Postpartum hemorrhage is one of the most common emergencies faced by obstetricians, complicating 1 in 20 to 1 in 100 deliveries.¹ Not only is it a leading cause of maternal morbidity, but it also remains one of the top three causes of maternal mortality throughout the world.^2,3 In order to manage postpartum hemorrhage effectively, the obstetrician must have a thorough understanding of normal delivery-related blood loss, physiological adaptation to hemorrhage, the most common etiologies of postpartum hemorrhage, and appropriate therapeutic interventions.

Normal delivery-related blood loss depends on mode of delivery. The average blood loss for a vaginal delivery, cesarean delivery, and cesarean hysterectomy has been estimated at 500, 1000, and 1500 mL, respectively. While recent data based upon objective quantification supports these values, clinicians often underestimate blood loss and its clinical implications due to the significant blood volume expansion that accompanies pregnancy.^4,5

Postpartum hemorrhage has been variably defined in published literature.^4-6 Definitions have included subjective assessments greater than the standard norms, a 10% decline in hematocrit, and need for blood transfusion. For practical purposes, postpartum hemorrhage is best defined as excessive bleeding that causes the patient to be hemodynamically symptomatic and/or hypovolemic.

The obstetric patient can adapt to hemorrhage more effectively than her nonpregnant counterpart due to five primary hemodynamic changes that accompany pregnancy. These changes include: (1) increased red cell mass, (2) increased plasma volume, (3) increased cardiac output, (4) decreased systemic vascular resistance, and (5) increased procoagulant blood factors. In the early phases of hemorrhage, the body compensates by raising systemic vascular resistance to maintain blood pressure and perfusion to vital organs. However, as bleeding continues, further vasoconstriction is impossible, resulting in reduced blood pressure, cardiac output, and end-organ perfusion.^7,8 Table 3-1 classifies the physiological adaptation that occurs with various stages of hemorrhage. It is important for the obstetrician to recognize these responses since the quantity of blood loss that occurs during a postpartum hemorrhage is often underestimated as stated previously.

There are two categories of postpartum hemorrhage etiologies. Primary (or early) causes are those that occur within 24 hours of delivery; whereas, secondary (or late) causes are those that occur 24 hours after delivery until 12 weeks postpartum.^2,9 Table 3-2 lists the most common etiologies of primary and secondary postpartum hemorrhages. Since the obstetrician is faced with primary postpartum hemorrhage more often than secondary postpartum hemorrhage, the remainder of this chapter focuses on its risk factors and therapy.

Uterine Atony

Uterine atony, or the inability of the uterine myometrium to contract effectively, is the most common cause of primary postpartum hemorrhage. Not only does it complicate 1 in 20 births, but it is also responsible for 80% of all postpartum hemorrhage cases.^9,10 At term, blood flow through the placental site averages 500 to 700 mL/min.² After placental delivery, the uterus controls bleeding by contracting its myometrial fibers in a tourniquet fashion around its spiral arterioles. If inadequate uterine contraction occurs, rapid blood loss will ensue.

Risk factors for uterine atony include uterine overdistention (multiple gestation, polyhydramnios, fetal macrosomia), induction of labor, rapid or prolonged labor, grand multiparity, chorioamnionitis, retained products of conception, uterine inversion, abnormal placentation, and use of uterine-relaxing agents (tocolytic therapy, halogenated anesthetics, nitroglycerin).¹¹

Genitourinary Tract Lacerations

The second most common cause of postpartum hemorrhage is genitourinary tract lacerations. These injuries may complicate both vaginal and cesarean deliveries. While instrumented vaginal delivery remains the most significant risk factor for a genitourinary tract laceration, other sources of obstetrical trauma can contribute to this cause of hemorrhage. These sources include fetal malpresentation, fetal macrosomia, episiotomy, precipitous delivery, prior cerclage placement, Dührssen incisions, and shoulder dystocia.

A genitourinary tract laceration should be suspected, if persistent bleeding occurs after delivery despite good uterine tone. Occasionally, the bleeding may be masked due to its location, such as within the broad ligament. In these circumstances, large amounts of blood loss may occur in an unrecognized hematoma. The astute obstetrician must be aware of the risk factors for this type of laceration as well as the patient’s initial presenting symptoms of pain and physiological signs of shock.

Retained Products of Conception

Retained products of conception, such as placental tissue and/or amniotic membranes, can inhibit the uterus from adequate contraction and result in hemorrhage. Risk factors for retained products of conception include midtrimester delivery, chorioamnionitis, and accessory placental lobes.

Invasive Placentation or Morbidly Adherent Placenta

Although uncommon, invasive placentation or morbidly adherent placenta can result in massive postpartum hemorrhage. Placenta accreta represents the abnormal attachment of the placenta to the uterine lining due to an absence of the decidua basalis and an incomplete development of the fibrinoid layer. Placenta increta and percreta represent attachments to and through the uterine myometrium, respectively. Attempts to remove an invasive or morbidly adherent placenta from its attachment site will result in rapid blood loss, often necessitating emergent surgical intervention.

Major risk factors for invasive placentation or morbidly adherent placenta include prior uterine surgery (curettage, myomectomy, hysteroscopic adhesiolysis, corneal resection, endometrial ablation), advanced maternal age, multiparity, cesarean scar pregnancy, history of pelvic irradiation, infertility and/or infertility procedures, placenta previa, and previous cesarean delivery.^12-18 As exemplified in Table 3-3, the combination of placenta previa and previous cesarean delivery should alert the physician to a substantial risk of invasive placentation and subsequent hemorrhage.¹⁹ In these circumstances, an attempt for antepartum detection should be undertaken, and a scheduled cesarean hysterectomy should be performed at the time of delivery if no future fertility is desired.

Uterine Rupture

Uterine rupture refers to the complete nonsurgical disruption of all uterine layers. Despite an uncommon incidence of 1 in 2000 deliveries, uterine rupture represents a potential catastrophic event for both mother and fetus and can cause significant hemorrhage, if the placental implantation site is involved.²⁰ While multiple risk factors have been associated with uterine rupture, no single or combination of factors is able to reliably predict all cases.^21-23 Despite this, consistent data demonstrate strong associations for trial of labor after cesarean delivery and one or more of the following: prior uterine rupture, previous fundal or vertical hysterotomy, induction of labor, prolonged labor, and labor dystocia.^24-30 Additional risk factors inconsistently associated with uterine rupture include advanced maternal age, postterm gestation, no prior vaginal delivery, fetal macrosomia, short interpregnancy interval, single layer and/or locked uterine incision closure, multiple prior cesarean deliveries, thin uterine scar identified by ultrasound, multiple gestation, and postcesarean delivery infection.^31-46

Uterine Inversion

Uterine inversion, or the collapse of the fundus into or through the uterine cavity, is a rare event, complicating approximately 1 in 1200 to 57,000 deliveries.^47-49 Uterine inversion is classified by degree and timing. With respect to degree, uterine inversion may be first degree (incomplete), second degree (complete), third degree (uterine prolapse), or fourth degree (total uterine and vaginal) (Fig. 3-1). The timing of uterine inversion is described as acute (within 24 hours of delivery), subacute (>24 hours after delivery but <4 weeks postpartum), and chronic (>4 weeks postpartum).⁵⁰

While the most commonly reported cause of uterine inversion is excessive cord traction with fundal pressure during the third stage of labor, the pathogenesis is incompletely known.^51,52 Other possible risk factors include fetal macrosomia, precipitous labor, short umbilical cord, use of uterine-relaxing agents, congenital uterine malformations, fibroids, nulliparity, retained placenta, invasive placentation, and Ehlers Danlos syndrome.⁴⁹

Coagulopathy

Coagulopathy represents the final major etiology of postpartum hemorrhage. Coagulopathies may be hereditary or acquired in origin. Although rare, hereditary coagulopathies may present challenging clinical courses if appropriate therapy is unavailable. In general, most of these coagulopathies are effectively treated with replacement of coagulation factors and/or additional pharmaceutical agents in the third stage of labor or at the time of cesarean delivery.

While several obstetrical scenarios may lead to acquired coagulopathy (anticoagulant administration, sepsis, severe preeclampsia, amniotic fluid embolus, tissue necrosis, and placental abruption), the most common etiology in the setting of primary postpartum hemorrhage is clotting factor consumption. Figure 3-2 reviews the pathophysiology of consumptive coagulopathy and its association with uterine atony.

When the obstetrician is faced with a postpartum hemorrhage, an organized care plan needs to be set in motion to minimize further bleeding and associated morbidity and mortality. Table 3-4 lists the components of such a care plan.

Blood Loss Needs

When faced with a postpartum hemorrhage, the clinician should first assess patient’s blood loss needs. Appropriate intravenous (IV) access is critical. This includes two large-bore (16-gauge) IV catheters. In addition, the patient’s blood type should be confirmed and held for possible cross-matching needs. The patient should be provided supplemental oxygen and attempts should be made to keep the patient warm (eg, Bair Hugger warming unit). Finally, need for ancillary support should be assessed. This support may include additional nursing assistance, operating room staff, physician assistance, anesthesiologist, and hospital’s rapid response team.

Loss Estimation

Many instances of hemorrhage result in compounded morbidity secondary to an inadequate blood loss estimation on the part of the obstetrician and healthcare team. At the onset of a postpartum hemorrhage, it is important for the clinician to realistically estimate the amount of blood loss that has occurred. This may be assisted by collection of blood in graduated cylinders or calibrated drapes that quantify blood loss, using visual aids that correlate the size of blood on specific surfaces to actual volume, and weighing bloody materials and subtracting the dry weight from the wet weight.² In addition, assessing the patient’s clinical response to hemorrhage will help to classify the extent of the bleeding. For example, if the patient has moderate tachycardia and tachypnea with a narrowed pulse pressure, she has lost at least 20% to 25% of her total blood volume.

Baseline laboratory evaluations of hemoglobin, hematocrit, platelet count, coagulation studies (fibrinogen, prothrombin time, and partial thromboplastin time), potassium, and ionized calcium should be taken.² If timely laboratory assessment is unavailable, drawing 5 mL of maternal blood into an empty red top tube and observing for clot formation will provide the clinician a rough estimate of the patient’s coagulopathy. If a clot is not visible within 6 minutes or forms and lyses within 30 minutes, the fibrinogen level is usually less than 150 mg/dL. The fibrinogen level at the onset of a postpartum hemorrhage is predictive of its severity as it falls sooner than other coagulation studies.⁵³

Etiology

After assessing blood loss needs and estimation, a rapid yet thorough exploration for the hemorrhage etiology must be undertaken. A poorly contractile uterus suggests uterine atony. If atony is not the source of bleeding, further exploration should occur. This exploration should begin with the most superior aspect of the genital tract and progress inferiorly since heavy downward blood flow may make visualization of the more inferior landmarks difficult.