Hemorrhagic complications during pregnancy are a significant causative factor of adverse maternal-fetal outcomes. Major blood loss predisposes the woman to an increased risk of hypovolemia, anemia, infection, preterm labor/birth, and maternal death. Although bleeding can cause considerable problems for the mother, the fetus is especially in jeopardy because significant maternal blood loss can result in negative alterations in maternal hemodynamic status and decreased oxygencarrying capacity. When bleeding decreases blood flow to the placenta, maternal-fetal gas exchange is reduced and the fetus is at risk for progressive physiologic deterioration (e.g., hypoxemia, hypoxia, asphyxia, and death). This risk is directly related to the amount and duration of blood loss.

Hemorrhage during pregnancy is one of the leading causes of maternal death in the United States, along with embolism and hypertensive disorders (Berg, Callaghan, Syverson, & Henderson, 2010; Paxton & Wardlaw, 2011; The Joint Commission [TJC], 2010). According to the most recent data available from the Centers for Disease Control and Prevention (Berg et al., 2010), the aggregate pregnancy-related mortality ratio for the 8-year period from 1998 to 2005 was 14.5 per 100,000 live births, which is higher than any period in the previous 20 years of the Pregnancy Mortality Surveillance System. African American women continued to have a threefold to fourfold higher risk of pregnancy-related death (Berg et al., 2010), which may reflect social, economic, and cultural barriers to healthcare (Mahlmeister, 2010).The proportion of deaths attributable to hemorrhage and hypertensive disorders declined from previous years, whereas the proportion from medical conditions, particularly cardiovascular, increased (Berg et al., 2010). Nevertheless, hemorrhage related to pregnancy remains a significant issue in the United States as seven causes of death, including hemorrhage, thrombotic pulmonary embolism, infection, hypertensive disorders of pregnancy, cardiomyopathy, cardiovascular conditions, and noncardiovascular medical conditions, each contributed 10% to 13% of maternal deaths (Berg et al., 2010). It is estimated that 70% to 92% of maternal deaths from hemorrhage are preventable (Berg et al., 2005). When considering all maternal deaths, the outcome of pregnancy was helpful in identifying specific risks. For example, no maternal deaths were reported as a result of a molar pregnancy, while 93% of deaths of women with ectopic pregnancy were hemorrhage related (Berg et al., 2010). When the outcome of pregnancy was live birth, maternal deaths were caused by a number of factors, including uterine rupture, placental abruption, placenta previa, placenta accreta, retained placental fragments, coagulopathies, and uterine atony (Berg et al., 2010). Significant causes of death in women whose pregnancy ends in stillbirth are hemorrhage from placental abruption and uterine rupture (Berg et al., 2010; Chang et al., 2003). Placental abruption and uterine rupture also are significant causes of fetal death (Silver, 2007).

As noted in The Joint Commission’s (2010) Sentinel Event Alert Preventing Maternal Death, the nurse must be alert to the symptoms of hemorrhage and shock and be prepared to act quickly to minimize blood loss and hasten maternal and fetal stabilization. Up to 15% of maternal cardiac output (750 mL to 1,000 mL/min) flows through the placental bed at term; unresolved bleeding can result in maternal exsanguination in 8 to 10 minutes (Rajan & Wing, 2010). In addition to the physiologic implications of bleeding during pregnancy,
the mother experiences emotional stress as she worries about the outcome for herself and her baby. Although maternal mortality decreased approximately 99% during the 20th century, hemorrhage remains a major cause of maternal death in all parts of the world. According to the most recent data, maternal mortality rates in the United States increased from 7.6 per 100,000 live births in 1996, 9.8 per 100,000 live births in 2000, and 12.1 per 100,000 live births in 2003 to approximately 15.4 per 100,000 live births in 2005 (Berg et al., 2010; Hoyert, 2007). The increase is significant as these rates had remained constant for the previous two decades (Clark et al., 2008) after many years of decreasing (e.g., 607.9 per 100,000 live births in 1915; 83.3 per 100,000 live births in 1950) (Hoyert, 2007). It is unclear whether the increase represents more women actually dying or improved coding and data collection methods (Berg et al., 2010).

Bleeding complicates approximately one in five pregnancies; the incidence and cause of bleeding vary by trimester (MacMullen, Dulski, & Meagher, 2005). Most bleeding occurring in the first trimester of pregnancy is related to spontaneous abortion and is generally not life threatening. Ectopic pregnancy is the leading cause of life-threatening hemorrhage during the first trimester, although the maternal mortality rate declined from 13.0% of all maternal deaths from 1970 to 1989 and to 6.0% from 1991 to 1999 (Creanga et al., 2011). Hemorrhage during the antepartum period usually results from disruption of the placental implantation site (involving a normally implanted placenta or placenta previa) (Hull & Resnik, 2009). Most serious obstetric hemorrhage occurs in the postpartum period as a result of uterine atony after placental separation (American College of Obstetricians and Gynecologists [ACOG], 2006; Driessen et al., 2011). Other causes of postpartum hemorrhage include retained placenta, uterine rupture, abnormal placental implantation, uterine inversion, genital tract trauma, and coagulopathy (ACOG, 2006; Oyelese & Ananth, 2010).

Symptomatic placenta previa is identified in approximately 0.3% to 0.5% of pregnancies (Harper, Obido, Macones, Crane, & Cahill, 2010; Oyelese & Smulian, 2006). Low implantation of the placenta is much more common during early pregnancy; however, most of these cases resolve or are not found to be clinically significant as pregnancy progresses (Harper et al., 2010; Oyelese & Smulian, 2006). Placentas may be classified as low lying during the second trimester by routine abdominal ultrasonography because it is difficult to determine which placentas cross the cervical os during ultrasonographic examination in early pregnancy. Transvaginal ultrasound remains a more accurate way to diagnose placenta previa and to measure the distance from the placental edge to the cervical os (Oyelese & Smulian, 2006; Vergani et al., 2009). The incidence of placenta previa is increasing, most likely secondary to the increasing cesarean birth rate (Hull & Resnik, 2009).

Placenta accreta is an uncommon abnormality of placental implantation where the placenta is abnormally adherent. Placenta accreta is one of the most serious complications of placenta previa. In addition to placenta previa, prior uterine surgery significantly increases the risk of placenta accreta (Comstock, 2011). With placenta previa, the risk of developing placenta accreta is 10% to 25% for women with a history of one prior cesarean birth and rises to more than 38% for women with two or more cesarean births or second-trimester pregnancy terminations (Comstock, 2011; Snegovskikh, Clebone, & Norwitz, 2011). The incidence of placenta accreta is rising secondary to an increase in the cesarean birth rate (Eller et al., 2011; Mahlmeister, 2010).

The incidence of abruptio placentae varies in the literature according to the population studied and diagnostic criteria. In the United States, the reported incidence of abruptio placentae is approximately 1% of all pregnancies (Hull & Resnik, 2009). Risk of recurrence in subsequent pregnancies has been reported to be as high as 5.5% to 16.6%. This rate is approximately 30 times higher than the rate for pregnant women without a history of prior abruptio placentae. The strongest risk factor for abruption is a history of placental abruption in a previous pregnancy (Hull & Resnik, 2009). The risk of recurrence for women with a history of two placental abruptions increases to approximately 25% (Hull & Resnik, 2009).

Vasa previa is a condition in which umbilical arteries and veins abnormally implanted throughout the amnion traverse the cervical os in front of the presenting part of the fetus. Vasa previa is a rare but life-threatening complication for the fetus at the time of rupture of membranes (Oyelese & Smulian, 2006; Robinson & Grobman, 2011). The reported incidence of vasa previa is approximately 1 in 2,500 births (Robinson & Grobman, 2011). Rupture of the vessels during spontaneous or artificial rupture of membranes usually leads to fetal exsanguination or severe neurologic fetal injury secondary to fetal hemorrhage before the cause of bleeding is recognized and before an emergent cesarean birth can be accomplished (Silver, 2007). Fetal death occurs in 60% to 75% of cases of ruptured vasa previa (Oyelese & Smulian, 2006).

Uterine rupture is another significant cause of maternal hemorrhage. The risk of uterine rupture for women attempting vaginal birth after cesarean birth (VBAC) is less than 1%; however, the consequences can be catastrophic for the mother and baby (ACOG, 2010; Spong & Queenan, 2011; Tillett, 2010). The risk of uterine rupture depends on the number, type, and location of the previous incisions (ACOG, 2010; Lang & Landon, 2010).
Although risk of uterine rupture has been reported as nearly five times greater for women with a history of two prior low transverse cesarean births when compared to women with one prior cesarean birth (ACOG, 2010), a large multicenter study did not find a difference in rupture rates in these two groups (Cahill & Macones, 2007; Landon et al., 2006; Lang & Landon, 2010). Women with a previous lowvertical uterine incision have a similar success rate for having a VBAC as those women with a previous low transverse incision (ACOG, 2010; Cahill & Macones, 2007). The risk of uterine rupture is increased for women with a T-shaped incision (ACOG, 2010).

Waiting for spontaneous labor, thus avoiding pharmacologic cervical ripening agents and oxytocin, appears to significantly decrease the risk of uterine rupture for women attempting VBAC (ACOG, 2010; Landon et al., 2005; Lang & Landon, 2010). There are enough data to suggest that prostaglandins and high rates of oxytocin infusion increase the risk for rupture (ACOG, 2010; Lang & Landon, 2010). Uterine ruptures at the scar site and remote from the previous scar site have been reported with high doses of oxytocin (Lang & Landon, 2010). It has been theorized that prostaglandins induce local biochemical modifications that weaken the prior uterine scar, thus predisposing it to rupture (Lang & Landon, 2010). Due to the risk of uterine rupture with the use of misoprostol or any prostaglandin agent for cervical ripening or induction, ACOG (2010) does not recommend prostaglandins for women attempting VBAC. If labor needs to be induced in a patient with a previous scar for a clear and compelling clinical indication, the potential increased risk of uterine rupture with the use of prostaglandins should be discussed with the patient and documented in the medical record (ACOG, 2010).

The incidence of uterine inversion is approximately 1 case in 2,500 births, although the range varies among studies (You & Zahn, 2006). It is difficult to ascertain the true incidence because uterine inversion is not often reported in the literature. Improper management of the third stage of labor increases the likelihood of iatrogenic uterine inversion (Oyelese & Ananth, 2010).

Postpartum hemorrhage remains one of the leading causes of maternal death worldwide (Burke, 2010; Callaghan, Kuklina, & Berg, 2010; Oyelese & Ananth, 2010). Early or primary postpartum hemorrhage (within 24 hours after birth) is most frequently caused by uterine atony, retained placental fragments, lower genital tract lacerations, uterine rupture, uterine inversion, placenta accreta, and coagulopathies. Late or secondary postpartum hemorrhage (> 24 hours to 6 weeks after birth) is more likely to be caused by infection, placental site subinvolution, retained placental fragments, and coagulopathy (Rajan & Wing, 2010).

The definitions, cause, pathophysiology, and clinical manifestations of the most frequently occurring causes of bleeding and bleeding disorders in pregnancy are described in the following sections. A diagnosis-specific summary of expected management is included. A more detailed summary of nursing interventions for bleeding during pregnancy concludes this section.