised their definition of PPH from the classic one
described above to: cumulative blood loss ≥1000 mL or bleeding associated with signs/symptoms of hypovolemia
within 24 hours of the birth process regardless of delivery route [2]. The new definition should reduce the number of
women inappropriately labeled with this diagnosis. However, they went on to state that despite this new definition, a
blood loss greater than 500 mL in a vaginal delivery should be considered abnormal and should serve as an
indication for the health care provider to investigate the increased blood deficit.
INCIDENCE
The incidence of PPH varies widely, depending upon the criteria used to diagnose the disorder. Sites utilizing
quantitative blood loss may report a higher PPH rate than sites using estimated blood loss.
The incidence of PPH using estimated blood loss has been reported to be 1 to 3 percent of deliveries [3,4]. In an
analysis of population-based data from the United States National Inpatient Sample, the incidence was 3 percent in
2014 and was rising over time [4]. However, when blood loss is measured quantitatively, prospective studies show a
PPH rate as high as 10 percent [5].
PHYSIOLOGIC MECHANISMS THAT LIMIT POSTPARTUM BLOOD LOSS
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 [6,7], type-1 plasminogen activator inhibitor [8,9], 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).
The potential for massive hemorrhage from pathology in normal physiologic mechanisms at 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.
CAUSES OF POSTPARTUM HEMORRHAGE
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 approximately 1 in 40 births in the United States and is responsible for at
least 80 percent of cases of PPH [4]. 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 [10].
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 [11].
(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 uterine 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 or other bleeding diathesis — Coagulopathy complicates approximately one in 500 births in the
United States and is responsible for less than 7 percent of cases of PPH [4]. Coagulopathy or platelet dysfunction can
contribute to PPH in women with an inherited or acquired bleeding diathesis. Coagulopathy can also be 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. (See "Approach to the adult with a suspected bleeding disorder".)
Women with von Willebrand disease are especially at risk for PPH because von Willebrand factor levels, which
typically increase during pregnancy, decline rapidly after delivery. (See "von Willebrand disease (VWD): Treatment of
minor bleeding and routine care", section on 'Delivery and postpartum care'.)
Acute acquired coagulopathies can be caused by amniotic fluid embolism, placental abruption, preeclampsia with
severe features, or HELLP syndrome (Hemolysis, Elevated Liver enzymes, Low Platelets).
RISK FACTORS AND SPECIFIC ETIOLOGIES
Many risk factors for PPH have been reported and are often interdependent. Although there are many known risk
factors for PPH, knowledge of these risk factors is not always clinically useful for prevention of hemorrhage.
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 with controls without hemorrhage,
factors significantly associated with hemorrhage were, in decreasing order of frequency [12]:
• 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 [13]:
• 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, anemia, and use of some drugs (uterine relaxants, antithrombotic drugs, antidepressants
[particularly selective serotonin reuptake inhibitors and serotonin-norepinephrine reuptake inhibitors]) [10,14-25].
ASSESSMENT OF SEVERITY OF HEMORRHAGE
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.
A large reduction in blood pressure is a late sign of severe PPH as it is 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 [26]. Hemoglobin and hematocrit values are also poor indicators of acute
blood loss since they may not decline immediately after an acute bleed. (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 Emergency Management Plan table chart describes the following stages of PPH [27]:
● Stage 0 – Every woman in labor/giving birth.
● 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 percent).

● Stage 2 – Continued bleeding with total blood loss <1500 mL.
● Stage 3 – Total blood loss >1500 mL or transfusion of more than two 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 [28]. 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 — From a pragmatic perspective, it is wise to always
assume, and rule out, PPH as the cause of symptoms of hypovolemia before assigning a less concerning diagnosis.
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. Women identified prenatally as high risk
for PPH should plan to be delivered in a facility that has an appropriate level of care for their needs.
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 [29]. (See "Postpartum hemorrhage: Management
approaches requiring laparotomy", section on 'Role of intraoperative cell salvage'.)
Routine prophylactic use of uterotonic drugs, such as oxytocin alone or in combination with misoprostol, reduces the
risk of PPH by at least 30 percent in the overall obstetric population. Prophylactic administration of tranexamic acid is
under investigation [30]. (See "Management of the third stage of labor after vaginal delivery: 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 "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", section on 'Management decisions' and "von Willebrand disease (VWD):
Treatment of minor bleeding and routine care", section on 'Obstetric considerations')
However, for most patients, knowledge of risk factors for PPH is not useful clinically because many women without
risk factors experience PPH [22,31], and most high-risk women do not experience significant hemorrhage (risk of
severe hemorrhage ranges from 2 to 7 percent [31,32]). As an example, although the California obstetric hemorrhage
quality improvement toolkit classifies patients as low, medium, or high risk for PPH, 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 [31]. The California risk classification scheme is as
follows [33]:
● Low risk
• Singleton pregnancy
• ≤4 previous vaginal deliveries
• No previous uterine surgery
• No history of PPH
• No known bleeding disorder
● Medium risk
Prior uterine surgery

• >4 previous vaginal deliveries

• Multiple gestation
• Large fibroids
• Chorioamnionitis
• History of PPH
● High risk
• Morbidly adherent placenta or placenta previa or low lying placenta

• Hematocrit <30 percent and other risk factors
• Active bleeding (greater than show) at admission
• Known coagulopathy
• Platelet count <100,000
Another risk stratification and planning system is shown in the table (table 3).
Since hemorrhage may occur in low-risk women, a postdelivery management plan should always consider not only
the blood loss at delivery, but also any complications that may increase the risk of continued bleeding. While evidence
is lacking regarding the optimal approach to medium term postpartum management in women who have experienced
PPH, it seems reasonable to prolong the duration of postpartum oxytocin administration when the cause was atony. In
addition, monitoring the complete blood count and coagulation profile is advisable in any woman at risk for
coagulopathy or symptomatic anemia from acute blood loss.
PPH protocols and algorithms — Ideally, each hospital labor and delivery unit should have a PPH protocol and
provide ongoing training to their staff regarding its use [34-36]. 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 appear to result in improved outcomes for
these women [37-39]. 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 [40].
The California Maternal Quality Care Collaborative provides comprehensive information in several formats for
management of PPH.
The following tables and figure provide additional examples (table 3 and table 4 and figure 1).
Massive transfusion (MT) is often required with severe PPH and can be facilitated by use of an algorithm (algorithm 1)
specific to the hospital. All providers should be well versed in the application of such a protocol. In addition, regular
simulation of PPH and MT protocol activation will improve compliance and facilitate the performance of the team in
low-frequency/high-complexity/high-risk events [41,42]. (See 'Training and simulation' below.)
MT protocols should include specific recommendations for empiric calcium replacement, potassium monitoring
(hyperkalemia), and core body temperature management. Calcium is often necessary in severe PPH due to the
citrate used for anticoagulation in blood products [43]. Rapid infusion is important to manage hypovolemia, which will
hamper efforts to reverse coagulopathy, but rapid infusion of cold fluids can lead to substantial heat loss [44]; thus,
direct warming of fluids should occur during resuscitation.

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 5) [42].
Training and simulation — The Joint Commission recommends that obstetric staff [45]:
● 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 obstetric outcomes
through safety sciences", section on 'Postpartum hemorrhage'.)
GENERAL PRINCIPLES OF MANAGEMENT
Quantify blood loss — Routine quantification of blood loss (QBL) with standardized processes is strongly
recommended for all births. Delay in the recognition of significant blood loss is a common finding in cases of maternal
morbidity and mortality from hemorrhage, and a policy of waiting to quantify blood loss only after the excessive loss is
appreciated does not address this problem.
The standardization of as many procedures as possible is an important principle for improving quality and safety; if
QBL is reserved only for cases of significant bleeding, staff may be unfamiliar with the process and procedures and
thus less likely to obtain valid data. With practice and routine adoption, QBL requires only minutes to perform in the
majority of births [27]. This is an important factor for early recognition of excessive blood loss and timely initiation of
life-saving interventions [46-48]:
● 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.
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.
A systematic review concluded evidence was insufficient to support the use of one method over another for estimating
blood loss after vaginal birth [49]. However, the American College of Obstetricians and Gynecologists considers
quantitative methods more accurate than visual methods and notes that visual estimation is more likely to
underestimate the actual blood loss when volumes are high and overestimate when volumes are low [50].
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 [51,52]. 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 in detail separately. (See "Postpartum
hemorrhage: Medical and minimally invasive management" and "Postpartum hemorrhage: Management approaches
requiring laparotomy".)
Several maternal mortality review committees have found that delayed response to abnormal vital signs is a common
factor in preventable mortality [53,54]. Limited evidence suggests that maternal early warning systems that target
specific vital sign criteria (eg, tachycardia, hypotension) and mandate an immediate response may reduce maternal
morbidity [55,56]. (See 'PPH protocols and algorithms' above.)
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 [57].
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 6) 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 Ts mnemonic: Tone: uterine
atony; Trauma: laceration, hematoma, inversion, rupture; Tissue: retained tissue or invasive placenta; and Thrombin:
coagulopathy [58].
● Treatment of atony, the most common cause of PPH, is influenced by both the route of delivery and severity of
bleeding (table 7). 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 obstetric 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, reversal of anticoagulation (if
present), and correction of clotting factor deficiencies, if needed.
● Early administration of tranexamic acid, an antifibrinolytic drug, can reduce death due to bleeding in women with
PPH 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 1). There are no data from
clinical trials of PPH to help guide management of transfusion specifically in PPH [59] (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'.)
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If the patient is coagulopathic with an extremely low fibrinogen level (50 to 100 mg/dL), cryoprecipitate and/or 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".)
Unstable patients in a coagulopathic state with active bleeding should be managed in the most appropriate area for
resuscitation and emergency surgery. Under most circumstances, this is a warm operating room with a full
multidisciplinary team in attendance. If the abdomen has been opened, temporarily closing it with towel clips enables
the surgical team direct access to the pelvis to repack or readdress ongoing bleeding. The aorta can also be directly
visualized if necessary, and direct pressure or temporary clamping can be undertaken. The author is aware of
situations where unstable, actively bleeding patients in a coagulopathic state have had their abdomen packed and
then were transported to an intensive care unit (ICU) where they expired. In the author's opinion, in these desperate
situations, having the patient under anesthesia on a surgical table in a warm environment while acid-base
resuscitation and volume, electrolyte, and blood product replacement are carried out gives the team the most options.
Keeping the hemodynamically unstable patient in the operating room for a few hours after surgery while gaining
control of the situation may be logistically difficult but should be encouraged as opposed to taking the patient to an
ICU. ICU consultants can be summoned to the operating room for assistance. Teams should remember that even in
the most dire situations, as long as transfusion of appropriate blood products can be continued and the volume of
such products exceeds the volume of the ongoing loss, blood pressure can be maintained, and efforts to reverse the
coagulopathy, acidosis, and hypothermia may ultimately be successful and should be continued.
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 [60]. 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
[61]. 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 [62]. By comparison, the rate of transfusion in the overall obstetric population of the United States is 4 to 7
per 1000 deliveries [63], and the frequency of transfusion in PPH deliveries was 16 percent in 2014 [4]. 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 [62]. In the United States, 2.1 percent of women with PPH underwent hysterectomy in 2014, and
atony accounted for almost 60 percent of these cases [4].
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 [62].
Thromboembolism prophylaxis — In trauma patients, transfusion is an independent risk factor for development
of thromboembolism [64]. 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 [65]. 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 [62]. 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 [66].
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 [67,68]. Uterine compression sutures used to treat PPH
have also been associated with the development of intrauterine adhesions [69-72].
Treatment is discussed separately. (See "Intrauterine adhesions: Clinical manifestation and diagnosis".)
Postpartum anemia — Postpartum anemia is common: One classic criterion 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 one week postpartum and <12 g/dL at eight weeks postpartum [73].
● 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 [2]. (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 [74,75]. In a systematic review on treatment of postpartum anemia with oral
versus intravenous iron, intravenous iron replacement resulted in a higher hemoglobin concentration when
measured six weeks postpartum, with few side effects, and a 0.6 percent event rate for anaphylaxis [75].
Nevertheless, most women with mild to moderate anemia resolve the anemia sufficiently rapidly with oral iron,
and it is cheap and convenient [76-78]. A ferritin level at approximately six weeks postpartum helps to guide
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 [79]. It is no more
effective than iron therapy in this setting [80], 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 [73].
RECURRENCE
Women with a prior PPH have as much as an 18 percent risk of recurrence in a subsequent pregnancy [81-83]. 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 [84]. However, unexplained PPH that does not respond to
general measures should alert clinicians to the possibility of a bleeding disorder as a causative factor [85], especially
in women with a history of heavy menstrual bleeding, 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 after vaginal delivery: 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
● All hospitals managing pregnant and postpartum women should have postpartum hemorrhage (PPH) and
massive transfusion protocols in force, and all providers should be made aware of and be familiar with these
protocols. Regular in-training and simulation drills should be instituted to ensure compliance, emergency stage-
based response, and unit preparedness. (See 'Planning' above.)
● 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. The author recommends keeping the fibrinogen level above 300 mg/dL in patients at high risk for, or
experiencing, PPH. (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, availability of PPH kits (table 5), and training/simulation. (See 'Planning' above.)
● Active management of the third stage of labor and the routine prophylactic use of uterotonic drugs, such as
oxytocin, reduce 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 6). The approach to management of PPH varies
depending on the cause and severity of bleeding (table 7) 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.)

● Both oral and intravenous iron are options for patients with mild to moderate postpartum anemia. If oral iron is
poorly tolerated or ineffective, intravenous iron is an effective alternative. Severe anemia may require transfusion.
(See '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 heavy menstrual bleeding, 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.
Use of UpToDate is subject to the Subscription and License Agreement.
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84. Kadir RA, Kingman CE, Chi C, et al. Is primary postpartum haemorrhage a good predictor of inherited bleeding
disorders? Haemophilia 2007; 13:178.
85. Kadir RA, Aledort LM. Obstetrical and gynaecological bleeding: a common presenting symptom. Clin Lab
Haematol 2000; 22 Suppl 1:12.
Topic 6710 Version 118.0

GRAPHICS
Symptoms related to blood loss with postpartum hemorrhage
Blood loss, % (mL) Blood pressure, mmHg Signs and symptoms
10 to 15 (500 to 1000) Normal Palpitations, lightheadedness, mild increase in heart rate
15 to 25 (1000 to 1500) Slightly low Weakness, sweating, tachycardia (100 to 120 beats/minute)
25 to 35 (1500 to 2000) 70 to 80 Restlessness, confusion, pallor, oliguria, tachycardia (120 to 140 beats/minute)
35 to 45 (2000 to 3000) 50 to 70 Lethargy, air hunger, anuria, collapse, tachycardia (>140 beats/minute)
Adapted from: Bonnar J. Massive obstetric haemorrhage. Baillieres Best Pract Res Clin Obstet Gynaecol 2000; 14:1.
Graphic 56885 Version 5.0

Examples of definitions for postpartum hemorrhage
Organization Definition of PPH
World Health Organization [1] Blood loss ≥500 mL within 24 hours after birth.
Severe PPH: Blood loss ≥1000 mL within the same time frame.
American College of Obstetricians and Cumulative blood loss ≥1000 mL or blood loss accompanied by signs or
Gynecologists [2] symptoms of hypovolemia within 24 hours after the birth process (includes
intrapartum loss) regardless of route of delivery.
Royal College of Obstetricians and Gynaecologists [3] Minor PPH (500 to 1000 mL) and major PPH (>1000 mL). Subdivisions of major
PPH include moderate (1001 to 2000 mL) or severe (>2000 mL).
International expert panel [4] Active bleeding >1000 mL within the 24 hours following birth that continues
despite the use of initial measures, including first-line uterotonic agents and
uterine massage.
Society of Obstetricians and Gynaecologists of Any amount of bleeding that threatens the patient's hemodynamic stability.
Canada [5]
California Maternal Quality Care Collaborative [6] Stage 0: Every woman in labor/giving birth.
Stage 1: Blood loss >500 mL after vaginal or >1000 mL after cesarean delivery;
or change in vital signs >15% or heart rate ≥110 beats/minute, blood pressure
≤85/45 mmHg, O 2 saturation <95%.
Stage 2: Continued bleeding with total blood loss <1500 mL.
Stage 3: Total blood loss >1500 mL or >2 units packed red cells transfused; or
unstable vital signs; or suspicion of disseminated intravascular coagulation.
PPH: postpartum hemorrhage.
References:
1. World Health Organization. WHO recommendations for the prevention and treatment of postpartum haemorrhage. Geneva: World Health
Organization; 2012.
2. American College of Obstetricians and Gynecologists. ACOG Practice Bulletin Number 183, October 2017: Postpartum hemorrhage. Obstet
Gynecol 2017; 130:e168.
3. Prevention and management of postpartum haemorrhage: Green-top guideline No. 52. BJOG 2017; 124:e106.
4. Abdul-Kadir R, McLintock C, Ducloy AS, et al. Evaluation and management of postpartum hemorrhage: Cnsensus from an international
expert panel. Transfusion 2014; 54:1756.
5. Leduc D, Senikas V, Lalonde AB, et al. Active management of the third stage of labour: Pevention and treatment of postpartum hemorrhage.
J Obstet Gynaecol Can 2009; 31:980.
6. CMQCC. www.cmqcc.org/resources-tool-kits/toolkits/ob-hemorrhage-toolkit (Accessed on May 17, 2017).

Sample approach to risk stratification and delivery preparation for PPH
Prenatal assessment and planning
Identify and prepare for patients at risk: previa/accreta, bleeding disorder, those who refuse transfusion
Screen and treat for anemia (iron panel, hemoglobin electrophoresis, consider oral versus IV iron)
Low Medium High
≤4 previous SVD Hgb <8 Placenta previa
Singleton Platelets <100,000 Suspected accreta
<2 prior CD ≥3 prior CD or previous myomectomy Abruption
No previous PPH >4 vaginal births Coagulopathy
No known bleeding disorder Chorioamnionitis
Magnesium sulfate use
Multiple gestation
Large uterine fibroids
EFW >4250 g
Black race
History of PPH
Morbid obesity (BMI >40)
Oxytocin preparation: 30 international units in 500 cc solution. 167 cc = 10 international units.

Low:
Type and screen on admission (if antibody positive, then will need crossmatch)
Postpartum order: Oxytocin 167 cc bolus, then 42 cc/hour for 4 hours
Medium:
Type and screen on admission
Discuss risk of PPH with patient
Postpartum orders: Oxytocin 167 cc bolus, then 42 cc/hour for 8 hours
Medium "plus" (>1 medium risk factor):
Crossmatch 2 units
Discuss risk of PPH with patient
High:
Crossmatch 4 (or more) units
Discuss risk of PPH and transfusion with patient
Observation on L&D postoperatively based on QBL or at least 4 hours (whichever is longer)
PPH: postpartum hemorrhage; IV: intravenous; SVD: small-vessel disease; Hgb: hemoglobin; CD: cesarean delivery; EFW: estimated fetal
weight; BMI: body mass index; cc: cubic centimeter; L&D: labor and delivery; QBL: quantification of blood loss.
Courtesy of Christina Davidson, MD and Catherine Eppes, MD, MPH.

Guidelines for rapid identification and treatment of hemorrhage in the postpartum patient
Sample protocol for assessment and prevention of postpartum hemorrhage (PPH, cumulative blood loss ≥1000 mL or blood loss accompanied
by signs or symptoms of hypovolemia within 24 hours after birth [includes intrapartum loss]) regardless of the route of delivery
I. Review patient history for the following risk factors:
A. Grand multiparity (>4 vaginal deliveries, >3 previous cesarean deliveries)
B. Obesity (BMI >40 kg/m 2)
C. Macrosomic infant (estimated fetal weight >4250 grams)
D. Previous history of hemorrhage
E. Uterine fibroids >5 centimeters in diameter
F. Chorioamnionitis
G. Multiple gestation
H. Magnesium sulfate administration
I. Placenta previa
J. Suspected placental accreta spectrum
K. Placental abruption
L. Coagulopathy
II. Actively manage the third stage of labor:
A. Controlled gentle cord traction
B. Administer oxytocin: 30 units in 500 mL IV and/or 10 units IM, with delivery of placenta
C. Uterine massage every 15 minutes for 2 hours after delivery
D. Closely examine the placenta for signs of retained tissue
E. Carefully examine the vagina and cervix for lacerations
F. Quantify and document blood loss
III. Postpartum period, assess for:
A. Excessive lochia and/or blood clots
B. Displaced and/or boggy uterine fundus
C. Bladder distention
D. Vital signs alterations:
1. Blood pressure decreased
2. Pulse increased
3. Respiratory rate increased
4. Alteration in level of consciousness
5. Skin changes such as pallor, cyanosis, clamminess
E. Visible hematoma or laceration:
1. Vaginal hematoma: Ecchymosis, swelling, tenderness of perineum, and rectal pressure
BMI: body mass index; IV: intravenous; IM: intramuscular.

Sample checklist for managing postpartum hemorrhage
OB: obstetrician; RN: registered nurse; IV: intravenous; QBL: quantity of blood loss; IM: intramuscular; OR: operating room; CBC: complete
blood count; PT: prothrombin time; PTT: partial thromboplastin time; INR: international normalized ratio; RBC: red blood cell; TXA:
tranexamic acid; TEG: thromboelastography; ROTEM: rotational thromboelastography.

Sample massive transfusion algorithm
Texas Children's Pavilion for Women massive transfusion protocol.
MTP: massive transfusion protocol; PRBC: packed red blood cells; PCA: patient-controlled analgesia; RRT:
rapid response team; BB: blood bank; Hg: hemoglobin; Hct: hematocrit; DIC: disseminated intravascular
coagulation; PT: prothrombin time; INR: international normalized ratio; PTT: partial thromboplastin time;
ABG: arterial blood gas; RBC: red blood cells; FFP: fresh frozen plasma; OB: Obstetrics; Anes: Anesthesia;
OR: operating room; CRNA: certified registered nurse anesthetist; Chrg: charge; RN: registered nurse;
Lab: laboratory; Tech: technician; MD: medical doctor; L&D: labor and delivery; iCa: ionized calcium; K:
potassium; Glu: glucose; PCA: patient care assistant.
* Every two packages or based on lab results.
Reproduced with permission. Accessed on February 19, 2013. Copyright © Evidence-Based Outcomes
Center, 2013. Quality and Outcomes Center, Texas Children's Hospital. This guideline was prepared by the
Evidence-Based Outcomes Center (EBOC) team in collaboration with content experts at Texas Children's
Hospital Pavilion for Women. Development of this guideline supports the TCH Quality and Patient Safety
Program initiative to promote clinical guidelines and outcomes that build a culture of quality and safety
within the organization. Guideline recommendations are made from the best evidence, clinical expertise
and consensus, in addition to thoughtful consideration for the patients and families cared for within the
Integrated Delivery System. When evidence was lacking or inconclusive, content experts made consensus
recommendations. Expert consensus is implied when a reference is not otherwise indicated. The guideline

is not intended to impose standards of care preventing selective variation in practice that is necessary to
meet the unique needs of individual patients. The physician must consider each patient and family's
circumstance to make the ultimate judgment regarding best care.

Example of instruments, equipment, and medications to assemble for a postpartum hemorrhage

emergency cart
Equipment/supplies for starting an intravenous line (14-, 16-, 18-, and 20-gauge peripheral venous catheter, 1 L Lactated Ringer's
solution for injection, intravenous tubing, four-way stopcock, tape)
Urinary catheter kit, urimeter
Lubricating gel
Assorted sizes of sterile gloves, including elbow-length gloves
Vaginal retractors, including a long right-angle retractor
Sterile speculum, long weighted speculum
Sponge forceps
Vaginal packs, 2 by 2 and 4 by 4 sponge gauze packs, gauze bandage rolls
Balloon catheter kit for intrauterine tamponade
Sterile utility bowl, 20 and 60 mL syringes, irrigation water
Banjo curettes
Long needle holder
Appropriate sutures for cervical and vaginal laceration repair and for uterine compression sutures
Uterine forceps
Freestanding mobile task light, battery-powered headlamp
Illustrations showing how to perform relevant procedures (eg, uterine compression, uterine artery ligation, intrauterine balloon placement,
replacement of inverted uterus)
Equipment/supplies for drawing blood (eg, syringes; needles; red, green, blue, and tiger top tubes; alcohol prep pads; tourniquet) for
laboratory studies (eg, type and cross, coagulation studies, CBC, platelets, electrolytes, ionized calcium, potassium) with prewritten lab
and blood bank requisition orders; instructions on how to order tests and blood and how to activate the massive transfusion protocol
Biohazard bag
Adult oxygen nonrebreather mask
Tubing and filter for blood transfusion
Equipment for warming irrigation and intravenous fluids
Pressure infusor bag
Tape, bandages
Medications:
Kit for transabdominal intramyometrial injection of carboprost under ultrasound guidance: 20 mL syringe, 20 mL sterile saline for
injection, 6 inch 20-gauge and 6 inch 22-gauge amniocentesis needles
Misoprostol, five 200 mcg tablets
Oxytocin, 10 to 40 units per 500 to 1000 mL NS 1 bag
Methylergonovine, 0.2 mg/mL 1 ampule (requires refrigeration)
Carboprost, 250 mcg/mL 1 ampule (requires refrigeration)
CBC: complete blood count; NS: normal saline.
Adapted from:
1. California Maternal Quality Care Collaborative Improving Response to Obstetric Hemorrhage Toolkit V2.0. www.cmqcc.org/resources-tool-
kits (Accessed on October 31, 2016).
2. Texas Children's Hospital-Pavilion for Women postpartum hemorrhage cart inventory list.

Visual aid for estimating intrapartum blood loss
Visual aid. Pocket card with images of measured volumes of artificial blood.
From: Zuckerwise LC, Pettker CM, Illuzzi J, et al. Use of a novel visual aid to improve estimation of obstetric blood loss. Obstet Gynecol 2014; 123:982.
DOI: 10.1097/AOG.0000000000000233. Copyright © 2014 American College of Obstetricians and Gynecologists. Reproduced with permission from
Wolters Kluwer Health. Unauthorized reproduction of this material is prohibited.

Potential interventions for treatment of postpartum hemorrhage
Pharmacologic interventions
Drug Dosing
Oxytocin 10 to 40 units in 500 to 1000 mL normal saline infused at a rate sufficient to control atony or 10 units IM
Tranexamic acid 1 g (10 mL of a 100 mg/mL solution) is infused over 10 to 20 minutes; if bleeding persists after 30 minutes,
a second 1 g dose is administered
Ergots Methylergonovine 0.2 mg IM every 2 to 4 hours or ergometrine 0.5 mg IV or IM or ergonovine 0.25 mg IM or

IV every 2 hours
Carboprost 0.25 mg IM every 15 to 90 minutes up to 8 doses or 500 mcg IM incrementally up to 3 mg or 0.5 mg

intramyometrial
Misoprostol 800 to 1000 mcg rectally
Dinoprostone 20 mg vaginally or rectally every 2 hours
Recombinant human 50 to 100 mcg/kg every 2 hours

factor VIIa
Surgical interventions
Repair lacerations
Curettage
Uterine compression suture (eg, B-Lynch suture)
Uterine artery ligation
Utero-ovarian artery ligation or cross clamp
Pelvic packing
Uterine tourniquet
Focal myometrial excision
Use of fibrin glues and patches to cover areas of oozing and promote clotting
Placement of figure 8 sutures or other hemostatic sutures directly into the placental bed
Resuscitative endovascular balloon occlusion of the aorta (REBOA)
Internal iliac artery (hypogastric artery) ligation
Aortic/iliac artery compression
Hysterectomy, supracervical
Hysterectomy, total
Interventional endovascular procedures

Selective arterial embolization
Intermittent aortic balloon occlusion
Common iliac artery balloon occlusion
Blood bank
Packed red blood cells
Platelets
Fresh frozen plasma
Cryoprecipitate
Nonsurgical interventions
Uterine massage
Intravenous fluids
Tamponade
Intrauterine tamponade with an intrauterine balloon or alternative device (eg, bladder catheter bulb, Sengstaken-Blakemore tube)
Uterine packing (eg, 4 inch gauge packing)
Consultations
General surgery
Trauma surgery

Anesthesia team
Interventional radiology
Gynecologic oncology
Urology
IV: intravenous; IM: intramuscular; mcg: micrograms; kg: kilogram.
Data from: Dahlke JD, Mendoz-Figueroa H, Maggio L, et al. Prevention and management of postpartum hemorrhage: a comparison of 4 national
guidelines. Am J Obstet Gynecol 2015; 213.e1.

Overview of management of postpartum hemorrhage based on estimated blood loss and

hemodynamic stability
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. Intervention is based, in
part, on the severity of hemorrhage.
Quantify blood loss.
Initiate additional measures to control bleeding based on severity of obstetric hemorrhage.
Blood loss >500 mL and <1000 mL at vaginal delivery or >1000 mL and <1500 mL at cesarean delivery with ongoing excessive
bleeding and/or mild tachycardia and/or hypotension.
Get help and notify obstetric hemorrhage team.
Continue to monitor vital signs and quantify blood loss.
Ensure intravenous access with a large gauge catheter(s).
Begin bimanual uterine massage.
Increase oxytocin flow rate (avoid direct intravenous injection of undiluted oxytocin).
Volume resuscitation, preferably with blood and blood products if bleeding is heavy and coagulopathy is imminent.
Give a second uterotonic (eg, methylergonovine, carboprost tromethamine).
Examine for lacerations, retained products of conception, uterine inversion, and other causes of bleeding. Consider bedside
ultrasound of uterus. Treat as appropriate (eg, repair lacerations, curettage, reposition uterus, etc).
If cesarean delivery: Apply conservative surgical interventions to control bleeding (eg, uterine artery/ovarian artery ligation,
uterine compression sutures).
Blood loss >1000 mL and <1500 mL at vaginal delivery or >1500 mL at cesarean delivery with ongoing excessive bleeding and/or
hemodynamic instability.
Do all of the above.
Draw blood for baseline labs (complete blood count, coagulation studies) and clot observation test.
Insert intrauterine balloon for tamponade.
Transfuse two units packed red cells and one to two units fresh frozen plasma. Activate a massive transfusion protocol if bleeding
is heavy and transfusion of four or more units of blood is likely.
If vaginal delivery: Move the patient to an operating room to perform conservative surgical interventions to control bleeding.
Consider selective arterial embolization only if patient is hemodynamically stable. This should preferably be performed in an
operating room or hybrid suite if available. Bleeding patients should only be moved to a radiology suite for embolization if they
are hemodynamically stable and blood products are being replaced at a rate that can exceed that of the bleeding. Arterial
embolization outside of an operating room is not an option in situations where there is catastrophic bleeding in a
decompensating patient.
If cesarean delivery: Continue to apply conservative surgical interventions to control bleeding (eg, uterine artery/ovarian artery
ligation, uterine compression sutures).
Blood loss >1500 mL, ongoing excessive bleeding, and hemodynamic instability despite initial therapy.
Initiate massive transfusion protocol (transfuse appropriate ratio of red cells, fresh frozen plasma/cryoprecipitate, and platelets).
If conservative surgical interventions are not successful, perform hysterectomy. Hysterectomy should not be delayed in women
who require prompt control of uterine hemorrhage to prevent death.
Keep patient warm.
Treat acidosis.
Check ionized calcium and potassium levels every 15 minutes once a massive transfusion protocol has been initiated and treat
hypocalcemia and hyperkalemia aggressively. Continue until the emergency has been contained and the protocol for massive
transfusion has been stopped.
Maintain oxygen saturation >95%.

Contributor Disclosures
Michael A Belfort, MBBCH, MD, PhD, D.A. (SA), FRCSC, FRCOG, FACOG Equity Ownership/Stock Options: Glenveigh
Medical. Patent Holder: Clinical Innovations [Postpartum hemorrhage]. Charles J Lockwood, MD, MHCM Nothing to
disclose Vanessa A Barss, MD, FACOG Nothing to disclose
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are addressed by vetting
through a multi-level review process, and through requirements for references to be provided to support the content. Appropriately
referenced content is required of all authors and must conform to UpToDate standards of evidence.
Conflict of interest policy

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Official reprint from UpToDate®

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PHYSIOLOGIC MECHANISMS THAT LIMIT POSTPARTUM BLOOD LOSS

CAUSES OF POSTPARTUM HEMORRHAGE

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RISK FACTORS AND SPECIFIC ETIOLOGIES

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

ASSESSMENT OF SEVERITY OF HEMORRHAGE

● Stage 0 – Every woman in labor/giving birth.

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

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Prior uterine surgery

• >4 previous vaginal deliveries

• Morbidly adherent placenta or placenta previa or low lying placenta

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GENERAL PRINCIPLES OF MANAGEMENT

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Treatment goals — Treatment goals are to:

● Restore or maintain adequate circulatory volume to prevent hypoperfusion of vital organs

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● Traumatic, hemorrhaging lacerations need to be controlled surgically, either transvaginally or transabdominally.

Approach to hemodynamically unstable patients — When hemorrhage is suspected as the cause of

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MORBIDITY AND MORTALITY

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

Abdominal compartment syndrome — Abdominal compartment syndrome (organ dysfunction caused by

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SOCIETY GUIDELINE LINKS

INFORMATION FOR PATIENTS

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

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SUMMARY AND RECOMMENDATIONS

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27. https://www.cmqcc.org/resource/ob-hem-emergency-management-plan-table-chart (Accessed on September 1

33. https://www.cmqcc.org/resource/ob-hem-risk-factor-assessment (Accessed on December 02, 2019).

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Topic 6710 Version 118.0

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Symptoms related to blood loss with postpartum hemorrhage

Blood loss, % (mL) Blood pressure, mmHg Signs and symptoms

10 to 15 (500 to 1000) Normal Palpitations, lightheadedness, mild increase in heart rate

Graphic 56885 Version 5.0

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Examples of definitions for postpartum hemorrhage

Organization Definition of PPH

PPH: postpartum hemorrhage.

Graphic 113123 Version 3.0

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Sample approach to risk stratification and delivery preparation for PPH

Prenatal assessment and planning

Low Medium High

≤4 previous SVD Hgb <8 Placenta previa

Singleton Platelets <100,000 Suspected accreta

<2 prior CD ≥3 prior CD or previous myomectomy Abruption