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

There has been much controversy concerning the preferred methods of managing the third stage of labor in terms of decreasing bleeding complications. The debate concerns active versus expectant management. Expectant management consists of waiting for separation and expulsion of the placenta, with minimal intervention except for gentle fundal massage. Active management of the third stage of labor involves three components. The first consists of administering a uterotonic drug, usually oxytocin, immediately after delivery of the fetus to promote contraction of the uterus and subsequent expulsion of the placenta. The second maneuver consists of gentle traction on the umbilical cord after the uterus is well contracted and then using countertraction against the uterine fundus.⁹ The third maneuver is uterine massage after delivery of the placenta. The two modalities were compared in five randomized, controlled trials in a Cochrane meta-analysis of studies enrolling more than 6000 women. A 60% decrease in PPH was associated with active management of the third stage of labor.¹⁰

General Treatment Measures

Many deaths associated with PPH may have resulted because clinicians underestimated the extent of blood loss and failed to provide rapid and aggressive resuscitation with fluids and blood products. Several authors have suggested the use of specific management protocols for the care of patients with PPH.^4,11,12 These guidelines can expedite rapid diagnosis and management of obstetric hemorrhage. A general assessment of the patient, evaluation of vital signs, a detailed physical examination, and a review of the obstetrical delivery details are all necessary for the clinician to formulate a comprehensive evaluation and critique of the situation. The general treatment measures for PPH are the same as those for any patient with acute hemorrhage (Box 161-3). Oxygen should be administered routinely. At least two large-caliber IV lines should be placed immediately. Central venous access is usually unnecessary unless peripheral access cannot be obtained quickly. Aggressive volume resuscitation should be instituted immediately, because this intervention can be life saving in patients with ongoing bleeding and hemodynamic instability. Either normal saline or lactated Ringer’s solution is the preferred fluid for aggressive resuscitation. Isotonic electrolyte solutions provide transient intravascular volume expansion. Monitoring of changes in blood pressure, heart rate, and pulse pressure can help the clinician to determine the amount of blood loss, particularly in cases in which bleeding is internal (Table 161-2).

TABLE 161-2 Therapeutic Response to Initial Fluid Resuscitation

General guidelines for fluid resuscitation of patients with hemorrhagic shock are based on the “3 : 1” rule. This recommendation derives from the empirical observation that patients require about 300 mL of crystalloid fluid replacement for every 100 mL of blood loss. This rule must be applied in the context of the clinical scenario. Applied blindly, this guideline can result in either excessive or inadequate volume resuscitation. Patients with expanding hematomas or areas of concealed active bleeding have hypotension out of proportion to the obvious blood loss and require resuscitation in excess of the 3 : 1 recommendation. In contrast, patients with ongoing blood losses that are being replaced with blood transfusions typically require less electrolyte fluid replacement. Although initial fluid resuscitation is critical, caution should be exercised to prevent abdominal compartment syndrome that may occur when more than 10 liters of fluids are administered. Red blood cell transfusions to replace ongoing blood loss remain the mainstay of fluid replacement.

Blood transfusions usually are necessary for patients with severe ongoing PPH. Healthy pregnant patients usually do not require transfusion if blood loss is 2000 mL or less. However, if blood loss is greater than 2 L or there is ongoing hemorrhage and hemodynamic instability, transfusion can be life saving. Crossmatched packed red blood cells or type-specific blood can be infused rapidly using a blood warming device in cases of severe ongoing hemorrhage (Box 161-4). Recombinant activated factor VII (rFVIIa) has been recommended in cases of refractory postpartum hemorrhage that has not responded to medical measures including blood product administration.¹³ Although supported by few and uncontrolled studies, the available data suggest a potential role of rFVIIa in the management of severe PPH prior to performing a definitive hysterectomy.

Manual external uterine massage should be performed immediately to stimulate uterine contractions and express clots if uterine atony is suspected or confirmed. If the uterus does not respond to vigorous manual external massage and the rapid administration of oxytocin, bimanual massage with one hand on the uterus and the other hand placed anterior to the cervix in the vagina should be performed. Aggressive uterine manipulation can result in uterine inversion. Direct pressure should be maintained over visible perineal, vaginal, or cervical lacerations. These general treatment measures can control excessive bleeding and even stop the hemorrhage in a significant proportion of patients.

Specific Treatment Measures

Oxytocic (uterotonic) drugs administered IV, intramuscularly, or intramyometrially are used to stimulate the uterus by producing rhythmic contractions and control the degree of hemorrhage. Dosing regimens for oxytocic drugs are listed in Table 161-3.

TABLE 161-3 Dosing Regimens for Oxytocic Drugs

IM, intramuscular; IV, intravenous; PR, per rectum.

Oxytocin (Pitocin) remains first-line therapy for most obstetricians. Prophylactic oxytocin, given either before or after placental delivery, decreases the incidence of PPH up to 40%.¹⁴ It is also used prophylactically after delivery of the fetus but before delivery of the placenta to decrease the duration of the third stage of labor and the amount of blood loss. In an RCT, the incidence of PPH was similar regardless of whether oxytocin was given before or after placental delivery.⁶ Additionally, the incidence of retained placenta was similar for patients treated with oxytocin before or after delivery of the placenta. Oxytocin should be used with caution in patients with hyperactive uterine contractions or hypertension, because the pressor effect of sympathomimetic drugs can increase if they are used with oxytocin.

Methylergonovine (Methergine) is now considered second-line therapy. It is a direct uterotonic agent that reduces uterine bleeding and shortens the third stage of labor. Hypertension is a relative contraindication for the use of Methergine. Carboprost tromethamine (Hemabate), a synthetic prostaglandin similar to prostaglandin F_2α but with a longer duration, produces myometrial contractions that induce hemostasis at the placentation site, reducing postpartum bleeding. It is used in some centers as a second-line uterotonic agent. Asthma is a relative contraindication to the use of carboprost. Carboprost has been shown to be as effective in decreasing PPH refractory to oxytocin and ergonovine. Misoprostol, prostaglandin E₁, causes uterine contractions, and rectal administration of this drug has been shown to be useful in refractory PPH. Although oxytocin is considered the standard of care for treating postpartum hemorrhage, it is not always viable nor available, particularly in resource-poor clinical settings, because of refrigeration requirements and the need for IV administration. In a large randomized prospective trial, the efficacy and acceptability of 800 µg of sublingual misoprostol was compared to 40 International Units of IV oxytocin to control postpartum bleeding.¹⁵ The primary endpoints were cessation of active bleeding within 20 minutes and additional blood loss of 300 mL or more after treatment. The findings suggested that sublingual misoprostol is a viable alternative to 40 International Units of IV oxytocin for treatment of primary postpartum hemorrhage after oxytocin prophylaxis during the third stage of labor. Misoprostol stopped bleeding as rapidly as oxytocin and with a similar quantity of additional blood loss.

The practice of uterine packing to control bleeding remains somewhat controversial. Although this practice had been abandoned for many years, it has recently resurged as an effective method for tamponade of bleeding from the uterus. Opponents of this practice argue that significant amounts of blood may be sequestered behind the uterine packing and that infection risks are increased. The packing can conceal the actual amount of bleeding, leading to gross underestimation of the extent of hemorrhage. The packing usually is removed in 24 to 36 hours. Uterine packing has been proposed as a temporizing maneuver to stop or decrease PPH before surgery or selective arteriography. Balloon occlusion catheters also have been used in the treatment of PPH.¹⁶ Placement of a Sengstaken-Blakemore tube also has been used for control of bleeding.¹⁷

If there is a suspicion of retained placenta, examination of the uterus is both diagnostic and therapeutic. The uterus must be explored digitally and retained placental fragments removed either manually or with instruments. Because this procedure can be difficult and quite painful, it may be necessary to use regional or general anesthesia to obtain optimal visualization and manipulation of the uterus. Administration of oxytocic drugs should continue during manual extraction of placental fragments. Administration of broad-spectrum antibiotics has been recommended whenever there is manipulation or instrumentation of the uterus.

Compression of the abdominal aorta against the vertebral column, which can be achieved by pressing a fist on the abdomen cephalad to the umbilicus, can be a lifesaving temporizing maneuver to control hemorrhage before surgery in the presence of fulminant bleeding with severe hemodynamic compromise. If there is persistent and significant bleeding despite the therapeutic measures described, consideration should be given to arteriography with selective arterial embolization. This procedure requires the expertise of an interventional radiologist and may not be readily available in many hospitals. Successful embolization of the bleeding sites can be accomplished, obviating the need for surgical intervention.¹⁸ Fertility can be preserved with this procedure.¹⁹ Prophylactic placement of embolectomy catheters in patients at high risk for PPH to minimize the procedural delay in the presence of active bleeding has also been utilized in some centers. If embolization is unsuccessful, balloon catheter occlusion of the hypogastric and iliac arteries has been successfully performed as a temporizing measure before surgery.^20–22 Complications are minimal, and post-procedural fever appears to be the most common complication of the procedure.

Surgical Therapy

Surgical therapy is reserved for cases not amenable to medical therapy. Patients with ongoing hemorrhage despite aggressive medical therapy are candidates for operation. Surgery is the treatment of choice for uterine rupture. Lacerations, if visible, are directly repaired and oversewn. Lacerations high in the vaginal vault or in the cervix may require operative repair, primarily for improved visualization of the lesions. Hematomas of the lower genital tract are incised and drained. Arterial embolization of vaginal and vulvar lesions has been used. Hematomas of the broad ligament and in the retroperitoneal space are often managed conservatively if there is only minimal further expansion of the hematoma, but surgical exploration or embolization is mandated if additional significant bleeding occurs. Radiographic imaging with computed tomography, magnetic resonance imaging, and/or ultrasonography is a useful adjunct to monitor the expansion of these hematomas.

Ligation of the uterine, ovarian, or internal iliac (hypogastric) arteries can be performed. The uterine arteries provide 90% of uterine blood flow. Ligation of these arteries can often control bleeding with success rates of up to 92% and a complication rate of 1%.²³ If hemostasis is not achieved with uterine artery ligation, the ovarian and internal iliac arteries can be ligated as well. Ligation of the internal iliac arteries is technically more difficult, and success rates range from 40% to 100%.^23–24 Ligation of the internal iliac arteries usually is done only if ligation of the uterine and ovarian arteries has proved unsuccessful in halting bleeding.

Uterine compression sutures running through the full thickness of both uterine walls (posterior as well as anterior) have recently been described for surgical management of atonic PPH.^25–27 The different uterine suture techniques have proved to be valuable and safe alternatives to hysterectomy in the control of massive PPH. In contrast, hysterectomy remains the definitive surgical therapy to control bleeding. Hysterectomy is required if bleeding continues despite ligation of the internal iliac arteries. Subtotal or total hysterectomy is curative in PPH. In cases of uterine rupture, it is the only surgical option, and nonsurgical modalities are only temporizing measures until the patient can be brought to the operating room. In developed countries, the incidence of postpartum emergent hysterectomy is approximately 1 in 2000 deliveries. Rossi et al. reviewed 24 articles that included 981 cases of emergency postpartum hysterectomy. They found women at highest risk of emergency hysterectomy are those who are multiparous, had a cesarean delivery in either a previous or the present pregnancy, or had abnormal placentation.²⁸

Complications

Serious morbidity may follow postpartum hemorrhage. Complications from postpartum bleeding include hematologic abnormalities such as DIC and dilutional coagulopathy from massive fluid resuscitation and/or massive transfusion (greater than 10 units of packed red blood cells). Dilutional coagulopathy occurs when more than 80% of the original blood volume has been replaced. Life-threatening complications of hemorrhagic shock, including renal failure and liver failure, acute respiratory distress syndrome (ARDS), and pituitary necrosis (Sheehan’s syndrome), can occur. Sheehan’s syndrome can result from severe PPH that causes permanent hypopituitarism from avascular necrosis of the pituitary gland.²⁹

Prognosis

The prognosis of PPH depends on many factors, some of which are directly related to prompt diagnosis and treatment. The cause of bleeding, the duration of bleeding, and the extent of bleeding all affect the likelihood of a good outcome.

Key Points