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Overview of postpartum hemorrhage

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
Literature review current through: Aug 2021. | This topic last updated: Jul 26, 2021.

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].

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. Prior PPH and prolonged labor are the most well-established risk factors for atony-related PPH, but many other risk factors have been suggested [10].

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 [11].

Trauma — Trauma-related bleeding can be due to lacerations (including uterine rupture) or surgical incisions. In one series, trauma (genital or surgical) was the most common cause of PPH >2500 mLs, more common than atony alone (192 versus 80 of 349 cases) [12].

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 [13]. (See "Uterine rupture: Unscarred uterus" and "Uterine rupture: After previous cesarean birth".)

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 (eg, placenta accreta spectrum). (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(See 'Assessment and management of risk' below.)

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 [14]:

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 [15]:

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, sepsis, fetal demise), assisted reproductive technology, anemia, gestational age 41 to 42 weeks, and use of some drugs (uterine relaxants, antithrombotic drugs, antidepressants [particularly selective serotonin reuptake inhibitors and serotonin-norepinephrine reuptake inhibitors]) [11,16-29].

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. It was the most frequently observed coagulation deficit in a cohort of patients with massive PPH, occurring in 17 percent of cases [12].

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 [30]. 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 [31]:

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 [32]. 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

Assessment and management of risk

Assessment — In the US, The Joint Commission recommends that hospitals use an evidence-based assessment tool for determining maternal hemorrhage risk on admission to the labor and delivery unit and on admission to the postpartum unit [33]. Those with risk factors for PPH should be counseled as appropriate for their level of risk and gestational age. (See 'Risk factors and specific etiologies' above.) However, for most patients, knowledge of risk factors for PPH is not useful clinically because many women without risk factors experience severe PPH (40 percent in one study [11]) [24,34], and most high-risk women do not experience significant hemorrhage (risk of severe hemorrhage ranges from 2 to 7 percent [34,35]). 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 [34].

Two examples of risk scoring systems are described below, and others are available (eg, Association of Women’s Health, Obstetric and Neonatal Nurse; New York Safety Bundle for Obstetric Hemorrhage). No risk scoring or prognostic model for prediction of PPH has proven utility in the general obstetric population [36].

Risk stratification and planning system (table 3)

California Maternal Quality Care Collaborative risk classification scheme for patients admitted to the labor unit [37]:

Low risk (transfusion preparation: clot only)

-Singleton pregnancy

-≤4 previous vaginal deliveries

-No previous uterine surgery

-No history of PPH

-No known bleeding disorder

Medium risk (transfusion preparation: type and screen)

-Prior uterine surgery

->4 previous vaginal deliveries

-Multiple gestation

-Large fibroids

-Chorioamnionitis

-History of PPH

High risk (transfusion preparation: type and crossmatch)

-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

Subsequent intrapartum and postpartum red flags associated with increased risk for PPH include a prolonged second stage of labor, prolonged oxytocin administration for induction or augmentation of labor, active bleeding, chorioamnionitis, assisted vaginal delivery (vacuum or forceps), emergency cesarean birth, and retained placenta.

Management — Planning for PPH involves ensuring availability of resources that might be needed, including personnel, uterotonic and other medications, equipment for control of bleeding, adequate intravenous access, topical hemostatic agents, 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.

Based on the risk assessment system used by the hospital facility, when the patient arrives on the labor unit for delivery, a clot should be sent to the blood bank for women at low risk of PPH, blood should be typed and screened for women with a medium risk factor for PPH, and blood should be typed and crossmatched for those at high risk of 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 [38]. (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 [39]. 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 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. (See "Management of the third stage of labor: Prophylactic 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 "Placenta accreta spectrum: Management" 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')

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 [40-42]. 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 [43-45]. 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 [46].

The California Maternal Quality Care Collaborative provides comprehensive information in several formats for management of PPH, including as a table (table 4).

The following tables and figure provide additional examples (table 3 and table 5 and figure 1), and links to additional society and government-sponsored guidelines from selected countries and regions around the world are provided separately. There appears to be a large variation in obstetric and hematologic management of severe PPH across resource-abundant countries [47]. (See 'Society guideline links' below.)

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 [48,49]. (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 [50]. 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 [51]; 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 6) [49].

Training and simulation — The Joint Commission recommends that obstetric staff [52]:

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 [31]. This is an important factor for early recognition of excessive blood loss and timely initiation of life-saving interventions [53-55]:

Volumetric measurement – Collect blood in graduated measurement containers, such as V-drapes with calibrated pockets and calibrated suction canisters.

Visual aids – 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.

Gravimetry – 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 [56]. 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 [57].

Colorimetry addresses some of the limitations of other methods. A smartphone application calculates blood loss by taking photographs of used surgical gauze and canisters and then filtering out the effects of non-blood components mixed into each sponge and canister. The hemoglobin mass present in the gauze or canister is then calculated from the image and subtracted from the preoperative hemoglobin level. A meta-analysis found this method correlated well with a validated reference, but more data are needed before it can be recommended for clinical use [58].

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 [59,60]. 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 [61,62]. 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 (table 7) [63,64]. (See 'PPH protocols and algorithms' above.)

In ambulances and facilities where definitive treatment of PPH is not possible or will be delayed because of lack of resources, use of a non-pneumatic anti-shock garment (NASG) may reduce bleeding, stabilize patients until they are transferred to an appropriate referral/tertiary facility, and decrease mortality from hypovolemic shock [65-69]. It consists of nine articulated segments that are wrapped tightly and sequentially around the legs, pelvis, and abdomen and then closed with Velcro. It is thought to work by applying circumferential counterpressure, thus decreasing blood flow to the compressed area (abdomen, pelvis, and lower extremities), and increasing blood flow to the heart, lungs, and brain. The addition of a small foam ball provides uterine compression. Intrauterine balloon tamponade can also be employed. With minimal training, NASG can be applied within two minutes and is reusable. In an analysis of five observational studies, NASG use was associated with a ≥50 percent reduction in median blood loss in three of four studies and a smaller reduction in one study [65]. The analysis also found a 38 percent reduction in mortality overall across the five studies, although one study reported increased mortality.

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 [70]. 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. Point-of-care testing provides nearly real-time data for guiding transfusion of blood products. Viscoelastic testing is a point of care method for monitoring coagulation function. Its use leads to better hemorrhage control, in part because of rapid detection and targeted treatment of hypofibrinogenemia and thrombocytopenia. (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 8) 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 [71].

Treatment of atony, the most common cause of PPH, is influenced by both the route of delivery and severity of bleeding (table 9). 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 "Placenta accreta spectrum: Management".)

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 [72], our approach is described separately (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 also addressed separately. (See "The approach to the patient who declines blood transfusion".)

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

If the patient is coagulopathic with an extremely low fibrinogen level (50 to 100 mg/dL), cryoprecipitate and/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 [73]. 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 [74]. 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 [75]. By comparison, the rate of transfusion in the overall obstetric population of the United States is 4 to 7 per 1000 deliveries [76], and the frequency of transfusion in PPH deliveries was 16 percent in 2014 [4]. (See "Postpartum hemorrhage: Medical and minimally invasive management", section on 'Transfuse red blood cells, platelets, plasma'.)

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 [75]. 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 [75].

Thromboembolism prophylaxis — In trauma patients, transfusion is an independent risk factor for development of thromboembolism [77]. 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 [78]. 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 [75]. 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 [79].

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 [80,81]. Uterine compression sutures used to treat PPH have also been associated with the development of intrauterine adhesions [82-85].

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 [86].

Treatment – Severe anemia due to PPH may require one or more 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 [87,88]. 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 [88]. Nevertheless, most women with mild to moderate anemia resolve the anemia sufficiently rapidly with oral iron, and it is cheap and convenient [89-91]. 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 [92]. It is no more effective than iron therapy in this setting [93], 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 [86].

RECURRENCE — Women with a prior PPH have as much as an 18 percent risk of recurrence in a subsequent pregnancy [94-96]. 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 [97]. However, unexplained PPH that does not respond to general measures should alert clinicians to the possibility of a bleeding disorder as a causative factor [98], 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: Prophylactic 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

Definitions:

Primary postpartum hemorrhage (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.)

Causes:

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

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.)

Clinical findings and diagnosis:

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

Planning and prevention:

All hospitals managing pregnant and postpartum women should have 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.)

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 6), and training/simulation. However, only a small proportion of at-risk women develop PPH (abnormal placentation is an exception), and many women without risk factors experience PPH. (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. (See 'Assessment and management of risk' above.)

Management:

Many interventions are available for management of PPH (table 8). The approach to management of PPH varies depending on the cause and severity of bleeding (table 9) 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.)

Recurrence:

Women with a prior PPH have as much as an 18 percent risk of recurrence in a subsequent pregnancy. (See 'Recurrence' above.)

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

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  80. March CM. Intrauterine adhesions. Obstet Gynecol Clin North Am 1995; 22:491.
  81. Schenker JG. Etiology of and therapeutic approach to synechia uteri. Eur J Obstet Gynecol Reprod Biol 1996; 65:109.
  82. Poujade O, Grossetti A, Mougel L, et al. Risk of synechiae following uterine compression sutures in the management of major postpartum haemorrhage. BJOG 2011; 118:433.
  83. Rasheed SM, Amin MM, Abd Ellah AH, et al. Reproductive performance after conservative surgical treatment of postpartum hemorrhage. Int J Gynaecol Obstet 2014; 124:248.
  84. Rathat G, Do Trinh P, Mercier G, et al. Synechia after uterine compression sutures. Fertil Steril 2011; 95:405.
  85. Ibrahim MI, Raafat TA, Ellaithy MI, Aly RT. Risk of postpartum uterine synechiae following uterine compression suturing during postpartum haemorrhage. Aust N Z J Obstet Gynaecol 2013; 53:37.
  86. Milman N. Postpartum anemia II: prevention and treatment. Ann Hematol 2012; 91:143.
  87. Holm C, Thomsen LL, Norgaard A, Langhoff-Roos J. Single-dose intravenous iron infusion or oral iron for treatment of fatigue after postpartum haemorrhage: a randomized controlled trial. Vox Sang 2017; 112:219.
  88. Sultan P, Bampoe S, Shah R, et al. Oral vs intravenous iron therapy for postpartum anemia: a systematic review and meta-analysis. Am J Obstet Gynecol 2019; 221:19.
  89. Bhandal N, Russell R. Intravenous versus oral iron therapy for postpartum anaemia. BJOG 2006; 113:1248.
  90. Anemia during pregnancy and in the postpartum: intravenous iron therapy revisited. Eur J Obstet Gynecol Reprod Biol 2005; 123 Suppl 2:S1.
  91. Perelló MF, Coloma JL, Masoller N, et al. Intravenous ferrous sucrose versus placebo in addition to oral iron therapy for the treatment of severe postpartum anaemia: a randomised controlled trial. BJOG 2014; 121:706.
  92. Kotto-Kome AC, Calhoun DA, Montenegro R, et al. Effect of administering recombinant erythropoietin to women with postpartum anemia: a meta-analysis. J Perinatol 2004; 24:11.
  93. Wågström E, Akesson A, Van Rooijen M, et al. Erythropoietin and intravenous iron therapy in postpartum anaemia. Acta Obstet Gynecol Scand 2007; 86:957.
  94. Oberg AS, Hernandez-Diaz S, Palmsten K, et al. Patterns of recurrence of postpartum hemorrhage in a large population-based cohort. Am J Obstet Gynecol 2014; 210:229.e1.
  95. Ford JB, Roberts CL, Bell JC, et al. Postpartum haemorrhage occurrence and recurrence: a population-based study. Med J Aust 2007; 187:391.
  96. Ruiter L, Kazemier BM, Mol BWJ, Pajkrt E. Incidence and recurrence rate of postpartum hemorrhage and manual removal of the placenta: A longitudinal linked national cohort study in The Netherlands. Eur J Obstet Gynecol Reprod Biol 2019; 238:114.
  97. Kadir RA, Kingman CE, Chi C, et al. Is primary postpartum haemorrhage a good predictor of inherited bleeding disorders? Haemophilia 2007; 13:178.
  98. Kadir RA, Aledort LM. Obstetrical and gynaecological bleeding: a common presenting symptom. Clin Lab Haematol 2000; 22 Suppl 1:12.
Topic 6710 Version 135.0

References

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14 : Obstetric risk factors and outcome of pregnancies complicated with early postpartum hemorrhage: a population-based study.

15 : Massive blood transfusion during hospitalization for delivery in New York State, 1998-2007.

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49 : Patient blood management in obstetrics: prevention and treatment of postpartum haemorrhage. A NATA consensus statement.

50 : Preventing severe hypocalcemia during surgery for placenta accreta spectrum.

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53 : Measurement of blood loss: review of the literature.

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56 : Methods for blood loss estimation after vaginal birth.

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61 : Pregnancy-related mortality in California: causes, characteristics, and improvement opportunities.

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63 : Use of Maternal Early Warning Trigger tool reduces maternal morbidity.

64 : The maternal early warning criteria: A proposal from the national partnership for maternal safety.

65 : Combined analysis of the non-pneumatic anti-shock garment on mortality from hypovolemic shock secondary to obstetric hemorrhage.

66 : A cluster randomized controlled trial of the non-pneumatic anti-shock garment for obstetric haemorrhage: sub-analysis of the Zimbabwean Arm.

67 : Implementation project of the non-pneumatic anti-shock garment and m-communication to enhance maternal health care in rural Tanzania.

68 : Non-pneumatic anti-shock garment for improving maternal survival following severe postpartum haemorrhage: a systematic review.

69 : Non-pneumatic anti-shock garment to stabilize women with hypovolemic shock secondary to obstetric hemorrhage.

70 : Non-pneumatic anti-shock garment to stabilize women with hypovolemic shock secondary to obstetric hemorrhage.

71 : Postpartum Hemorrhage: Prevention and Treatment.

72 : Postpartum hemorrhage: when uterotonics and sutures fail.

73 : Outcomes of pelvic arterial embolization in the management of postpartum haemorrhage: a case series study and systematic review.

74 : The WOMAN Trial (World Maternal Antifibrinolytic Trial): tranexamic acid for the treatment of postpartum haemorrhage: an international randomised, double blind placebo controlled trial.

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77 : A prospective study of venous thromboembolism after major trauma.

78 : Cutting-edge advances in the medical management of obstetrical hemorrhage.

79 : Normative postpartum intraabdominal pressure: potential implications in the diagnosis of abdominal compartment syndrome.

80 : Intrauterine adhesions.

81 : Etiology of and therapeutic approach to synechia uteri.

82 : Risk of synechiae following uterine compression sutures in the management of major postpartum haemorrhage.

83 : Reproductive performance after conservative surgical treatment of postpartum hemorrhage.

84 : Synechia after uterine compression sutures.

85 : Risk of postpartum uterine synechiae following uterine compression suturing during postpartum haemorrhage.

86 : Postpartum anemia II: prevention and treatment.

87 : Single-dose intravenous iron infusion or oral iron for treatment of fatigue after postpartum haemorrhage: a randomized controlled trial.

88 : Oral vs intravenous iron therapy for postpartum anemia: a systematic review and meta-analysis.

89 : Intravenous versus oral iron therapy for postpartum anaemia.

90 : Anemia during pregnancy and in the postpartum: intravenous iron therapy revisited.

91 : Intravenous ferrous sucrose versus placebo in addition to oral iron therapy for the treatment of severe postpartum anaemia: a randomised controlled trial.

92 : Effect of administering recombinant erythropoietin to women with postpartum anemia: a meta-analysis.

93 : Erythropoietin and intravenous iron therapy in postpartum anaemia.

94 : Patterns of recurrence of postpartum hemorrhage in a large population-based cohort.

95 : Postpartum haemorrhage occurrence and recurrence: a population-based study.

96 : Incidence and recurrence rate of postpartum hemorrhage and manual removal of the placenta: A longitudinal linked national cohort study in The Netherlands.

97 : Is primary postpartum haemorrhage a good predictor of inherited bleeding disorders?

98 : Obstetrical and gynaecological bleeding: a common presenting symptom.