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Official reprint from UpToDatewww.uptodate.com ©2016 UpToDate

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

Section EditorsCharles J Lockwood, MD, MHCMDeborah Levine, MD

Deputy Editor Vanessa A Barss, MD, FACOG

Overview of postpartum hemorrhage

All topics are updated as new evidence becomes available and our peer review process is complete.Literature review current through: Feb 2016. | This topic last updated: Feb 24, 2016.

INTRODUCTION — Postpartum hemorrhage (PPH) is an obstetrical emergency. It is a major cause of

maternal morbidity, and one of the top three 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 (1 in

100,000 deliveries in the United Kingdom versus 1 in 1000 deliveries in the developing world). With timely

diagnosis, appropriate resources, and appropriate management, however, PPH may be the most preventable

cause of maternal mortality.

This topic will present an overview of major issues relating to postpartum hemorrhage, including management

of secondary postpartum hemorrhage. Specific issues in management of PPH depend on the setting, vaginal or

cesarean delivery, and will be discussed separately:

DEFINITIONS — PPH is described as primary or secondary: 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).

PPH is classically defined by the volume of blood loss. The most common definition is estimated blood loss

≥500 mL after vaginal birth or ≥1000 mL after cesarean delivery. The inadequacy of this definition was

illustrated in studies that assessed blood loss using various objective methods: The mean blood loss reportedafter vaginal and cesarean deliveries was approximately 400 to 600 mL and 1000 mL, respectively, and

clinicians were likely to underestimate the volume of blood lost [1-3]. Another problem is that bleeding may not

be visible.

Another classic definition is a 10-point decline in postpartum hematocrit concentration from antepartum levels.

However, this is not a clinically useful definition for several reasons: Rapid blood loss may trigger a medical

emergency prior to observation of a fall in hematocrit concentration; laboratory changes not correlated with

events that endanger the patient should not be used to define a medical emergency; crystalloid and blood

product infusions before and during the delivery may obfuscate the findings; and antepartum

hemoconcentration (eg, from preeclampsia or dehydration) may cause a lar ge fall in hematocrit concentration

following delivery in the absence of excessive intrapartum blood loss.

The Royal College of Obstetricians and Gynaecologists defines PPH as minor (500 to 1000 mLs) or major

(>1000 mLs), with further subdivisions of major hemorrhage as moderate (1000 to 2000 mLs) or severe (>2000

mLs) [4]. An international expert panel defined PPH as "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" [5].

INCIDENCE — The incidence of PPH varies widely, depending upon criteria used to define the disorder. A

reasonable estimate is 1 to 5 percent of deliveries [ 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]. The incidence increased across the interval due to an increase in the proportion of women diagnosed withuterine atony, the most common cause of PPH in this series.

PATHOGENESIS — 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 about 15 percent of cardiac output. Normally,

®

®

(See "Management of postpartum hemorrhage at vaginal delivery".)●

(See "Management of postpartum hemorrhage at cesarean delivery".)●

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hemostasis occurs upon placental separation because uterine bleeding is controlled by a combination of two

mechanisms:

PPH occurs when there is a disturbance in one or both of these mechanisms. These disturbances includeincomplete placental separation, defective myometrial contraction, and bleeding diatheses.

Delivery-related trauma is another pathway to PPH.

CAUSES

Atony — The most common cause of PPH is uterine atony (ie, lack of effective contraction of the uterus after

delivery), which complicates 1 in 20 births and is responsible for at least 80 percent of cases of PPH [ 12,13].

Blood loss can be much greater than observed because a boggy and dilated uterus may contain a significant

amount of blood. The diagnosis is made if the uterus does not become firm after uterine massage and

administration of uterotonic agents.

Atony may be diffuse or localized to an area of uterine muscle. In the latter, the fundal region may be well

contracted while the lower uterine segment is dilated and atonic, which is difficult to appreciate on physical

examination. Women with persistent bleeding despite a firm fundus should undergo a vaginal examination to

identify ballooning of the lower uterus, as well as cervical and vaginal lacerations.

Although diffuse uterine atony is the most common cause of PPH, it is often responsive to uterotonic therapy,

thus it is not the most common reason for massive transfusion at delivery [ 14].

Trauma — Trauma-related bleeding can be due to lacerations, surgical incisions, or uterine rupture.

Cervical and vaginal lacerations may develop spontaneously 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 hematomas.

Corpus lacerations may be complete ruptures or incomplete lacerations of the inner myometrium [ 15]. (See

"Rupture of the unscarred uterus" and "Uterine dehiscence and 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 or bulging of the broad ligament at cesarean delivery can be signsof retroperitoneal hemorrhage.

Coagulopathy — Coagulopathy is both a cause and result of PPH since persistent heavy bleeding,

irrespective of the cause, leads to consumption of clotting factors and hemodilution of remaining clotting

factors.

RISK FACTORS — Many risk factors for PPH have been reported and they are often interdependent.

Contraction of the myometrium, which compresses the blood vessels supplying the placental bed and

causes mechanical hemostasis.

●

Local decidual hemostatic factors (tissue factor [8,9], type-1 plasminogen activator inhibitor [10,11],

systemic coagulation factors [eg, platelets, circulating clotting factors]), which cause clotting.

●

A study including 154,311 deliveries compared 666 cases of PPH to controls without hemorrhage [16].

Factors significantly associated with hemorrhage, in decreasing order of frequency, were:

●

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)•

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DIAGNOSIS — We make the diagnosis of PPH in postpartum women with bleeding that is greater than

expected and causes symptoms (eg, pallor, lightheadedness, weakness, palpitations, diaphoresis,restlessness, confusion, air hunger, syncope) and/or results in signs of hypovolemia (eg, hypotension,

tachycardia, oliguria, oxygen saturation 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 another large series, the most common risk factors associated with need for massive transfusion

during hospitalization for delivery were abnormal placentation (1.6/10,000 deliveries, adjusted OR [aOR]

18.5, 95% CI 14.7-23.3), placental abruption (1.0/10,000, aOR 14.6, 95% CI 11.2-19.0), severepreeclampsia (0.8/10,000, aOR 10.4, 95% CI 7.7-14.2), and intrauterine fetal demise (0.7/10,000, aOR

5.5, 95% CI 3.9-7.8) [17].

●

Other risk factors include personal or family history of previous PPH, obesity, high parity, Asian or

Hispanic race, precipitous labor, uterine overdistention (eg, multiple gestation, polyhydramnios,

macrosomia), uterine infection, uterine inversion, inherited bleeding diathesis, acquired bleeding diathesis

(eg, amniotic fluid embolism, abruptio placenta, sepsis, fetal demise), and use of some drugs, such as

uterine relaxants and drugs that affect coagulation (possibly including antidepressants) [ 14,18-26].

●

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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 [30]. 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.

PPH kits — In addition to a protocol, it is useful for labor and delivery units to assemble kits including

medications and instruments that may be needed to manage PPH so that this equipment is readily available

when needed (similar to a "code cart").

Training and simulation — The Joint Commission recommends that obstetrical staff 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 [31]. 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 floor or post-

anesthesia care unit, may also increase comfort with the protocols and teamwork required in such

emergencies.

MANAGEMENT — Timely, accurate diagnosis is important in order to initiate appropriate interventions (eg,

drugs, surgery, referral, consultation) and improve outcome [32]. Early intervention may prevent shock

(inadequate perfusion and oxygenation of tissues) and the development of the potentially lethal triad of

hypothermia, acidosis, and coagulopathy. Many potentially effective interventions are available for management

of PPH (table 2).

The management of PPH is multifaceted and requires care by several teams within the hospital (obstetricians,

midwives, nurses, anesthesiologists, hematologists/blood bank personnel, laboratory medicine, surgical

subspecialists [eg, vascular, urology], interventional radiology) [33]. These teams 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 these teams will communicate and

function together; the following table (table 3) and algorithms are representative examples (algorithm 1 and

algorithm 2). In addition, numerous professional organizations have provided guidance for team management of

PPH (eg, California Maternal Quality Care Collaborative). (See 'Guidelines from professional organizations'below.)

General principles — The rate and volume of bleeding, vital signs, and laboratory results should be closely

monitored to assess the best approach to and aggressiveness of intervention. It is important to not allow the

patient to become moribund before initiating life-saving measures. (See "Management of postpartum

hemorrhage at vaginal delivery", section on 'Initial interventions' and "Management of postpartum hemorrhage

at cesarean delivery", section on 'Initial management'.)

The obstetrical provider should initiate a sequence of nonoperative and operative interventions (table 4) for

control of PPH and promptly assess the success or failure of each measure. The goal is to:

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.

Although there are no data from clinical trials to help guide management of transfusion specifically in PPH,

management of blood component therapy is similar to that in other massive hemorrhage [ 34]. Development of a

standardized institutional approach improves outcome (algorithm 2).

The approach to treatment of PPH differs somewhat depending on the cause and whether hemorrhage occurs

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●

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after a vaginal birth or after a cesarean delivery. Traumatic, hemorrhaging lesions need to be controlled

surgically, either transvaginally or transabdominally. Coagulation defects can often be treated medically, with

transfusion of blood and blood products. The treatment of atony, the most common cause of PPH, depends on

the route of delivery. After a vaginal birth, treatment begins with less invasive interventions and progresses to

more invasive procedures until hemorrhage is controlled. It is usually possible to avoid laparotomy and its

associated morbidity.

By comparison, after a cesarean delivery where the abdomen is already open and adequate anesthesia has

already been administered, there is much less concern about open operative interventions. The frequency of the different causes of hemorrhage also differs by route of birth; retained products of conception are more likely

after a vaginal birth than after a cesarean delivery since the uterine cavity is readily accessed and visualized

during surgery.

If PPH does not occur while the patient is hospitalized, use of an antishock garment may be helpful for

reversing hypovolemic shock and decreasing obstetric hemorrhage while the patient is being transported to

emergency obstetrical care facilities and able to receive definitive therapies [35-37].

Key components of evaluation and treatment — Aggressive active evaluation and management of persistent

vaginal bleeding after delivery involves:

The Advanced Trauma Life Support manual describes four classes of hemorrhage to emphasize the early signs

of the shock state [41]. Clinicians should note that significant drops in blood pressure are generally not

manifested until class III hemorrhage develops, and up to 30 percent of a patient's blood volume can be lost

before this occurs. Hemoglobin and hematocrit values are poor indicators of acute blood loss since they may

not decline immediately after an acute bleed.

Cumulative measurement of blood loss at every delivery. This is an important factor for early recognitionof excessive blood loss and timely initiation of life saving interventions [38-40]:

●

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.

Bedside evaluation by the provider.●

Active management of the third stage with oxytocin and secondary uterotonic drugs, as needed (eg

carboprost, methylergonovine, misoprostol). (See "Management of postpartum hemorrhage at vaginal

delivery", section on 'Uterotonic drugs'.)

●

Early, adequate intravenous access (≥16 gauge) for massive transfusion.●

Frequent assessment of vital signs.●

Laboratory evaluation (complete blood count, coagulation studies, potassium and ionized calcium levels).●

Blood cross-match or activation of a massive transfusion protocol.●

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

●

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Hypovolemic hemorrhagic shock is treated by aggressive volume resuscitation with packed red blood cells and

other appropriate blood products. (See "Management of postpartum hemorrhage at vaginal delivery", section on

'Fluid resuscitation and transfusion'.)

In addition, the author believes early recourse to intrauterine balloon tamponade can be useful to decrease

ongoing blood loss and allow time for stabilization and institution of resuscitative procedures. (See

"Management of postpartum hemorrhage at vaginal delivery", section on 'Uterine tamponade'.)

If the patient is coagulopathic with an extremely low fibrinogen level, 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

"Management of postpartum hemorrhage at vaginal delivery", section on 'Repletion of clotting factors'.)

Arterial embolization is an appropriate treatment for persistent bleeding in a hemodynamically stable patient in

whom the capacity for blood replacement exceeds that of the ongoing hemorrhage. Generally, it should not beattempted in unstable patients who have to be transferred to a radiology suite for the procedure and it should

not be considered an emergency procedure for managing uncontrolled PPH of indeterminate cause. (See

"Management of postpartum hemorrhage at vaginal delivery", section on 'Arterial embolization'.)

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 hemorrhageand myocardial depression. (See "Management of postpartum hemorrhage at cesarean delivery", section on

'Temporizing measures' and "Management of postpartum hemorrhage at cesarean delivery", section on

'Conservative surgical interventions'.)

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 "Management of postpartum

hemorrhage at cesarean delivery", section on 'Hysterectomy'.)

Hemorrhage associated with vaginal versus cesarean delivery — A variety of medications and techniques

are available for control of PPH. The choice of technique depends, in part, on the setting: postvaginal delivery

or at cesarean delivery where the abdomen is already open. The approach to management of PPH after vaginal

birth and cesarean delivery are described in detail separately:

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 mustassume 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.

●

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Detailed discussions of specific techniques and patient support are also available:

Guidelines from professional organizations — Guidelines for diagnosis, management, and prevention of

postpartum hemorrhage have been developed by several organizations and are generally consistent with the

approach described in the UpToDate topics.

COMPLICATIONS — PPH is a major cause of maternal morbidity, including catastrophic sequelae:

Sheehan syndrome — Sheehan syndrome (ie, postpartum hypopituitarism) is a rare but potentially life-

(See "Management of postpartum hemorrhage at vaginal delivery".)●

(See "Management of postpartum hemorrhage at cesarean delivery".)●

(See "Intrauterine balloon tamponade for control of postpartum hemorrhage".)●

(See "Massive blood transfusion".)●

(See "Clinical use of plasma components".)●

(See "Intraoperative fluid management".)●(See "Overview of topical hemostatic agents and tissues adhesives used in the operating room".)●

(See "Management of hemorrhage in gynecologic surgery".)●

California Maternal Quality Care Collaborative best practices for management of obstetrical hemorrhage●

Royal College of Obstetricians and Gynaecologists guideline for prevention and management of

postpartum hemorrhage

●

World Health Organization guideline for prevention and treatment of postpartum haemorrhage●

Society of Obstetricians and Gynaecologists of Canada guideline for prevention and management of

postpartum hemorrhage

●

American College of Obstetricians and Gynecologists practice bulletin for postpartum hemorrhage [42]●

New York health advisory recommendations for reducing the risk of maternal death from hemorrhage●

International Expert Panel consensus statement [5]●

National Partnership for Maternal Safety: Consensus Bundle on Obstetric Hemorrhage [43]●

French College of Gynaecologists and Obstetricians [44]●

Death●

Hypovolemic shock and organ failure: renal failure, stroke, myocardial infarction, postpartum

hypopituitarism (Sheehan syndrome)

●

Fluid overload (pulmonary edema, dilutional coagulopathy)●

Abdominal compartment syndrome●

Anemia●

Transfusion-related complications, including severe electrolyte abnormalities (predominantly hyperkalemia

and hypocalcemia) (see "Use of blood products in the critically ill", section on 'Complications')

●

Acute respiratory distress syndrome●

Anesthesia-related complications●

Sepsis, wound infection, pneumonia●

Venous thrombosis and embolism●

Unplanned sterilization due to need for hysterectomy●

Asherman syndrome (related to curettage if performed for retained products of conception)●

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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 "Diagnosis of hypopituitarism".)

Abdominal compartment syndrome — Another rare but life-threatening complication is abdominal

compartment syndrome (organ dysfunction caused by intraabdominal hypertension). The diagnosis should be

considered in patients with a tensely distended abdomen and progressive oliguria who are developing

multiorgan failure (see "Abdominal compartment syndrome"). 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 [45].

Thromboembolism — In trauma patients, transfusion is an independent risk factor for development of

thromboembolism [46]. For this reason, all women who have been transfused for PPH should receive

mechanical thromboprophylaxis (graduated compression stockings or pneumatic compression device) as soonas feasible and continue thromboprophylaxis until discharge [47]. Twelve to 24 hours after bleeding has been

controlled, pharmacologic thromboprophylaxis should be added, providing coagulation tests are normal or close

to normal.

Severe postpartum anemia — Postpartum anemia is treated with oral iron supplementation. A single 325 mg

ferrous sulfate tablet taken orally three times daily between meals provides 195 mg of elemental iron per day.

This regimen 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. If the patient cannot tolerate

this dose, she should take a lower tolerable dose.

Hemoglobin levels rise faster with parenteral iron therapy than with oral therapy; however, most women resolvetheir anemia sufficiently rapidly with oral iron [48-50]. Administration of parenteral iron is rarely indicated, given

its risks (eg, anaphylaxis) and costs. If parenteral therapy is administered, ferric gluconate in sucrose complex

and iron sucrose are safer than iron dextran.

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 [51]. It is no more

effective than iron therapy in this setting [52], and is expensive. In a few women with severe anemia who do

not respond to iron alone because of blunted erythropoiesis due to infection and/or inflammation, some

hematologists consider recombinant human erythropoietin as an alternative to transfusion [53].

The indications for red blood cell transfusion and parenteral iron therapy are discussed separately. These

interventions may be needed instead of oral iron therapy in women who are unable to care for themselves or

their newborns because of severe anemia. (See "Indications and hemoglobin thresholds for red blood cell

transfusion in the adult" and "Treatment of iron deficiency anemia in adults".)

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

pregnancy [54,55]. 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 [ 56]. However, unexplained

PPH that does not respond to general measures should alert clinicians to the possibility of a bleeding disorder

as a causative factor [57], 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 patient with a bleeding

diathesis".)

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SECONDARY POSTPARTUM HEMORRHAGE — Secondary PPH refers to excessive uterine bleeding

occurring between 24 hours and 12 weeks postpartum. Most studies report peak incidence at one to two

weeks postpartum [58]. It affects 0.2 to 2 percent of women in high income countries [ 58-60].

The most common cause is diffuse uterine atony or subinvolution of the placental site secondary to retained

products of conception and/or infection. A bleeding diathesis may also be responsible. Pseudoaneurysm of the

uterine artery and arteriovenous malformations are rare causes of secondary PPH described in case reports

[61-68]. Choriocarcinoma is rare, but may present as prolonged, new, or increased bleeding postpartum. Some

cases have been attributed to excessively strong resumption of menses [58]. Sometimes the cause cannot bedetermined.

A history of primary PPH is a risk factor for severe secondary PPH [60,69,70]. Unlike primary PPH, bleeding

is not catastrophic in most patients. A previous history of secondary PPH appears to predispose to a

recurrence, as with primary PPH [70-72].

Our approach — Our approach to diagnosis and management of secondary PPH is illustrated by the algorithm

(algorithm 3).

Diagnostic evaluation — A thorough history and physical examination should be performed. Evaluation for

a bleeding diathesis, such as von Willebrand disease, should be considered, especially in women with a

history of menorrhagia or other personal or family history of excessive or unusual bleeding. Basic laboratoryscreening for a bleeding diathesis includes platelet count, prothrombin time, and activated partial

thromboplastin time; however, these tests may be normal in women with von Willebrand disease. (See

"Approach to the adult patient with a bleeding diathesis", section on 'Laboratory testing' and "Approach to the

adult patient with a bleeding diathesis", section on 'Diagnostic approach' .)

Ultrasound examination (including color and spectral flow Doppler) of the uterus may detect the cause of

bleeding, and will help exclude some potential bleeding sources in the differential diagnosis (see 'Ultrasound

images' below). However, the postpartum uterus has a variable appearance on ultrasound examination and

there is considerable overlap between normal postpartum findings and findings associated with secondary

bleeding [73,74]. In both cases, the uterus may be empty or contain gas, fluid, or echogenic material.

Vascularity of echogenic intracavitary material is a key finding as vascularity on color Doppler suggests

retained products whereas lack of vascularity is consistent with blood clot, but does not exclude the presence

of retained necrotic (avascular) placental tissue. If no intracavitary mass, endometrial fluid, or vascularity is

seen and the endometrial thickness is thin, retained products are not likely. (See "Overview of postpartum

care", section on 'Ultrasound of the involuting uterus'.)

In women with bleeding many weeks after delivery, a quantitative pregnancy test is useful for evaluating for

choriocarcinoma, retained products of conception, or even a new pregnancy. Ultrasound examination and serial

determinations of human chorionic gonadotropin may be needed to distinguish among these entities when the

test is positive. (See "Gestational trophoblastic neoplasia: Epidemiology, clinical features, diagnosis, staging,

and risk stratification".)

Ultrasound images

Management — There are no data from randomized controlled trials to guide management [59]. Because

sonographic evidence of accumulation of fluid and debris in the uterine cavity is a common finding in the

involuting uterus, ultrasound may not distinguish patients requiring surgical versus medical therapy [60,75,76].

If the uterus is atonic, uterotonic agents are given. Options include oxytocin infusion, methylergonovine (0.2 mg

intramuscularly, repeated every two to four hours up to three doses), or intramuscular carboprost tromethamine

Normal postpartum uterus (image 1)●

Retained products of conception (image 2)●

Vascularized retained products of conception (image 3)●

Blood clot in postpartum uterus (image 4)●

Endometritis (image 5)●

Choriocarcinoma (image 6 and image 7)●

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(Hemabate, 250 mcg intramuscularly; up to eight doses at intervals of no less than 15 minutes). These agents

will not be useful if the uterus is firm.

If bleeding is not massive and fever, uterine tenderness, and/or a malodorous discharge are present, then

endometritis should be suspected. Under these circumstances, we prescribe broad spectrum antibiotic therapy

(table 5). However, some clinicians administer antibiotics to all patients with secondary PPH, including those

without obvious signs of infection. Rare, but potentially lethal causes of endometritis include Clostridium

sordellii [77-80], Clostridium perfringens [81], and streptococcal or staphylococcal toxic shock syndrome [82-

84]. (See "Postpartum endometritis", section on 'Endometritis with toxic shock syndrome' .)

Women diagnosed with a bleeding diathesis should be treated as appropriate for the underlying disorder.

Consultation with a hematologist is advised.

Surgical procedures (dilation and curettage, suction curettage) are directed at evacuation of retained products

of conception, which are more common after vaginal than cesarean delivery and when a vascularized

endometrial mass is noted on color Doppler. However, these procedures are often effective when medical

management fails, even if retained placental or membrane fragments cannot be identified sonographically

[60,85]. As an example, a study of 132 consecutive women with secondary PPH reported 75 (57 percent) were

initially treated with surgical evacuation, which was successful in 67 (90 percent) [ 60]. Of the 57 women

initially managed medically, treatment was successful in 41 (72 percent); 16 women had continuing symptoms,

of whom 12 subsequently underwent surgical evacuation. Tissue specimens were obtained at surgery in only

38 women and just one-third of these had histological confirmation of placental tissue.

Ideally, curettage is performed under ultrasound guidance. This is likely to reduce the rate of perforation, will

allow identification of placental tissue, and confirm that this tissue has been evacuated [73]. Suction curettage

should be employed when bleeding is over 500 mL and is not controlled by medical measures. The size of the

suction cannula is determined by the size of the uterus. The diameter of the cannula is usually chosen

according to the uterine size by gestational age (eg, a 12 mm cannula for a uterus of 12 weeks size) with a

minimum diameter of 10 mm and a maximum diameter of 16 mm.

Uterine perforation and formation of intrauterine adhesions are the major complications of surgery. In the series

described above, perforation occurred in 3 percent of cases [ 60]. (See "Intrauterine adhesions".)

Selective arterial embolization is a good option for women with vascular lesions as the source of bleeding, but

has also been effective for controlling severe bleeding refractory to uterotonic drugs or uterine curettage

[58,86].

Management of patients with gestational trophoblastic disease is reviewed separately. (See "Gestational

trophoblastic neoplasia: Epidemiology, clinical features, diagnosis, staging, and risk stratification".)

Use of uterotonic drugs in breastfeeding women — Oxytocin can be administered to breastfeeding mothers.

Limited information indicates that maternal doses of methylergonovine up to 0.75 mg daily produce low levels

in milk and would not be expected to cause any adverse effects in breastfed infants. Although results of several studies are mixed, it appears that methylergonovine can decrease serum prolactin and possibly the

amount of milk production and duration of lactation, especially when used in the immediate postpartum period.

The effect seems to be related to the dosage and route of administration, with injected doses having a greater

impact than oral. A few oral doses may not severely affect lactation; however, methylergonovine should

probably not be the first-line uterotonic in mothers who wish to nurse. The US Food and Drug Administration

recommends women avoid breastfeeding for at least 12 hours after receiving their last dose of

methylergonovine and discard breast milk produced during this period. This recommendation was made in the

absence of any available evidence of risk to breastfed infants, and has not been endorsed by other experts

[87].

Ergotamine in breast milk may cause vomiting and diarrhea in exposed infants. The drug may also inhibitprolactin secretion and lower milk production. It is generally not recommended for breastfeeding women.

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 5 to 6th th

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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 10 to 12 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.)

SUMMARY AND RECOMMENDATIONS

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.

REFERENCES

th th

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

We make the diagnosis of postpartum hemorrhage (PPH) in women with excessive bleeding that causes

symptoms (eg, lightheaded, palpitations, diaphoresis, confusion) and/or results in signs of hypovolemia

(eg, hypotension, tachycardia, oliguria, decreased oxygen saturation). (See 'Diagnosis' 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 'Definitions' above.)

●

The most common causes of PPH are atony, trauma, and acquired or congenital coagulation defects.(See 'Pathogenesis' above.)

●

Although there are many known risk factors for PPH, knowledge of these risk factors is not always

clinically useful in prevention of hemorrhage. (See 'Pathogenesis' above.)

●

The approach to management of PPH varies depending on the cause 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 'Management' above.)

●

Massive transfusion requires close monitoring of volume status, hemodynamic effects, coagulation

parameters, and electrolyte levels. Resuscitative efforts can be compromised by cardiac dysfunction

from potassium and calcium imbalances that result from rapid transfusion of stored blood. (See 'Key

components of evaluation and treatment' above.)

●

Coordination is essential and can be facilitated by protocols and flow diagrams; the following table ( table

3) and algorithms are representative examples (algorithm 1 and algorithm 2). In addition, numerous

professional organizations have provided guidance for team management of PPH (eg, California Maternal

Quality Care Collaborative). (See 'Guidelines from professional organizations' above.)

●

Our approach to evaluation and management of women with secondary postpartum hemorrhage is

described in the algorithm (algorithm 3). (See 'Secondary postpartum hemorrhage' above.)

●

Because of ease of treatment and a lesser incidence of severe side effects, we recommend that patients

with anemia be treated with an oral, rather than a parenteral, iron preparation (Grade 1B). (See 'Severe

postpartum anemia' above.)

●

Women with a prior PPH have as much as a 10 percent risk of recurrence in a subsequent pregnancy.

(See 'Recurrence' above.)

●

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GRAPHICS

Symptoms related to blood loss with postpartum hemorrhage

Blood loss,

percent (mL)

Blood

pressure, mm

Hg

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. Baillieres Best Pract Res Clin Obstet Gynaecol 200 0; 14:1.

Graphic 56885 Version 3.0


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Potential interventions for treatment of postpartum hemorrhage

Pharmacologic interventions

Drug Dosing

Oxytocin 10 to 40 units in 500 to 1000 mL saline infused at a rate sufficient to

control atony or 10 units IM

Ergots Methyl-ergonovine 0.2 mg IM every two to four hours or ergometrine

0.5 mg IV or IM or ergonovine 0.25 mg IM or IV every two hours

Carboprost 0.25 mg IM every 15 to 90 minutes up to eight 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 two hours

Recombinant

human Factor

VIIa

50 to 100 mcg/kg every two hours

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

Internal iliac artery (hypogastric artery) ligation

Aortic compression

Hysterectomy, supracervical

Hysterectomy, total

Interve

overview of postpartum hemorrhage

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