Definition

The commonly accepted definition of postpartum hemorrhage (PPH) is excessive and life-threatening bleeding after 20 weeks of gestation, which occurs at the time of delivery of the fetus or placenta. Primary PPH is excessive blood loss within 24 hours of delivery. Secondary PPH is any abnormal or excessive bleeding that occurs between 24 hours and 12 weeks after delivery. Most commonly, bleeding occurs in the third stage of labor, which refers to the time between delivery of the fetus and delivery of the placenta after its separation and expulsion from the uterus. Defining excessive bleeding is somewhat problematic because it can be difficult to determine the exact amount of blood loss, and clinicians tend to underestimate blood loss. With a normal vaginal delivery, blood loss is typically 500 mL or less; after a normal cesarean section, it is usually 800 to 1000 mL. Blood loss greater than these amounts has been used to define PPH. However, uncomplicated vaginal and cesarean deliveries can occasionally occur with greater amounts of blood loss but without hemodynamic compromise. Therefore, a more comprehensive definition of PPH is bleeding (regardless of the volume of shed blood) that is severe enough to cause hemodynamic compromise.

A decrease in hematocrit greater than 10% as a diagnostic criterion has also been widely accepted as a definition of postpartum hemorrhage. The hematocrit level initially may be in the low-normal to normal range despite excessive bleeding, because hematocrit does not change quickly in response to rapid hemorrhage. The hematocrit is also determined in part by the volume of infused resuscitation fluid. Because the parturient’s blood volume is increased by 30% to 50%, she may not manifest signs of tachycardia and hypotension until blood loss exceeds 1500 mL. If the patient is hemodynamically unstable but the amount of blood visualized externally is relatively insignificant, occult sites of internal bleeding should be suspected immediately.

Incidence and Mortality

Maternal mortality has significantly decreased over the past 50 years in developed countries, in part because of improvements in obstetric care. According to the National Center for Health Statistics of the Centers for Disease Control and Prevention (CDC), in 2006 the national maternal mortality rate was 13.3 deaths per 100,000 live births.¹ Mortality rates are significantly higher for African American and Asian or Pacific Island women compared with Caucasian women.^2,3 According to a study by the CDC of pregnancy-related mortality in the U.S. between 1991 and 1997, the leading causes of maternal death are hemorrhage, hypertensive disorders, pulmonary and amniotic fluid emboli, infections, and preexisting chronic conditions (such as cardiovascular disease).²

Obstetric hemorrhage is the world’s leading cause of maternal mortality, causing 24% of maternal deaths or an estimated 127,000 maternal deaths annually. Postpartum hemorrhage is the most common type of obstetric hemorrhage and accounts for the majority of the 14 million cases of obstetric hemorrhage that occur each year.² In developing countries, PPH may cause up to 60% of all maternal deaths.³

Pathophysiology

At term, blood flow to the uterus and placenta increases to 600 to 1200 mL/min, accounting for 10% of the maternal cardiac output. To stem the flow of blood and provide immediate hemostasis after delivery of the fetus, the uterus begins to contract. Myometrial contraction is the primary mechanism for both placental separation and hemostasis. The myometrial muscle fibers of the uterus contract and simultaneously retract, causing compression and occlusion of the blood vessels. Uterine atony results when this adaptive mechanism fails and the myometrial fibers are unable to contract and retract normally. Excessive bleeding from the uterus and lower genital tract from many causes, including lacerations, placental anomalies, and trauma, is directly related to the increase in blood flow to the uterus and placenta. At term, there is a physiologic increase in the circulating concentrations of various clotting factors. This adaptive response also helps control the bleeding that is a normal consequence of delivery. However, these factors are overwhelmed by the excessive bleeding of PPH.

Presentation

PPH often manifests as brisk and excessive flow of blood from the vagina. This finding is easily observed on physical examination. If the placenta has been delivered, blood can be seen at the vaginal entrance. Maternal hemodynamics may be unaltered initially. If the bleeding is left untreated, typical presenting signs of hypovolemic shock (i.e., tachycardia, tachypnea, and hypotension) become apparent. Bonnar described the symptoms related to PPH in relation to the amount of blood loss (Table 161-1).⁴ However, the signs and symptoms of hemorrhagic shock may not occur immediately and may extend over a longer period of time if shed blood is sequestered in the uterus. Occult bleeding occurs most frequently with retained placental fragments, uterine atony, and concealed hematomas in the pelvis, perineum, or retroperitoneal space. Occult hemorrhage in the uterus or hematomas should be suspected in patients who are in the third stage of labor with hemodynamic instability but little or no evidence of external bleeding. Signs and symptoms of excessive bleeding also may be delayed because of the relative hypervolemic state of the patient and by the position of the patient after delivery with the legs elevated in stirrups.

TABLE 161-1 Presentation of Symptoms in Postpartum Hemorrhage

Causes of Postpartum Hemorrhage

Obtaining a detailed antenatal history is important in helping to determine a possible cause of PPH. A history of prior bleeding episodes associated with heavy menses or with dental or surgical procedures should raise the possibility of an underlying coagulation or bleeding disorder. Significant predisposing risk factors for the development of PPH include previous episodes of PPH, multiparity, and multiple fetuses. Women with a prior history of PPH can have up to a 15% risk of recurrence with subsequent pregnancies.⁵ Risk factors associated with the development of PPH are listed in Box 161-1. Early recognition of these risk factors may aid in the diagnosis and subsequently in the management of PPH. A randomized controlled trial (RCT) comparing oxytocin administration before and after delivery of the placenta found that birth weight, labor induction with augmentation, chorioamnionitis, use of magnesium sulfate infusions, and previous episodes of PPH increased the risk of developing PPH.⁶ However, a significant number of patients with PPH have no obvious predisposing factors.

Potential causes of PPH are listed in Box 161-2. The most frequent cause of PPH is uterine atony after delivery of either the fetus or placenta. Bleeding is from the uterine vessels or from the placental site of implantation if the placenta has been delivered. The incidence of uterine atony is approximately 1 in 20 deliveries. Uterine atony can lead to rapid and severe PPH. Overdistention of the uterus secondary to multiple gestation, fetal macrosomia, or polyhydramnios is a major predisposing risk factor for the development of uterine atony. Other predisposing factors are retained placenta, chorioamnionitis, uterine structural abnormalities, and muscle fatigue after prolonged or stimulated labor. General anesthesia, particularly with halogenated anesthetics, and magnesium sulfate infusions can inhibit effective uterine contractions and lead to uterine atony. The diagnosis of uterine atony is a clinical diagnosis made by assessing the tone of the uterus and its size by manually palpating the uterus externally. Bimanual examination of the uterus also can be performed to diagnose uterine atony. A boggy uterus associated with heavy vaginal bleeding or with an appreciable increase in the size of the uterus is diagnostic of uterine atony. The size of the uterus may be larger than normal due to accumulated blood within.

Lacerations of the lower genital tract are the second most frequent cause of PPH. Lacerations of the vagina and cervix can result from a number of causes. These lesions occur most commonly as a result of prolonged or tumultuous labor, particularly with uterine hyperstimulation with oxytocic agents. Nevertheless, lacerations can occur spontaneously as well. They are seen in deliveries associated with instrumentation, such as forceps deliveries, or with extrauterine or intrauterine manipulations of the fetus. Attempts to remove the placenta or placental fragments manually or with instrumentation can lead to traumatic lesions or hematomas. Excessive vaginal bleeding or traumatic hematomas can result from these lacerations. Careful examination with palpation of the vagina and cervix may reveal the presence of lacerations.

Retention of placental fragments or the entire placenta can lead to severe and life-threatening hemorrhage, which may be immediate or delayed depending on the extent of accumulated blood in the uterus. The most common definition of retention of the placenta in utero for more than 30 to 60 minutes after delivery of the fetus. Retained placenta is more likely to occur with a preterm gestation of less than 24 weeks. Placental abnormalities (i.e., placenta accreta, placenta increta, and placenta percreta) have been associated with retained placenta and failure of complete separation of the placenta from the uterus. Placenta accreta occurs when a portion or the entire surface of the placenta is abnormally attached to the uterus. Where placenta accreta is present, the failure of the placenta to separate normally from the uterus after delivery is accompanied by severe postpartum hemorrhage. Placenta increta involves actual invasion of the uterus by the placenta. If the placenta has been delivered, it is imperative to closely examine the placenta to look for missing fragments, a finding that suggests retained placental tissue.

Another less frequent cause of PPH is uterine rupture. Rupture is more common in patients with prior cesarean incisions and in those with any prior operative procedures of the uterus (e.g., intrauterine device placement, laparoscopy, hysteroscopy). Uterine rupture may manifest with severe and acute abdominal pain and hemodynamic instability, but there may not be significant bleeding initially. Uterine inversion is relatively uncommon but may be associated with blood losses of up to 2 L.

A defect in hemostasis resulting from an underlying coagulopathy should be considered if the uterus is contracting normally and manual exploration has excluded either placental retention or uterine rupture. Disseminated intravascular coagulation (DIC) associated with placental abruption (premature separation of a normally implanted placenta), the HELLP syndrome (hemolysis, elevated liver enzymes, and low platelets), intrauterine fetal death, acute fatty liver of pregnancy, sepsis, or amniotic fluid embolism may precipitate PPH. The incidence of severe DIC associated with PPH is estimated at 0.1% of pregnancies.⁷

Amniotic fluid embolism syndrome (AFES) is a catastrophic condition that can occur either during the pregnancy or after the delivery. AFES manifests with acute respiratory failure, cardiogenic shock, and/or DIC.⁸ As many as 80% of these patients develop DIC, and in some, DIC is the major clinical abnormality. Oozing from intravenous (IV) or skin puncture sites, mucosal surfaces, or surgical sites should raise the suspicion of DIC; confirmation of the diagnosis is made by laboratory coagulation studies. Although the coagulation profile is unlikely to be abnormal with acute postpartum bleeding in the absence of DIC, coagulation parameters are clearly abnormal in the presence of DIC regardless of the cause. In late pregnancy, the circulating fibrinogen level usually is two to three times the normal prenatal value, but fibrinogen concentration is dramatically decreased if DIC is present. Preexisting or pregnancy-acquired disorders of coagulation are relatively infrequent causes of significant PPH.

Diagnostic Studies

Although the diagnosis is obvious with significant and excessive bleeding after delivery, not all patients present with immediate bleeding, because of hematoma formation or accumulations in the interior of the uterus. Bedside ultrasonography can be used for the detection of clots, hematomas, and retained placental products. For patients who are at high for risk for development of PPH, periodic ultrasound examinations during pregnancy can offer invaluable information concerning the extent and progression of placental disease. Angiography with selective arterial embolization can be used both diagnostically and therapeutically. Bleeding sites can be visualized and embolized simultaneously. For evaluation of a proven or suspected case of PPH, the following laboratory studies are almost always indicated: complete blood count with platelet count, coagulation studies with prothrombin and activated partial thromboplastin times, fibrinogen, and D-dimer level. With acute hemorrhage, the measurements of hemoglobin concentration and hematocrit may be of limited use.

Prevention