Postpartum Hemorrhage

Abstract

Obstetric hemorrhage is the leading cause of maternal death in childbirth; it is estimated that one woman dies every four minutes from postpartum hemorrhage (PPH). PPH is the cause of approximately one-quarter of maternal deaths worldwide and is thus a major public health issue of great importance. Despite modern advances in medicine, hemorrhage continues to lead the causes of pregnancy-related death in most countries, with increasing disparity between countries with highly developed and underdeveloped national healthcare systems. Most deaths caused by PPH are preventable. All involved in the care of pregnant women must be aware of the gravity of this problem, ways of identifying women at risk for severe hemorrhage at childbirth, strategies for preventing and ameliorating blood loss at delivery, and finally ways to deal with obstetric hemorrhage when it does occur. This article reviews the impact of obstetric hemorrhage, the controversy regarding definitions, diagnosis, epidemiology, pathophysiology, and management of obstetric hemorrhage.

Introduction

Bleeding is an inevitable part of childbirth. Obstetric hemorrhage has through the ages been a major contributor to death in childbirth; it is estimated that one woman dies every four minutes from postpartum hemorrhage (PPH).¹ Indeed, PPH is the cause of approximately one-quarter of maternal deaths worldwide.² Thus, obstetric hemorrhage is a major public health issue of great importance. Despite modern advances in medicine, hemorrhage continues to lead the causes of pregnancy-related death in most countries, with increasing disparity between countries with highly developed and underdeveloped national healthcare systems.^3,4

The majority of deaths caused by PPH are preventable.^5,6 As such, all involved in the care of pregnant women must be aware of the gravity of this problem, ways of identifying women at risk for severe hemorrhage at childbirth, strategies for preventing and ameliorating blood loss at delivery, and finally ways to deal with obstetric hemorrhage when it does occur.^5,7 The purpose of this article is to review the impact of obstetric hemorrhage, the controversy regarding definitions, diagnosis, epidemiology, pathophysiology, and management of obstetric hemorrhage. As most of the obstetric hemorrhage occurs postpartum, this review focuses on PPH.

Definition

Defining PPH is problematic, not only because of varying definitions, but more importantly, because of the challenges in assessing the amount of blood loss at delivery.^7,8,9,10 Visual inspection tends to underestimate the blood lost at delivery, and quantitative blood loss assessment has been proposed as a method to reduce this systematic underestimation and to achieve more accurate estimates of blood loss.^11,12

PPH has traditionally been defined as a blood loss of greater than 500 mL after vaginal delivery and 1000 mL after cesarean delivery.⁵ Others have attempted to use other clinical criteria, such as a drop in hematocrit of 10% or greater, to define PPH. However, in 1990, the World Health Organization (WHO), which was one of the first medical governing bodies to use this definition, acknowledged that that figure of 500 mL was an arbitrary one and ‘not always of great clinical significance.^6,12 Furthermore, Pritchard and colleagues, in the 1960s, using radioactive chromium tagging of red blood cells, demonstrated that the average blood loss at vaginal delivery was about 500mL and at elective cesarean delivery was about 1000 mL.^13,14 Thus, the 500 mL definition for PPH, a historical definition based arbitrarily on expert consensus, has little value.⁹

In 2017, the American College of Obstetricians and Gynecologists changed the definition of PPH to blood loss of 1000 mL or greater, or blood loss that is accompanied by symptoms and signs of hypovolemia within 24 hours of delivery, regardless of mode of delivery.⁶ The Dutch Society of Obstetrics and Gynecology uses the same definition. However, the Royal College of Obstetricians and Gynaecologists (RCOG) uses a different definition, categorizing PPH into “minor” (500 mL-1000 mL) and “major” (blood loss > 1000 mL).⁵ The RCOG goes further, dividing “major” PPH into “moderate” (1001 mL-2000 mL), and “severe” (> 2000 mL).⁵ Both the International Federation of Gynecology and Obstetrics (FIGO) and the Society of Obstetricians and Gynaceologists of Canada define it as blood loss of > 500 mL after vaginal delivery or > 1000 mL after cesarean delivery or any blood loss with the potential to cause hemodynamic instability.⁷

These varying definitions affect the reported incidence of PPH as well as thresholds for treatment. Kerr and Weeks argued that a single definition is not adequate for PPH. These authors make a case that there should be one definition to decide when to start treatment, another for audit purposes, and another for research.⁹ Finally, secondary PPH has been defined as excessive bleeding from 24 hours after delivery until 12 weeks postnatally.⁵

Epidemiology

The incidence of PPH has increased in the United States and other high-income countries over the past 20 years.^1,15,16 It is estimated that PPH occurred in 3% of deliveries in the US in 2012-2013.¹⁷ PPH has also increased worldwide, both in high-income and low- to middle-income countries.^18,19 A systematic review and meta-analysis found that PPH complicated 17% and 6% of births when PPH was defined as blood loss > 500 mL and > 1000 mL, respectively.¹⁹

Risk factors

Several risk factors for PPH have been identified.^19,20,21 However, it is important to recognize that a substantial proportion of PPH occurs in women with no known risk factors.²² One of the strongest risk factors for PPH is a history of PPH in a prior birth.²⁰ Multiparity has long been recognized to increase the risk for PPH.²⁰ Hypertensive disorders have been associated with an increased risk of PPH.²¹ Placenta previa and low-lying placenta are also strongly associated with an increased risk for PPH.²³ Prior cesarean birth, polyhydramnios, large babies, multifetal pregnancies, placental abruption, prolonged labor, preexisting bleeding disorders, fibroids, genital tract trauma, episiotomy, obesity, retained placenta and assisted delivery are all risk factors for PPH.¹⁹

Pathophysiology

The major mechanism of stopping bleeding after delivery is uterine contraction.¹ The myometrial fibers run in different directions that intersect with vessels running between them. Thus, uterine contraction compresses these vessels and leads to cessation of hemorrhage. As such, in most cases, it is uterine contraction that is the primary mechanism of controlling bleeding, even in patients with impaired coagulation.¹ It is following uterine contraction that platelets and coagulation factors are effective in preventing further blood loss. If this first step in controlling hemorrhage (uterine contraction) fails, especially when intravenous crystalloids are administered, a dilutional coagulopathy often ensues. The bleeding then becomes a vicious cycle which worsens until uterine contraction and correction of coagulopathy can be achieved.

In pregnancy, some physiological changes occur to ameliorate the effect on the mother of blood loss at delivery. These include increase in red cell mass and circulating blood volume. As such, the blood loss at delivery has less impact than loss of similar amounts of blood would have in a non-pregnant individual. Traditionally, the etiologies of PPH have been considered to be caused by 4 “Ts”: Tone (uterine atony), Tissue (retained placenta and clots), Trauma (lacerations or injury of the vagina, cervix, or uterus), and Thrombin (coagulopathies).

The first “T”, uterine atony, is by far the leading cause of PPH. Uterine atony may result from such factors as prolonged labor, uterine overdistension from polyhydramnios, multifetal gestations, effects of anesthesia, and infection. The second “T” (tissue) has gained increased prominence recently as placenta accreta spectrum has become more frequent, primarily as a result of the trend of increasing cesarean deliveries. Retained placental fragments also are a frequent cause of PPH. The third “T” (trauma) occurs when there are spontaneous or iatrogenic lacerations to the vagina, cervix, or lower uterus. This occurs iatrogenically from cesarean delivery and episiotomy, or with trauma from instrumental delivery. Uterine rupture is another source of PPH resulting from trauma. Finally, the final “T”, coagulopathy, may be pre-existing such as in thrombocytopenia, von Willebrand’s disease, anticoagulant therapy, or may be the result of consumptive or dilutional coagulopathy that may occur during labor from such etiologies as placental abruption, HELLP syndrome, and acute fatty liver of pregnancy.

Prevention

Perhaps the most important strategy for prevention of PPH is identification of patients at risk for PPH and taking steps to prevent PPH. Several risk assessment tools have been developed to predict patients at risk for PPH.²⁴ Unfortunately, most risk assessment tools when applied on admission to labor and delivery are poor predictors of PPH.^24,25

In patients deemed to be at risk for PPH, delivery should take place in centers with adequate resources and personnel to deal with PPH. Use of standardized protocols have been shown to reduce morbidity and improve teamwork when caring for patients with PPH.²⁶ Regular drills should be instituted. All units where women give birth should have a dedicated equipment cart for PPH.²⁶ It is recommended that this cart should contain instruction charts for rarely used equipment used to manage PPH such as tamponade balloons and compression sutures.²⁶

In particular, women with placenta previa and prior cesarean are at risk for placenta accreta spectrum (PAS) and should be screened for PAS during pregnancy.²³ Those considered at risk for PAS should be delivered in centers with adequate resources and personnel as well as experience in treating patients with PAS.²³ A multidisciplinary team approach is recommended. Assessment for anemia prenatally and correction of anemia may help reduce the morbidity from blood loss at delivery.

Active management of the third stage of labor with uterotonics has been recognized as highly effective in reducing the risk for PPH.^5,7,27,28,29 FIGO recommends prophylactic uterotonics for the third stage of labor for all births.⁷ They recommend that intravenous oxytocin be used as the first line prophylactic uterotonic in a dose of 10 international units (IU) administered intravenously or intramuscularly.⁷ This should be given within one minute of the birth of the baby.²⁸ FIGO also recommends use of other injectable uterotonics such as ergometrine or methylergometrine when oxytocin is unavailable. However, ergometrine and its derivatives should not be given to women with hypertension, preeclampsia or heart disease.^5,6 An alternative is oral misoprostol (400-600 micrograms) or carbetocin 100 micrograms given IM. All women after delivery should have an evaluation to ensure that the uterus remains contracted.⁵ Uterine massage may be helpful to achieve this, and all those caring for women delivering babies should be trained in this.²

Management of postpartum hemorrhage

Initial management

Timely recognition and appropriate and prompt management of PPH will reduce maternal morbidity and possibly mortality.⁸ As such, all involved in caring for women during childbirth must be aware of how to recognize and manage PPH. Delays in instituting preventive and therapeutic measures for PPH have been shown to be associated with increased risk for severe PPH and for morbidity and mortality.³⁰ Of prime importance is early identification of the severity of the hemorrhage.⁵ This requires clinicians being aware that visual estimations of blood loss tend to be inaccurate and that assessment of clinical symptoms and signs are an essential part of management of PPH.^5,11 When quantified by visual estimation, estimated blood loss has been shown to significantly underestimate large volume blood loss by as much as 33-50% compared to direct or quantitative measurement.^31,32 Clear and calm communication of the clinical situation to the patient and her birthing partner are vital.⁵ Assembling a multidisciplinary team (when available) is essential when severe PPH occurs.

Bimanual uterine massage should be instituted to ensure that the uterus is contracted. At least 2 wide bore intravenous lines should be inserted. A call should be made for assistance from staff that have the appropriate expertise to deal with PPH.⁵ Careful inspection of the genital tract should be performed to rule out lacerations.

In patients with PPH, replacement of volume and blood products in a timely manner is crucial. FIGO recommends that intravenous (IV) isotonic crystalloids (as opposed to colloids) should be used as first line volume replacement.⁷ Blood should be drawn for a complete blood count, crossmatch and coagulation studies. Vital signs (BP, pulse) and urine output should be monitored closely. An algorithm for the prevention and management of PPH is shown in Fig. 1.

Figure 1.

An algorithm for the prevention and management of PPH. Used with permission from: Evensen A, Anderson JM, Fontaine P. Postpartum Hemorrhage: Prevention and Treatment. Am Fam Physician. 2017 Apr 1;95(7):442-449. PMID: 28409600. Copyright American Academy of Family Physicians. ^*The American College of Obstetricians and Gynecologists defines early postpartum hemorrhage as blood loss of 1000 mL or more accompanied by signs and symptoms of hypovolemia, cumulative blood loss of 500 to 999 mL alone should trigger increased supervision and potential interventions as clinically indicated. ^†Oxytocin should be used as a first-line agent, with other agents added only if needed to control hemorrhage. IM: Intramuscular; IU: International Unit; PPH: Postpartum hemorrhage.

Pharmacological therapies

Uterotonics

FIGO recommends that IV oxytocin alone should be used as the first line uterotonic for the treatment of PPH.⁷ Oxytocin has the advantages of being cheap, generally easily accessible, with few contraindications and side effects, and acts within 2-3 minutes. For intravenous administration, 10 IU of oxytocin can be added to 1000 milliliters of a non-hydrating IV solution and given over 30 minutes. Following the initial bolus or intramuscular dose of 10 IU, an additional 10-40 IU of oxytocin can be added to 1000 mL of a non-hydrating IV solution, which can be infused at a maintenance rate of 125 milliliters per hour to control uterine atony for the next 3-4 hours. However, when the PPH is not responsive to oxytocin, intramuscular ergometrine is recommended.⁷ Oxytocin requires careful storage and refrigeration, and the WHO and FIGO have given instruction on the importance of adequate storage facilities. In cases in which these are not available, carbetocin, a more stable alternative, may be used.⁸ Additional alternatives for uterotonics include carboprost (15-methyl PGF2α), a prostaglandin analogue administered as an intramuscular injection at a dose of 0.25 milligrams. It may also be injected directly through the abdominal wall into the uterus. Carboprost may be administered every 15-90 minutes, with a maximum of eight doses. Absolute contraindications for carboprost include asthma due to the potential risk of bronchospasm. Relative contraindications include hypertension, active hepatic, pulmonary, or cardiac disease.

Tranexamic acid

Tranexamic acid (TXA) is an antifibrinolytic that is now frequently used in the treatment of patients with PPH.^6,33,34,35 It is a synthetic analog of the amino acid lysine and exerts its effects by preventing conversion of plasminogen to plasmin. The fibrinolytic pathway is thought to be a factor in the pathogenesis of PPH, and hence antifibrinolytic therapy had been proposed as a potential therapy for PPH.³⁶ Early experience had found that TXA was highly effective in reducing blood loss in orthopedic surgery, trauma, dental surgery, cardiovascular surgery, and for menorrhagia. FIGO recommends the early use of intravenous tranexamic acid as soon as a diagnosis of PPH (defined as clinically estimated blood loss exceeding 500 mL after vaginal delivery or 1,000 mL following cesarean) is made. 7 However, TXA is ineffective when administered greater than 3 hours after delivery.³⁶ TXA is generally administered in a dosage of 1 gram intravenously over 10-20 minutes.⁷

The efficacy of TXA in reducing blood loss in patients with PPH and need for blood transfusions in both vaginal and cesarean delivery has been demonstrated in several randomized controlled trials and 2 recent metaanalyses.^37,38,39,40 The WOMAN (World Maternal Antifibrinolytic Trial), an RCT of over 20,000 women with a diagnosis of PPH following vaginal or cesarean delivery in 193 hospitals in 21 countries found a reduction of death from bleeding (Risk Ratio = 0.69; 95% confidence interval = 0.52–0.91; P = 0.008) among women who received TXA within 3 hours of delivery compared with those treated with placebo.⁴¹ A systematic review and meta-analysis found that use of tranexamic acid reduced hysterectomy for PPH.³³ A randomized controlled trial (RCT) of 212 patients at high risk of PPH undergoing cesarean delivery found and average of approximately 200 mL lower blood loss among those given prophylactic TXA when compared to those given placebo.⁴² However, there was no difference in need for additional uterotonics between the groups and no patients required transfusions.⁴² In addition, a large multicenter RCT of prophylactic TXA for blood loss at cesarean delivery did not demonstrate a reduction in blood transfusions or composite morbidity among those women who received TXA when compared those treated with placebo.⁴³ Thus, while TXA has proven effective in treating PPH, routine prophylactic administration of the agent to prevent PPH is not currently recommended.^7,36

TXA is not significantly excreted in breast milk and hence can be given safely in breastfeeding women.³⁶ Side effects are common with TXA. These include headaches in 50%, and abdominal, back, or musculoskeletal pain in up to 20% of patients.⁷ Importantly, large studies have not demonstrated an increased incidence of thromboembolic events in patients being treated for PPH with TXA.^34,36 In summary, tranexamic acid is an effective, inexpensive, and safe agent that should be used early in the treatment of PPH.^34,41

Blood transfusion and coagulation factor replacement

An essential component of managing PPH is correction of hypovolemia and treatment of coagulopathy.^5,6,7,44 The first recorded transfusion of human blood to another human was by an English obstetrician, James Blundell for the treatment of PPH in 1818. Blood transfusion may be life-saving when PPH occurs, and aggressive replacement of packed red blood cells and coagulation factors is an indispensable component of the treatment of acutely hemorrhaging patients with hypovolemic shock.⁴⁴ The RCOG states that “there are no firm criteria for initiating blood transfusion”.⁵ Blood transfusion administration should be determined by the clinical situation including amount of blood lost, the patient’s clinical status, risk factors, and the results of lab tests.^5,6,7 For instance, a patient with preexisting anemia may have a lower threshold for transfusion that one with a normal pre-delivery hemoglobin. Importantly, the hemoglobin level alone should not determine blood transfusion, since deaths have occurred in women with PPH and normal hemoglobin values.⁵ Furthermore, changes in vital signs such as tachycardia and hypotension may not occur until the amount of blood lost is critical.⁴⁵ It is generally recommended to replace coagulation factors when transfusion exceeds 2-3 units of packed red blood cells. In most situations, fresh frozen plasma (FFP) will be the first-line coagulation factor replacement. The first step in correcting coagulopathy is replacing fibrinogen, an essential clotting factor and the one that typically drops below critical values when PPH occurs.⁷ When the fibrinogen level drops to < 200 mg/dL, urgent replacement is indicated, and target values should be to maintain the fibrinogen at > 200 mg/dL. Typically, one unit of fresh frozen plasma is given per 2-3 units of packed red blood cells transfused. However, FFP is relatively low in fibrinogen, and cryoprecipitate, which contains 2g of fibrinogen per unit, may be more effective, with one unit (100mL) raising serum fibrinogen by 10 mg/dL.⁷ FIGO recommends a 1-1-1 ratio of packed red blood cells, FFP, and platelets, stating that “this is associated with fewer complications and better patient survival outcomes.”⁷ It is essential that obstetric units have adequate transfusion facilities. Protocols must include access to blood group O, Rh-negative and K-negative blood for emergencies with the ability to provide group-specific and cross-matched blood promptly.⁵ Massive transfusion protocols are recommended when severe PPH occurs, and all involved in childbirth should be familiar with their unit’s protocol. These generally involve requirements of > 4 units of packed red blood cells, replacement of whole blood volume within 24 hours or 50% of blood volume within 3 hours.⁷

Intraoperative cell salvage

Intraoperative red cell salvage allows use of the patient’s own blood to replace blood loss.^46,47,48 In this process, lost blood is collected, filtered, and washed, yielding autologous red blood cells which are then transfused back into the patient.⁴⁷ Cell salvage has been shown to be safe, and prior fears about the potential for amniotic fluid embolism have proven unfounded.^47,48 Some Jehovah’s Witnesses, who will generally not accept blood products, may agree to cell salvage with autologous blood.⁴⁹ However, PPH is often unanticipated prior to the event, and in severe cases, massive transfusions may be necessary, making cell salvage of limited utility. In a small percentage of cell salvage, maternal sensitization from fetal red blood cells may occur.^47,48

Recombinant factor VIIa

Recombinant Factor VIIa (rFVIIa) has been used to treat hemorrhage in orthopedics and trauma and was proposed as a possible agent for the management of intractable obstetric hemorrhage. There are limited data from case series or observational obstetric studies that have examined rFVIIa for PPH.^50,51,52 There is some data that suggests that rFVIIa off-label use for treating intractable PPH increases the risk for arterial thromboembolic events. For these reasons, routine use of rFVIIa for treating PPH is not recommended outside a clinical trial.⁵ However, in life-threatening situations where no other options exist, it may be considered as a therapeutic option.⁵

Intrauterine tamponade

Because approximately 70% of PPH is the result of uterine atony, PPH refractory to initial therapy with uterotonics may be treated with a variety of intrauterine tamponade devices and compressive surgical therapies.⁵³ Intrauterine tamponade has long been used as a method of controlling PPH. The proposed rationale for this is using intrauterine pressure to overcome the pressure from the bleeding uterine surface as well as creating greater pressure than that in the uterine arteries and thereby leading to a cessation of bleeding.

Uterine packing

Early attempts at intrauterine tamponade were achieved via uterine packing with gauze.⁵⁴ Subsequently, an intrauterine Foley catheter was inflated to achieve uterine tamponade.⁵⁵ While uterine packing fell into disrepute because of concerns for infection and limited efficacy, there has been a resurgence in its use, especially in low resource countries. Schmid and colleagues successfully used intrauterine chitosan covered gauze packing for treatment of PPH in 19 women with no side effects, while Dueckelmann and colleagues successfully treated refractory PPH in 47 women with the same intervention, and found it both safe and as efficacious as intrauterine balloons.^56,57

Uterine balloon tamponade devices

While uterine tamponade was performed using a Foley catheter or a Sengstaken-Blakemore tube, perhaps the first dedicated balloon designed for intrauterine tamponade in obstetrics was the Bakri balloon.^58,59 The Bakri balloon when inflated, is effective in treating PPH. It is inflated with 300-500 mL of saline. It exerts its effect via outward pressure on the inside of the uterus, leading to cessation of bleeding in most cases. In low resource countries, a Foley catheter balloon or inflated male condom may also be used. The vagina is typically packed with gauze to keep the balloon in place and a catheter inserted into the bladder to drain urine. In low resource countries, other balloons have been used for uterine tamponade, including inflated male condoms. A systematic review and meta-analysis found that intrauterine balloon tamponade was effective in 85.9% of cases of refractory PPH.⁶⁰

Intrauterine vacuum devices

In 2020, a novel vacuum device, the Jada System^TM was cleared by the United States Food and Drug Administration for the treatment of refractory PPH.^61,62 This vacuum device induces low-level negative pressure within the uterine cavity.^53,61 This negative pressure leads to uterine contraction and constriction of blood vessels. The Prospective Single Arm Pivotal Clinical Trial Designed to Assess the Safety and Efficacy of the Jada System in Treating Primary PPH (PEARLE trial) evaluated the use of the Jada System in patients with uterine atony and PPH (defined as blood loss of 500 mL to 1500 mL following vaginal delivery or 1000 mL to 1500 mL following cesarean delivery).⁶² One hundred and six women at 12 US hospitals participated in the study. Blood loss control was achieved in 100/106 patients (94%) with a median time of control of 3 minutes. This device is an elliptical loop made of silicone containing 20 vacuum pores which is inserted into the uterus and attached to a low-level vacuum of approximately 80 mmHg. A cervical seal allows achievement and maintenance of the vacuum. The vacuum evacuates the blood from the uterus and the uterine walls collapse inwards. Once there is bleeding cessation, the device is left in the uterus for a minimum of one hour.

Surgical interventions

Devascularization techniques

A strategy to treat PPH involves uterine devascularization. A variety of surgical ligation techniques have been used to reduce blood flow to the uterus and hence lead to less hemorrhage.⁶³

Uterine artery ligation

One of the earliest descriptions of bilateral ligation of the uterine artery was by Waters in 1952.⁶⁴ He proposed that this procedure would shut off approximately 90% of uterine blood flow, and in addition would induce uterine contraction due to myometrial hypoxia.⁶⁴ In 1966, O’Leary and O’Leary published a description of a technique for bilateral uterine artery ligation, and the procedure is now frequently referred to by their eponym.⁶⁵ This technique was used in 10 patients with intractable PPH resulting from uterine atony or placental site hemorrhage, and successfully controlled the hemorrhage in eight of them.⁶⁵ The procedure involves ligating the uterine artery after the cervical branch leaves the uterine artery.⁶⁵ The uterine wall and broad ligament are grasped and then a curved needle passed through the myometrium encompassing the uterine arteries and the suture is then tied in the avascular area of the broad ligament.⁶⁵ This technique typically uses an absorbable suture such as chromic catgut. This allows recanalization within a few weeks, and thus restores uterine blood flow and does not have an impact on future pregnancies. A case-control study comparing 25 women who underwent bilateral uterine artery ligation for intractable hemorrhage at cesarean with 24 controls found no differences in subsequent ovarian reserve or ovarian blood supply between the groups.⁶⁶ The procedure is simple to perform and can be performed quickly.⁸ FIGO recommends that bilateral uterine artery ligation be considered for the control of PPH that has not responded to uterotonics or compressive sutures.⁷

Internal iliac (hypogastric) artery ligation

Bilateral ligation of the internal iliac arteries has often been performed as a method of reducing blood flow to the uterus and controlling PPH.^67,68 This procedure was reportedly first performed at the end of the 19^th century for control of hemorrhage from uterine cancer.^63,68,69,70 Subsequently, by the mid-20^th century, it was often employed as a life-saving surgical technique for intractable obstetric hemorrhage.^70,71 At the time, extensive surgical training was a routine part of obstetrics and gynecology residency programs and this technique was widely taught and as such most obstetricians had some experience in the procedure. To perform the procedure, laparotomy is performed, and the uterus exteriorized. The posterior peritoneal surface is incised in the triangle where the common iliac artery bifurcates. The internal iliac artery is then identified, dissected out from surrounding structures, and ligated with an absorbable suture. This is done by passing a right-angle clamp with an absorbable suture grasped between its claws from outwards inwards underneath the dissected internal iliac artery.⁶³ This suture is then tied over the internal iliac artery to occlude it. It is crucial to identify and avoid the ureter by mobilizing it away from the area of the ligation prior to the ligation.⁶³ It is also important to avoid damaging the underlying internal iliac vein.⁶³ It is recommended to perform the ligation 2 cm below where the common iliac artery divides to prevent ligation of the posterior branch which supply the gluteus muscle.⁶³

Joshi and colleagues performed bilateral internal iliac artery ligation in 88 women for PPH following vaginal or cesarean delivery, with the majority of these (32.7%) being due to uterine atony.⁶⁷ Uterine salvage was possible in approximately 60% of 84 women. Importantly, of those who required hysterectomy, the reason was irreparable damage from uterine rupture. The authors stated that internal iliac artery ligation allowed better control of blood loss in these cases and made the hysterectomies easier.⁶⁷

While internal iliac artery ligation was initially considered highly effective in controlling PPH, more recent data suggests less success. A systematic review indicated that internal iliac artery ligation is successful an average of 69% of the time.⁷² Studies have demonstrated that following the procedure, collateral circulation develops and there is recanalization of the internal iliac vessels, and as such, the procedure does not have lasting effects, and has no impact on future fertility and childbearing.^68,73

However, internal iliac artery ligation requires good knowledge of abdominal and pelvic anatomy, good surgical skills, and experience operating in that region. In particular, the iliac veins and the ureters are at risk of damage, and therefore this procedure can only be performed where the necessary surgical expertise is available. These skills are no longer as widely taught as they were a generation or two ago. Obstetricians are generally more familiar and comfortable with uterine artery ligation and uterine compression sutures.⁷⁴ For these reasons, in most locations, internal iliac artery ligation is no longer a practical therapy, except when skilled pelvic surgeons are available.⁶³

Uterine compression sutures

Because the majority of PPH is the result of uterine atony, compression of the uterus may be effective in treating PPH. In 1997, B-Lynch and colleagues described use of a compression suture to treat PPH.⁷⁵ These authors used a no. 2 chromic catgut suture to apply a compression suture that resembles a pair of suspenders or braces. Essentially, this suture brought the anterior and posterior uterine walls together and thus compressed the uterus. The first report of its use in 5 women demonstrated efficacy in controlling PPH.⁷⁵ The B-Lynch suture remains the most widely known and used of these techniques.⁷⁶ Uterine compression techniques are relatively easy to learn and perform, which gives them an invaluable role in the armamentarium of those who treat PPH. A systematic review found that these techniques are effective overall in about 92% of cases.⁷⁷ However, uterine compressive sutures for the treatment of PPH have been associated with complications including uterine necrosis, pyometra, and intrauterine adhesions.^78,79

Internal iliac and uterine artery embolization

The earliest published reports of emergency transcatheter angiographic embolization of the internal iliac arteries for the treatment of PPH emerged in the 1980s.^80,81,82 Internal iliac and uterine artery embolization requires fairly sophisticated interventional radiology services. However, if successful, they allow uterine preservation and the opportunity for future fertility.⁶ Generally, the approach is via the femoral artery using Seldinger’s technique. Temporary embolic agents such as gelatin sponges, gels, or microparticles are mixed with contrast material and injected under direct visualization using fluoroscopy. When there is a bleeding vessel, extravasation of contrast may occur allowing visualization and embolization of the vessel. With placenta accreta being diagnosed more often prenatally, and with increasing availability of interventional radiology, prophylactic embolization or intravascular placement of balloon catheters are being used more frequently. Uterine artery embolization for PPH has a reported median success rate of 89% (range 58-98%).⁶ These techniques carry some risk for potentially severe complications including vessel injury and rupture, accidental embolization of other structures such as gluteal muscles, allergic reactions, contrast induced renal damage, and pseudoaneurysm formation.^83,84 Whether uterine artery embolization has an impact on future fertility remains questionable. Aortic balloons may be used in the management of PPH, although they are more often used prophylactically in severe placenta accreta spectrum when massive hemorrhage is anticipated. Interventional radiology techniques should be reserved for the hemodynamically stable patient. In unstable patients, other interventions such as hysterectomy are more appropriate.^5,6

Hysterectomy

In cases of intractable life-threatening hemorrhage recalcitrant to conservative measures, hysterectomy should be performed. Obviously, this therapy deprives the patient of future childbearing, and therefore should not be undertaken in most situations except as a last resort. Nonetheless, it should not be forgotten that the purpose of any therapy is to preserve life; it is therefore essential to not delay the decision to perform a hysterectomy to the point where the patient loses their life. Subtotal (supracervical) hysterectomy may be appropriate in cases of uterine atony. It requires a shortened operating time and reduced morbidity when compared with total hysterectomy. However, in bleeding due to placenta previa or accreta, removal of the cervix is often necessary.¹

Interventional radiology

Resuscitative endovascular balloon occlusion of the aorta

Resuscitative endovascular balloon occlusion of the aorta (REBOA) is a temporary, fluoroscopy-free, ultrasound-guided hemorrhage management strategy used in trauma and vascular surgery. It has recently been employed to manage life-threatening PPH in unstable patients and prophylactically to mitigate bleeding in cases of placenta accreta spectrum.^85,86,87

REBOA offers several benefits: rapid hemorrhage control, minimal invasiveness, and the ability to buy time for more definitive surgical therapies under controlled circumstances. The procedure is performed by an interventional radiologist who gains common femoral arterial access using Seldinger’s technique under ultrasound guidance. A semi-compliant balloon catheter is then introduced into the abdominal aorta and intermittently inflated with isotonic saline. The balloon is deflated once hemostasis is achieved.⁸⁵ While REBOA shows promise, further research is needed to determine appropriate indications for the procedure, as well as its outcomes and complication rates, particularly in the context of PPH.

Other nontraditional surgical methods

Aortic compression

Aortic compression is a technique in which substantial pressure is exerted on the aorta through the mother’s abdominal wall.⁷ This procedure, if performed appropriately, may be life-saving. The fist of the performer is placed slightly to the left of the maternal umbilicus, and then pressure applied downward to compress the aorta. The performer uses their other hand to palpate the femoral pulse. If performed appropriately, the femoral pulse should disappear. This will act as a temporizing measure while other interventions are utilized.

Non-pneumatic anti-shock garments

These garments, typically made of inexpensive lightweight articulated neoprene segments held together tightly with Velcro, shunt blood from the lower body to essential organs.⁸⁸ They cause circumferential compression of the abdomen and lower extremities, which results in a reduction in total vascular volume, redirecting blood centrally. They reduce blood loss and may help reverse hypovolemic shock. They have been used effectively in low- to middle- income countries and have the potential to reduce maternal mortality from PPH.⁸⁸

Complications and long-term outcomes following postpartum hemorrhage

PPH may lead to shock, need for intensive care unit admission, disseminated intravascular coagulopathy, massive blood transfusion, renal failure, adult respiratory distress syndrome, surgical injury, multi-organ failure, and even maternal death.^5,6 Postpartum pituitary necrosis (Sheehan’s Syndrome) rarely occurs in nations with adequate healthcare resources but remains a challenge in low resource countries. Furthermore, massive PPH is associated with substantial psychological impact on the patient and their families including postpartum depression and posttraumatic stress disorder.⁸⁹

Jehovah’s Witnesses

Jehovah’s Witnesses do not accept blood transfusions.^49,90 They are a Christian group founded in the US in 1872, with 1 million members in the US and 6 million worldwide. A core tenet of their belief system is refusal of blood products of any kind, even if it leads to loss of life.⁹⁰ Since childbirth is inevitably associated with blood loss, this presents a unique challenge. According to the Watchtower Society’s declaration of 1945, they refuse treatment with red blood cells, platelets, white blood cells, and plasma. It has been estimated that 1000 members die each year from refusing transfusions.⁹⁰ They also refuse autologous transfusions. For these reasons, they are at particular risk of death after childbirth, and it is important to take measures to mitigate that risk.

Religious or other convictions that may lead to declining blood products should be inquired about in all pregnant patients as part of their prenatal care. Regardless of the patient’s beliefs, they should be treated with respect. Importantly, the refusal of blood products does not constitute a refusal of all care. Pre-delivery correction of anemia and aggressive prophylactic measures to limit blood loss at delivery are mainstays of their care. Birthing staff should all be made aware of the patient’s choices and their autonomy should be respected. It is important to inquire about what products will not be accepted. Some Witnesses will accept intraoperative cell salvage. Every effort should be made to minimize blood loss at delivery. Patients may benefit from prophylactic antifibrinolytics such as tranexamic acid. Therapies that may be considered when PPH occurs include recombinant Factor VIIa, cryoprecipitate, fibrinogen, and hemoglobin-based oxygen carriers.⁹⁰

PPH strategies for patient with bleeding disorders, coagulopathy and anticoagulation

Pregnant patients with bleeding disorders, inherited coagulopathies, or those treated with anticoagulation are at particular risk for PPH.^91,92 Their care requires a cautious approach to both preventing PPH and treating it appropriately and quickly should it occur. Ideally, care for these patients should begin prenatally and be managed by a multidisciplinary team including a hematologist, perinatologist, anesthesiologist, and, if appropriate, a geneticist. While a detailed discussion is beyond the scope of this chapter, we will briefly describe the obstetric hemorrhage-related considerations for pregnant patients with von Willebrand disease, hemophilia, inherited thrombocytopenic purpura (ITP), and those treated with anticoagulation.

For patients with von Willebrand disease, von Willebrand factor levels (FVIII or FIX) should be measured in each trimester and specifically in the third trimester close to the planned delivery.⁹³ Factor levels should be targeted to be at 50 IU/dL to 100 IU/dL, with a plan for treatment with factor concentrate or desmopressin at the time of delivery to maintain these levels.⁹⁴ Factor infusion is recommended to avoid long-term postpartum bleeding. Additionally, tranexamic acid should be administered prophylactically at the time of delivery. A similar approach is recommended for hemophilia carriers, including laboratory factor level assessment, peri-delivery factor or desmopressin infusion, and postpartum administration of tranexamic acid.

For patients with ITP, the risk of PPH increases, particularly if platelet count falls below 20,000/uL; however, severe bleeding is typically rare. Target platelet counts for both vaginal or Cesarean delivery and regional anesthesia are recommended to be between 50,000/uL and 80,000/uL.⁹⁵

For patients on prophylactic or therapeutic anticoagulation during pregnancy, it is important to have a plan for timing the cessation of anticoagulation prior to delivery and for resuming it postpartum. This should be discussed with a multidisciplinary team, including perinatology and anesthesia, to ensure safe administration of neuraxial anesthesia if indicated and to mitigate the risks of postpartum bleeding. In the event of significant postpartum bleeding, options include delaying the resumption of postpartum anticoagulation if safe, initiating a heparin drip, or considering the placement of a vena cava filter.

Low-resource settings

PPH continues to be associated with a disproportionately high mortality and morbidity in low resource settings.^4,28 In these settings, frequently the resources and strategies that are available in more developed healthcare systems may not be available or practical. Often, basic necessities such as clean water, electricity, and blood products may not be easily accessible in these locations. Yet, this is where the scourge of PPH carries its highest lethality. Thus, agents that can be administered orally, intramuscularly, intravaginally or intrarectally may be preferable to those which require intravenous access. Use of tranexamic acid and misoprostol may be beneficial.^28,96,97 Non-pneumatic anti-shock garments have the potential to reduce maternal mortality from PPH in low- to middle- income countries.⁸⁸ Finally, education of women and those who care for pregnancies is essential, and international initiatives will be necessary to train locals in the best methods of preventing and treating PPH.²⁸

Global strategies and collaborations to combat postpartum hemorrhage

Given the high incidence of PPH and its significant contribution to maternal morbidity and mortality, it is imperative for both national and international entities to prioritize the prevention and management of PPH. In recent years, numerous initiatives have been launched by a variety of organizations, leading to substantial decreases in PPH-related fatalities. These efforts encompass a broad spectrum of strategies, including the training of healthcare professionals, funding of research into PPH, the development and implementation of PPH care bundles, meticulous data collection, the conduct of drills and simulations, and the adoption of evidence-based protocols for the prevention and treatment of PPH.^26,99

Organizations such as the WHO and the FIGO, and the United Nations Population Fund have been at the forefront of international efforts to combat PPH.^2,7,99,100 These bodies advocate for global standards in maternal care, support research into effective interventions, and facilitate the sharing of best practices among member states. On a national level, initiatives like the California Maternal Quality Care Collaborative in the United States have developed PPH bundles that include tools and protocols designed to improve the identification, prevention, and management of PPH.²⁶ In addition, several national obstetrics and gynecology societies have created robust evidence-based guidelines dealing with prevention and management of PPH.^5,6,29 These comprehensive approaches ensure a standardized response to PPH, enhancing the capability of healthcare providers to deliver timely and effective care. Through the collaborative efforts of such organizations and the implementation of targeted interventions, significant progress has been made in reducing the global burden of PPH, underscoring the importance of continued commitment and support from all stakeholders in the fight against this life-threatening condition.

Conclusion

PPH, a major cause of maternal death with rising incidence, is often preventable. Current risk assessment tools for PPH are largely ineffective. Effective management hinges on preparation, prophylaxis, and prompt evidence-based treatment. The administration of uterotonics in the third stage of labor and early tranexamic acid use are evidence-supported, and cost-effective in low-resource areas. Balloon tamponade is simple and helps reduce mortality. High-risk patients should be delivered to well-equipped centers with fluid and blood access, but many regions lack such resources. New techniques like intrauterine tamponade and vacuum devices must be made more affordable and accessible in low-resource settings. In addition, training for birth attendants is essential. Innovations should focus on developing cost-effective, practical interventions to combat high PPH mortality in underserved regions.

Funding

YO has received honoraria from UpToDate and BMJ Best Practice as an author on chapters on placental abruption. He also is on the Scientific Advisory Board of Sonio, LLC, for which he receives honoraria.

Conflicts of Interest

None.