Williams Obstetrics, 24th Edition

CHAPTER 41. Obstetrical Hemorrhage













Obstetrics is a bloody business.

Dr. Jack Pritchard (1976b)

Obstetrical hemorrhage continues along with hypertension and infections as one of the infamous “triad” of causes of maternal deaths in both developed and underdeveloped countries. It is a leading reason for admission of pregnant women to intensive care units (ICUs) (Crozier, 2011; Small, 2012; Zeeman, 2003; Zwart, 2008). Hemorrhage was a direct cause of nearly 13 percent of 4693 pregnancy-related maternal deaths in the United States documented by the Pregnancy Mortality Surveillance System of the Centers for Disease Control and Prevention (Berg, 2010). Similarly, Clark and coworkers (2008) reported that 12 percent of maternal deaths recorded in the Hospital Corporation of America database were caused by hemorrhage. In developing countries, its contribution is even more striking. Indeed, hemorrhage is the single most important cause of maternal death worldwide and is responsible for half of all postpartum deaths in developing countries (Lalonde, 2006; McCormick, 2002).


The decreasing maternal mortality rate from hemorrhage in this country has been a major achievement. Decreased deaths from hemorrhage have been a major contributor to the decrease in the maternal mortality rate during the 20th century—from approximately 1000 to only 10 per 100,000 births (Hoyert, 2007). But, as discussed in Chapter 1 (p. 5), probably half of maternal deaths are not reported, and at least a third are considered preventable. It thus seems unlikely that deaths from hemorrhage have reached an irreducible minimum.

image Mechanisms of Normal Hemostasis

A major concept in understanding the pathophysiology and management of obstetrical hemorrhage is the mechanism by which hemostasis is achieved after normal delivery. Recall that near term an incredible amount of blood—at least 600 mL/min—flows through the intervillous space (Pates, 2010). As described in Chapter 5 (p. 96), this prodigious flow circulates through the spiral arteries, which average 120 in number. Also recall that these vessels have no muscular layer because of their endotrophoblastic remodeling, which creates a low-pressure system. With placental separation, these vessels at the implantation site are avulsed, and hemostasis is achieved first by myometrial contraction, which compresses this formidable number of relatively large vessels (Chap. 2p. 26). Contractions are followed by clotting and obliteration of vessel lumens.

If after delivery, the myometrium within and adjacent to the denuded implantation site contracts vigorously, fatal hemorrhage from the placental implantation site is unlikely. Importantly, an intact coagulation system is not necessary for postpartum hemostasis unless there are lacerations in the uterus, birth canal, or perineum. At the same time, however, fatal postpartum hemorrhage can result from uterine atony despite normal coagulation. Adhered placental pieces or large blood clots that prevent effective myometrial contraction will serve to impair hemostasis at the implantation site.

image Definition and Incidence

Traditionally, postpartum hemorrhage has been defined as the loss of 500 mL of blood or more after completion of the third stage of labor. This is problematic because almost half of all women delivered vaginally shed that amount of blood or more when losses are measured quantitatively (Pritchard, 1962). These results are depicted in Figure 41-1 and show further that approximately 5 percent of women delivering vaginally lose more than 1000 mL of blood. These studies also showed that estimated blood loss is commonly only approximately half the actual loss. Because of this, estimated blood loss in excess of “average” or 500 mL should alert the obstetrician to possible excessive bleeding. Calibrated delivery-drape markings improve estimation accuracy, but even this technique underestimates blood loss compared with more precise methods (Sosa, 2009; Toledo, 2007).


FIGURE 41-1 Blood loss associated with vaginal delivery, repeat cesarean delivery, and repeat cesarean delivery plus hysterectomy. (Data from Pritchard, 1962.)

The blood volume of a pregnant woman with normal pregnancy-induced hypervolemia usually increases by half, but increases range from 30 to 60 percent—1500 to 2000 mL for an average-sized woman (Pritchard, 1965). The equation to calculate blood volume is shown in Table 41-1. It is axiomatic that a normal pregnant woman tolerates, without any decrease in postpartum hematocrit, blood loss at delivery that approaches the volume of blood that she added during pregnancy. Thus, if blood loss is less than the pregnancy-added volume, the hematocrit remains the same acutely and during the first several days. It then increases as nonpregnant plasma volume normalizes during the next week or so. Whenever the postpartum hematocrit is lower than one obtained on admission for delivery, blood loss can be estimated as the sum of the calculated pregnancy-added volume plus 500 mL for each 3 volume percent decrease of the hematocrit. Blood loss in these women can also be calculated using the formula of Hernandez and associates (2012). Briefly, these investigators used admission-to-discharge red cell volumes to compute total blood loss.

TABLE 41-1. Calculation of Maternal Total Blood Volume

Nonpregnant blood volumea:


Pregnancy blood volume:

Average increase is 30 to 60 percent of calculated nonpregnant volume

Increases across gestational age and plateaus at approximately 34 weeks

Usually larger with low normal-range hematocrit (–30) and smaller with high normal-range hematocrit (–40)

Average increase is 40 to 80 percent with multifetal gestation

Average increase is less with preeclampsia—volumes vary inversely with severity

Postpartum blood volume with serious hemorrhage:

Assume acute return to nonpregnant total volume after fluid resuscitation

Pregnancy hypervolemia cannot be restored postpartum

aFormula arrived at by measuring blood volume and blood loss in more than 100 women using 51Cr-labeled erythrocytes.

Modified from Hernandez, 2012

Excessive blood loss has been estimated by several methods that include measuring loss directly, using a predetermined decline in hematocrit or hemoglobin concentration, or counting the number of women transfused. Of these, direct measurement was performed in a two-center investigation done in Argentina and Uruguay (Sosa, 2009). Specially constructed drapes were used to collect blood at vaginal delivery. These investigators reported that 10.8 percent of women had hemorrhage in excess of 500 mL, whereas 1.9 percent lost > 1000 mL. These estimates likely are too low.

Tita and colleagues (2012) used a 6- volume percent decrease in the postpartum hematocrit to define clinically significant blood loss with vaginal delivery. This decrease easily signifies greater than 1000-mL blood loss in the averaged-sized women. They documented this amount in a fourth of women, which agrees with the findings in Figure 41-1.

A final marker used to estimate the hemorrhage incidence is the transfusion rate. Because of prevailing conservative attitudes toward blood replacement, rates cited more recently are lower than transfusion rates described in older studies. In the study by Tita and colleagues (2012) cited above, more than 6 percent of women delivered vaginally underwent interventional treatment and blood transfusions. In a study of more than 66,000 women delivered at Parkland Hospital from 2002 to 2006, Hernandez and associates (2012) reported that 2.3 percent overall were given blood transfusions for hypovolemia. Half of these women had undergone cesarean delivery. Importantly, for those transfused, these investigators calculated blood loss to average approximately 3500 mL! In a recent study from Australia, 1.6 percent of women delivered in 2010 were transfused (Patterson, 2014). Last, from a registry-based Norwegian study, Skjeldestad and Øian (2012) reported that blood loss exceeded 1250 mL in 2.7 percent of women undergoing cesarean delivery.

Thus, it is apparent that significant blood loss accompanies about a fourth of vaginal deliveries. The amounts and proportions for cesarean delivery are much greater.

When audits of discharge statistics are evaluated, it is apparent that hemorrhage is also underreported. In one example, Bateman and associates (2010) queried the Nationwide Inpatient Sample for 2004 and found a 2.9-percent reported rate of postpartum hemorrhage. Similarly, using a sample of nearly 185,000 delivery outcomes from the National Hospital Discharge Summary database that represented more than 40 million deliveries, Berg and coworkers (2009) reported postpartum hemorrhage incidence of 2.0 and 2.6 percent, for two epochs. In a population-based Canadian study, the incidence of postpartum hemorrhage from atony increased from 3.6 to 4.8 percent from 2001 to 2009 (Mehrabadi, 2013). In contrast, a study encompassing 1999 to 2008 by Kramer and associates (2013) cited a rate of severe postpartum hemorrhage that increased from only 1.9 to 4.2 per 1000 births. At the same time, reported transfusion rates between 1991 and 2003 increased from only 3 to 5 per 1000 deliveries—all rather meager compared with rates in previously cited prospective studies.

Predisposing Conditions

There are myriad clinical circumstances in which risks for obstetrical hemorrhage and its consequences are appreciably increased. The imposing list shown in Table 41-2 illustrates that hemorrhage can manifest at any time throughout pregnancy, delivery, and the puerperium. Thus, any description of obstetrical hemorrhage should include gestational age. Use of terms such as third-trimester bleeding is not recommended because of imprecision.

TABLE 41-2. Obstetrical Hemorrhage: Causes, Predisposing Factors, and Vulnerable Patients


Importantly, inadequate obstetrical and anesthetic services in some areas contribute to maternal death from hemorrhage. This undoubtedly includes facilities in the United States. It was quantified in the United Kingdom by the 2002 Confidential Enquiry into Maternal and Child Health, which concluded that most maternal deaths from hemorrhage were associated with substandard care (Weindling, 2003). Similar experiences were reported from Japan and from the Netherlands (Nagaya, 2000; Zwart, 2008).

image Timing of Hemorrhage

It is has been traditional to classify obstetrical hemorrhage as antepartum—such as with placenta previa or placental abruption, or as postpartum—commonly caused by uterine atony or genital tract lacerations. In individual women, however, these terms are nonspecific, and it is reasonable to specify the cause and gestational age as descriptors.

Antepartum Hemorrhage

Bleeding during various times in gestation may give a clue as to its cause. Many aspects of bleeding during the first half of pregnancy from abortion or ectopic pregnancy are discussed in detail in Chapters 18and 19, respectively. Discussions that follow concern pregnancies with a viable mature living fetus. In these cases, rapid assessment should always consider the deleterious fetal effects of maternal hemorrhage.

Slight vaginal bleeding is common during active labor. This “bloody show” is the consequence of effacement and dilatation of the cervix, with tearing of small vessels. Uterine bleeding, however, coming from above the cervix, is concerning. It may follow some separation of a placenta previa implanted in the immediate vicinity of the cervical canal, or it may be from a placental abruption or uterine tear. Rarely, there may be velamentous insertion of the umbilical cord, and the involved placental vessels may overlie the cervix—vasa previa. Fetal hemorrhage follows laceration of these vessels at the time of membrane rupture. In many women near term, the source of uterine bleeding is not identified, symptomless bleeding ceases, and no apparent anatomical cause is found at delivery. In most of these cases, bleeding likely resulted from a slight marginal placental separation. Despite this, any pregnancy with antepartum bleeding remains at increased risk for an adverse outcome even though bleeding has stopped and placenta previa has been excluded sonographically.

Several reports address mid- to early third-trimester bleeding. Lipitz and colleagues (1991) reported that a fourth of 65 consecutive women with uterine bleeding between 14 and 26 weeks had placental abruption or previa, and a third of all 65 fetuses ultimately were lost. Similar outcomes were described subsequently (Ajayi, 1992; Leung, 2001). The Canadian Perinatal Network described 806 women with hemorrhage between 22 and 28 weeks’ gestation (Sabourin, 2012). Placental abruption (32 percent), previa (21 percent), and cervical bleeding (6.6 percent) were the most common causes identified, and in a third, no cause was found. Of all women, 44 percent were delivered ≤ 29 weeks. Clearly, second- and third-trimester bleeding are associated with a poor pregnancy prognosis.

Postpartum Hemorrhage

In most cases, the cause of postpartum hemorrhage can and should be determined. Frequent causes are uterine atony with bleeding from the placental implantation site, genital tract trauma, or both (see Table 41-2). Postpartum hemorrhage is usually obvious. Important exceptions are unrecognized intrauterine and intravaginal blood accumulation and uterine rupture with intraperitoneal bleeding. Initial assessment should attempt to differentiate uterine atony from genital tract lacerations. Primary considerations are the predisposing risk factors shown in Table 41-2, lower genital tract examination, and uterine tone assessment. Atony is identified by a boggy, soft uterus during bimanual examination and by expression of clots and hemorrhage during uterine massage.

Persistent bleeding despite a firm, well-contracted uterus suggests that hemorrhage most likely is from lacerations. Bright red blood further suggests arterial bleeding. To confirm that lacerations are a source of bleeding, careful inspection of the vagina, cervix, and uterus is essential. Sometimes bleeding may be caused by both atony and trauma, especially after forceps or vacuum-assisted vaginal delivery. Importantly, if significant bleeding follows these deliveries, then the cervix and vagina are carefully examined to identify lacerations. This is easier if conduction analgesia was given. If there are no lower genital tract lacerations and the uterus is contracted, yet supracervical bleeding persists, then manual exploration of the uterus is done to exclude a uterine tear. This also is completed routinely after internal podalic version and breech extraction.

image Blood Loss Estimation

Estimated blood loss—like beauty—is in the eye of the beholder.

Estimation is notoriously inaccurate, especially with excessive bleeding (p. 781). Instead of sudden massive hemorrhage, postpartum bleeding is frequently steady. If atony persists, bleeding may appear to be only moderate at any given instant but may continue until serious hypovolemia develops. Bleeding from an episiotomy or a vaginal laceration can also appear to be only minimal to moderate. However, constant seepage can lead to enormous blood loss relatively quickly. In some cases, after placental separation, blood may not escape vaginally but instead may collect within the uterine cavity, which can become distended by 1000 mL or more of blood. In others, postpartum uterine massage is applied to a roll of abdominal fat mistaken for the uterus. Thus, monitoring of the uterus immediately postpartum must not be left to an inexperienced person (Chap. 27p. 547).

All of these factors can lead to an underappreciation of the magnitude of hemorrhage over time. The effects of hemorrhage depend to a considerable degree on the maternal nonpregnant blood volume and the corresponding degree of pregnancy-induced hypervolemia as previously discussed. For this and other reasons, hypovolemia may not be recognized until very late. A treacherous feature of postpartum hemorrhage is the failure of the pulse and blood pressure to undergo more than moderate alterations until large amounts of blood have been lost. The normotensive woman initially may actually become somewhat hypertensive from catecholamine release in response to hemorrhage. Moreover, women with preeclampsia may become “normotensive” despite remarkable hypovolemia.

Late Postpartum Hemorrhage

Bleeding after the first 24 hours is designated late postpartum hemorrhage. Such bleeding is found in up to 1 percent of women and may be serious (American College of Obstetricians and Gynecologists, 2013b). It is discussed in Chapter 36 (p. 670).

Special Considerations

In certain conditions, a pregnant woman may be particularly susceptible to hemorrhage because her blood volume expansion is less than expected. This situation is most commonly encountered in small women—even those with normal pregnancy-induced hypervolemia. Women with severe preeclampsia or eclampsia are also more vulnerable to hemorrhage because they frequently do not have a normally expanded blood volume. Specifically, Zeeman and associates (2009) documented a mean increase above nonpregnant volume of only 10 percent in eclamptic women (Chap. 40p. 737). A third example is the moderate to severely curtailed pregnancy-induced volume expansion in women with chronic renal insufficiency (Chap. 53p. 1061). When excessive hemorrhage is suspected in these high-risk women, crystalloid and blood are promptly administered for suspected hypovolemia.


The most important causes—because of their incidence or consequence—of severe obstetrical hemorrhage and their contribution to maternal mortality rates are shown in Figure 41-2. Fatal hemorrhage is most likely in circumstances in which blood or components are not immediately available. As discussed on page 815, the ability to provide prompt resuscitation of hypovolemia and blood administration is an absolute requirement for acceptable obstetrical care.


FIGURE 41-2 Contributions to maternal death from various causes of obstetrical hemorrhage. Percentages are approximations because of different classification schemata used. DIC = disseminated intravascular coagulation. (Data from Al-Zirqi, 2008; Berg, 2010; Chichakli, 1999; Zwart, 2008.)

image Uterine Atony

The most frequent cause of obstetrical hemorrhage is failure of the uterus to contract sufficiently after delivery and to arrest bleeding from vessels at the placental implantation site (p. 780). That said, some bleeding is inevitable during third-stage labor as the placenta begins to separate. Blood from the implantation site may escape into the vagina immediately—the Duncan mechanism of placental separation, or it remains concealed behind the placenta and membranes until the placenta is delivered—the Schultze mechanism.

With bleeding during the third stage, the uterus should be massaged if it is not contracted firmly. After the signs of separation, placental descent is indicated by the cord becoming slack. Placental expression should be attempted by manual fundal pressure (Chap. 27p. 546). If bleeding continues, then manual removal of the placenta may be necessary. Separation and delivery of the placenta by cord traction, especially when the uterus is atonic, may cause uterine inversion, which is discussed on page 787.

Third-Stage Bleeding

If significant bleeding persists after delivery of the infant and while the placenta remains partially or totally attached, then manual placental removal is indicated (Chap. 27p. 546). For this, adequate analgesia is mandatory, and aseptic surgical technique should be used. As illustrated in Figure 41-3, the placenta is peeled off its uterine attachment by a motion similar to that used in separating the pages of a book. After its removal, trailing membranes are removed by carefully teasing them from the decidua and using ring forceps for this as necessary. Another method is to wipe out the uterine cavity with a gauze-wrapped hand.


FIGURE 41-3 Manual removal of placenta. A. One hand grasps the fundus. The other hand is inserted into the uterine cavity, and the fingers are swept from side to side as they are advanced. B. When the placenta has become detached, it is grasped and removed.

Uterine Atony after Placental Delivery

The fundus should always be palpated following placental delivery to confirm that the uterus is well contracted. If it is not firm, then vigorous fundal massage usually prevents postpartum hemorrhage from atony (Hofmeyr, 2008). Simultaneously, 20 units of oxytocin in 1000 mL of crystalloid solution will often be effective given intravenously at 10 mL/min for a dose of 200 mU/min. Higher concentrations are minimally more effective (Tita, 2012). Oxytocin should never be given as an undiluted bolus dose because serious hypotension or cardiac arrhythmias may develop.

Risk Factors

In many women, uterine atony can at least be anticipated well in advance of delivery (see Table 41-2). In one study, however, up to half of women who had atony after cesarean delivery were found to have no risk factors (Rouse, 2006). Thus, the ability to identify which individual woman will experience atony is limited. Risk factors for retained placenta are similar (Endler, 2012).

The magnitude of risk imposed by each of these factors shown in Table 41-2 varies considerably between reports. Primiparity has been cited as a risk factor (Driessen, 2011). High parity is a long-known risk factor for uterine atony. The incidence of postpartum hemorrhage was reported to increase from 0.3 percent in women of low parity to 1.9 percent with parity of 4 or greater. It was 2.7 percent with parity of 7 or greater (Babinszki, 1999). The overdistended uterus is prone to hypotonia after delivery, and thus women with a large fetus, multiple fetuses, or hydramnios are at greater risk. Labor abnormalitiespredispose to atony and include hyper- or hypotonic labor. Similarly, labor induction or augmentation with either prostaglandins or oxytocin is more likely to be followed by atony (Driessen, 2011). Finally, the woman who has had a prior postpartum hemorrhage is at risk for recurrence with a subsequent delivery.

Evaluation and Management

With immediate postpartum hemorrhage, careful inspection is done to exclude birth canal laceration. Because bleeding can be caused by retained placental fragments, inspection of the placenta after delivery should be routine. If a defect is seen, the uterus should be manually explored, and the fragment removed. Occasionally, retention of a succenturiate lobe may cause postpartum hemorrhage (Chap. 6p. 117). During examination for lacerations and causes of atony, the uterus is massaged and uterotonic agents are administered.

image Uterotonic Agents

There are several compounds that prompt the postpartum uterus to contract (Chap. 27p. 547). One of these is routinely selected and given to prevent postpartum bleeding by ensuring uterine contractions. Most of these same agents are also used to treat uterine atony with bleeding. Moreover, because many trials combine results from atony prophylaxis and treatment, evaluation of these studies is problematic. For example, oxytocin has been used for more than 50 years, and in most cases, it is infused intravenously or given intramuscularly after placental delivery. Neither route has been shown to be superior (Oladapo, 2012). This or other uterotonins given prophylactically will prevent most cases of uterine atony.

When atony persists despite preventive measures, ergot derivatives have been used for second-line treatment. These include methylergonovine—Methergine—and ergonovine. Only methylergonovine is currently manufactured in the United States. Given parenterally, these drugs rapidly stimulate tetanic uterine contractions and act for approximately 45 minutes (Schimmer, 2011). A common regimen is 0.2 mg of either drug given intramuscularly. A caveat is that ergot agents, especially given intravenously, may cause dangerous hypertension, especially in women with preeclampsia. Severe hypertension is also seen with concomitant use of protease inhibitors given for human immunodeficiency viral (HIV) infection (Chap. 65p. 1279). These adverse effects notwithstanding, it is speculative whether there are superior therapeutic effects of ergot derivatives compared with oxytocin.

In more recent years, second-line agents for atony have included the E- and F-series prostaglandins. Carboprost tromethamine—Hemabate—is the 15-methyl derivative of prostaglandin F2α. It was approved more than 25 years ago for uterine atony treatment in a dose of 250 μg (0.25 mg) given intramuscularly. This dose can be repeated if necessary at 15- to 90-minute intervals up to a maximum of eight doses. Oleen and Mariano (1990) reported its use for postpartum hemorrhage from 12 obstetrical units. Bleeding was controlled in 88 percent of 237 women treated. Another 7 percent required other uterotonics to control hemorrhage, and the remaining 5 percent required surgical intervention. Carboprost causes side effects in approximately 20 percent of women. These include, in descending order of frequency, diarrhea, hypertension, vomiting, fever, flushing, and tachycardia (Oleen, 1990). Another pharmacological effect is pulmonary airway and vascular constriction. Thus, carboprost should not be used for asthmatics and those with suspected amnionic-fluid embolism (p. 812). We have occasionally encountered severe hypertension with carboprost given to women with preeclampsia, and it has also been reported to cause arterial oxygen desaturation that averaged 10 percent (Hankins, 1988).

E-series prostaglandins have been used to prevent or treat atony. Dinoprostone—prostaglandin E2—is given as a 20-mg suppository per rectum or per vaginam every 2 hours. It typically causes diarrhea, which is problematic for the rectal route, whereas vigorous vaginal bleeding may preclude its use per vaginam. Intravenous prostaglandin E2—sulprostone—is used in Europe, but it is not available in this country (Schmitz, 2011).

Misoprostol—Cytotec—is a synthetic prostaglandin E1 analogue that has also been evaluated for both prevention and treatment of atony and postpartum hemorrhage (Abdel-Aleem, 2001; O’Brien, 1998). Most studies have addressed prevention and have conflicting conclusions. In a Cochrane review, Mousa and Alfirevic (2007) reported no added benefits to misoprostol use compared with oxytocin or ergonovine. Derman and coworkers (2006) compared a 600-μg oral dose given at delivery against placebo. They found that the drug decreased hemorrhage incidence from 12 to 6 percent and that of severe hemorrhage from 1.2 to 0.2 percent. In another study, however, Gerstenfeld and Wing (2001) concluded that 400-μg misoprostol administered rectally was not more effective than intravenous oxytocin in preventing postpartum hemorrhage. From a systematic review, Villar (2002) found that oxytocin and ergot preparations administered after delivery were more effective than misoprostol for prevention of postpartum hemorrhage (Chap. 27p. 547).

Bleeding Unresponsive to Uterotonic Agents

Hemorrhage that persists despite uterine massage and continued uterotonin administration may be from a yet unrecognized genital tract laceration, for example, uterine rupture. Thus, if bleeding persists after initial measures for atony have been implemented, then the following management steps are performed immediately and simultaneously:

1. Begin bimanual uterine compression, which is easily done and controls most cases of continuing hemorrhage (Fig. 41-4). This technique is not simply fundal massage. The posterior uterine wall is massaged by one hand on the abdomen, while the other hand is made into a fist and placed into the vagina. This fist kneads the anterior uterine wall through the anterior vaginal wall. Concurrently, the uterus is also compressed between the two hands.

2. Immediately mobilize the emergent-care obstetrical team to the delivery room and call for whole blood or packed red cells.

3. Request urgent help from the anesthesia team.

4. Secure at least two large-bore intravenous catheters so that crystalloid with oxytocin is continued simultaneously with blood products. Insert an indwelling Foley catheter for continuous urine output monitoring.

5. Begin volume resuscitation with rapid intravenous infusion of crystalloid (p. 815).

6. With sedation, analgesia, or anesthesia established and now with optimal exposure, once again manually explore the uterine cavity for retained placental fragments and for uterine abnormalities, including lacerations or rupture.

7. Thoroughly inspect the cervix and vagina again for lacerations that may have escaped attention.

8. If the woman is still unstable or if there is persistent hemorrhage, then blood transfusions are given (p. 815).


FIGURE 41-4 Bimanual compression for uterine atony. The uterus is positioned with the fist of one hand in the anterior fornix pushing against the anterior wall, which is held in place by the other hand on the abdomen. The abdominal hand is also used for uterine massage.

At this juncture, after causes other than atony have been excluded and after hypovolemia is reversed, several other measures are considered if bleeding continues. Their use depends on several factors such as parity, desire for sterilization, and experience with each method.

Uterine Packing or Balloon Tamponade. Uterine packing was popular to treat refractory uterine atony during the first half of the 20th century. It subsequently fell from favor because of concerns regarding concealed bleeding and infection (Hsu, 2003). Newer techniques have been described that alleviate some of these concerns (Zelop, 2011). In one technique, the tip of a 24F Foley catheter with a 30-mL balloon is guided into the uterine cavity and filled with 60 to 80 mL of saline. The open tip permits continuous drainage of blood from the uterus. If bleeding subsides, the catheter is typically removed after 12 to 24 hours. Similar devices that have been used for tamponade include Segstaken-Blakemore and Rusch balloons and condom catheters (Georgiou, 2009; Lo, 2013a,b). Alternatively, the uterus or pelvis may be packed directly with gauze (Gilstrap, 2002).

Enthusiasm has developed for specially constructed intrauterine balloons to treat hemorrhage from uterine atony and other causes (Barbieri, 2011). A Bakri Postpartum Balloon (Cook Medical) or BT-Cath(Utah Medical Products) may be inserted and inflated to tamponade the endometrial cavity and stop bleeding (Fig. 41-5). Insertion requires two or three team members. The first performs abdominal sonography during the procedure. The second places the deflated balloon into the uterus and stabilizes it. The third member instills fluid to inflate the balloon, rapidly infusing at least 150 mL followed by further instillation over a few minutes for a total of 300 to 500 mL to arrest hemorrhage.


FIGURE 41-5 Intrauterine balloon for postpartum hemorrhage.

There have been few prospective studies with these uterine balloons, and thus data are observational (Aibar, 2013; Grönvall, 2013; Laas, 2012). In all, more than 150 women were managed for postpartum hemorrhage. Perhaps a fourth were caused by uterine atony. For all causes, the success rate was noted to be approximately 85 percent. Combinations of balloon tamponade and uterine compression sutures have also been described (Diemert, 2012; Yoong, 2012). Failures for all of these require various surgical methods including hysterectomy. Well-designed studies are needed before instituting intrauterine balloon tamponade as a second-line treatment for atony.

Surgical Procedures. Several invasive procedures can be used to control hemorrhage from atony. These include uterine compression sutures, pelvic vessel ligation, angiographic embolization, and hysterectomy. These are discussed on page 818.

image Uterine Inversion

Puerperal inversion of the uterus is considered to be one of the classic hemorrhagic disasters encountered in obstetrics. Unless promptly recognized and managed appropriately, associated bleeding often is massive. Risk factors include alone or in combination:

1. Fundal placental implantation,

2. Delayed-onset or inadequate uterine contractility after delivery of the fetus, that is, uterine atony,

3. Cord traction applied before placental separation, and

4. Abnormally adhered placentation such as with the accrete syndromes (p. 804).

Depending on which of these factors is contributory, the incidence and severity of uterine inversion varies, with the worst scenario being complete inversion with the uterus protruding from the birth canal as shown in Figure 41-6. There is progressive severity of inversion as shown in Figure 41-7.


FIGURE 41-6 Maternal death from exsanguination caused by uterine inversion associated with a fundal placenta accreta during a home delivery.


FIGURE 41-7 Progressive degrees of uterine inversion depicted. After the fundus begins and continues to invert (Nos. 1 and 2), it would not be visible externally until it was at the level of the introitus (No. 3) or completely inverted (No. 4).

The incidence of uterine inversion is variable and is usually different for vaginal and for cesarean delivery. Incidences range from approximately 1 in 2000 to 1 in 20,000 deliveries (Baskett, 2002; Ogah, 2011; Rana, 2009; Witteveen, 2013). Our experiences at Parkland Hospital comport with the higher 1:2000 incidence. This is despite our policy to discourage placental delivery by cord traction alone and before certainty of its separation. It is unknown if active management of third-stage labor with cord traction applied ostensibly after signs of placental separation increases the likelihood of uterine inversion (Deneux-Tharaux, 2013; Gülmezoglu, 2012; Peña-Marti, 2007; Prick, 2013).

Recognition and Management

Immediate recognition of uterine inversion improves the chances of a quick resolution and good outcome. That said, inexperienced attendants may have a delayed appreciation for an inverting uterus, especially if it is only partial and thus not protruding through the introitus. In these cases, continued hemorrhage likely will prompt closer examination of the birth canal. Even so, the partially inverted uterus can be mistaken for a uterine myoma, and this can be resolved by sonography (Pauleta, 2010; Rana, 2009). Many cases are associated with immediate life-threatening hemorrhage, and at least half require blood replacement (Baskett, 2002). It was previously taught that associated shock was disproportionate to blood loss because of parasympathetic stimulation from stretching pelvic tissues. This has been refuted (Watson, 1980).

Once any degree of uterine inversion is recognized, several steps must be implemented urgently and simultaneously:

1. Immediate assistance is summoned, including obstetrical and anesthesia personnel.

2. Blood is brought to the delivery suite in case it may be needed.

3. The woman is evaluated for emergency general anesthesia. Large-bore intravenous infusion systems are secured to begin rapid crystalloid infusion to treat hypovolemia while awaiting arrival of blood for transfusion.

4. If the recently inverted uterus has not contracted and retracted completely and if the placenta has already separated, then the uterus may often be replaced simply by pushing up on the inverted fundus with the palm of the hand and fingers in the direction of the long axis of the vagina (Fig. 41-8). Some use two fingers rigidly extended to push the center of the fundus upward. Care is taken not to apply so much pressure as to perforate the uterus with the fingertips.

5. If the placenta is still attached, it is not removed until infusion systems are operational and a uterine relaxant drug administered. Many recommend a trial of an intravenously administered tocolytic drug such as terbutaline, magnesium sulfate, or nitroglycerin for uterine relaxation and repositioning (Hong, 2006; You, 2006). If these fail to provide sufficient relaxation, then a rapidly acting halogenated inhalational agent is administered.

6. After removing the placenta, steady pressure with the fist, palm, or fingers is applied to the inverted fundus in an attempt to push it up into and through the dilated cervix as described in Step 4.

7. Once the uterus is restored to its normal configuration, tocolysis is stopped. Oxytocin is then infused, and other uterotonics may be given as described for atony (p. 785). Meanwhile, the operator maintains the fundus in its normal anatomical position while applying bimanual compression to control further hemorrhage until the uterus is well contracted (see Fig. 41-4). The operator continues to monitor the uterus transvaginally for evidence of subsequent inversion.


FIGURE 41-8 The incompletely inverted uterus is repositioned by using the abdominal hand for palpation of the crater-like depression while gently pushing the inverted fundus up out of the lower segment and to its normal anatomical position.

Surgical Intervention

In most cases the inverted uterus can be restored to its normal position by the techniques described above. Occasionally, manual replacement fails. One cause is a dense myometrial constriction ring (Kochenour, 2002). At this point, laparotomy is imperative. The anatomical configuration found at surgery can be confusing as shown in Figure 41-9. With agents given for tocolysis, a combined effort is made to reposition the uterus by simultaneously pushing upward from below and pulling upward from above. Application of atraumatic clamps to each round ligament and upward traction may be helpful—the Huntington procedure. In some cases, placing a deep traction suture in the inverted fundus or grasping it with tissue forceps may be of aid. However, these may be technically difficult (Robson, 2005). If the constriction ring still prohibits repositioning, a longitudinal surgical cut—Haultain incision—is made posteriorly through the ring to expose the fundus and permit reinversion (Sangwan, 2009). After uterine replacement, tocolytics are stopped, oxytocin and other uterotonics are given, and the uterine incision is repaired. Risks of separation of this posterior hysterotomy incision during subsequent pregnancy, labor, and delivery are unknown.


FIGURE 41-9 Surgical anatomy of a completely inverted uterus viewed from above at laparotomy. The uterine fundus is not visible and the tubes and ovaries have been drawn into the birth canal.

In some cases, the uterus will again invert almost immediately after repositioning. If this is a problem, then compression sutures shown on page 819 can be used to prevent another inversion (Matsubara, 2009; Mondal, 2012). Occasionally, chronic puerperal uterine inversion may become apparent weeks after delivery.

image Injuries to the Birth Canal

Childbirth is invariably associated with trauma to the birth canal, which includes the uterus and cervix, vagina, and perineum. Injuries sustained during labor and delivery range from minor mucosal tears to lacerations that create life-threatening hemorrhage or hematomas.

Vulvovaginal Lacerations

Small tears of the anterior vaginal wall near the urethra are relatively common. They are often superficial with little to no bleeding, and their repair is usually not indicated. Minor superficial perineal and vaginal lacerations occasionally require sutures for hemostasis. Those large enough to require extensive repair are typically associated with voiding difficulty, and an indwelling bladder catheter will obviate this.

Deeper perineal lacerations are usually accompanied by varying degrees of injury to the outer third of the vaginal vault. Some extend to involve the anal sphincter or varying depths of the vaginal walls. In more than 87,000 deliveries in the Consortium on Safe Labor database, the frequency of third- or fourth-degree perineal lacerations was 5.7 percent in nulliparas and 0.6 percent in multiparas (Landy, 2011). Bilateral vaginal lacerations are usually unequal in length, and they are separated by a tongue of vaginal tissue. Lacerations involving the middle or upper third of the vaginal vault usually are associated with injuries of the perineum or cervix. These sometimes are missed unless thorough inspection of the upper vagina and cervix is performed. Bleeding despite a firmly contracted uterus is strong evidence of genital tract laceration. Those that extend upward usually are longitudinal. They may follow spontaneous delivery but frequently result from injuries sustained during operative vaginal delivery with forceps or vacuum extractor. Most involve deeper underlying tissues and thus usually cause significant hemorrhage. Bleeding is typically controlled by appropriate suture repair.

Extensive vaginal or cervical tears should prompt a careful search for evidence of retroperitoneal hemorrhage or peritoneal perforation or hemorrhage. If this is strongly suspected, then laparotomy is considered (Rafi, 2010). Extensive vulvovaginal lacerations should also prompt intrauterine exploration for possible uterine tears or rupture. For deep vulvovaginal lacerations, suture repair is usually required, and effective analgesia or anesthesia, vigorous blood replacement, and capable assistance are mandatory. In the study reported by Melamed and colleagues (2009), 1.5 percent of women with these lacerations required blood transfusions. Repair of vulvovaginal lacerations is detailed in Chapter 27 (p. 548).

Levator Sling Injuries

The levator ani muscles, described in Chapter 2 (p. 22), are usually involved with deep vaginal vault lacerations. They also sustain stretch injuries that result from overdistention of the birth canal. Muscle fibers are torn and separated, and their diminished tone may interfere with pelvic diaphragm function to cause pelvic relaxation. If the injuries involve the pubococcygeus muscle, urinary incontinence also may result.

Cervical Lacerations

Superficial lacerations of the cervix can be seen on close inspection in more than half of all vaginal deliveries. Most of these are less than 0.5 cm and seldom require repair (Fahmy, 1991). Deeper lacerations are less frequent, but even these may be unnoticed. Due to ascertainment bias, variable incidences are described. For example, in the Consortium database, the incidence of cervical lacerations was 1.1 percent in nulliparas and 0.5 percent in multiparas (Landy, 2011). But the overall incidence reported by Melamed and coworkers (2009), in a study of more than 81,000 Israeli women, was only 0.16 percent. Parikh and associates (2007) reported a 0.2-percent incidence of lacerations that needed repair.

Cervical lacerations are not usually problematic unless they cause hemorrhage or extend to the upper third of the vagina. Rarely, the cervix may be entirely or partially avulsed from the vagina—colporrhexis—in the anterior, posterior, or lateral fornices. These injuries sometimes follow difficult forceps rotations or deliveries performed through an incompletely dilated cervix with the forceps blades applied over the cervix. In some women, cervical tears reach into lower uterine segment and involve the uterine artery and its major branches. They occasionally extend into the peritoneal cavity. The more severe lacerations usually manifest as external hemorrhage or as a hematoma, however, they may occasionally be unsuspected. In the large Israeli study reported by Melamed and colleagues (2009), almost 11 percent of women with a cervical laceration required blood transfusions.

Other serious cervical injuries fortunately are uncommon. In one, the edematous anterior cervical lip is caught during labor and compressed between the fetal head and maternal symphysis pubis. If this causes severe ischemia, the anterior lip may undergo necrosis and separate from the rest of the cervix. Another rare injury is when the entire vaginal portion of the cervix is avulsed. Such annular or circular detachment of the cervix is seen with difficult deliveries, especially forceps deliveries.

Diagnosis. A deep cervical tear should always be suspected in women with profuse hemorrhage during and after third-stage labor, particularly if the uterus is firmly contracted. It is reasonable to inspect the cervix routinely following major operative vaginal deliveries even if there is no third-stage bleeding. Thorough evaluation is necessary, and often the flabby cervix interferes with digital examination. The extent of the injury can be more fully appreciated with adequate exposure and visual inspection. This is best accomplished when an assistant applies firm downward pressure on the uterus while the operator exerts traction on the lips of the cervix with ring forceps. A second assistant can provide even better exposure with right-angle vaginal wall retractors.

Management. In general, cervical lacerations of 1 and even 2 cm are not repaired unless they are bleeding. Such tears heal rapidly and are thought to be of no significance. When healed they result in the irregular, sometime stellate appearance of the external cervical os that indicates previous delivery of a viable-size fetus.

Deep cervical tears usually require surgical repair. When the laceration is limited to the cervix or even when it extends somewhat into the vaginal fornix, satisfactory results are obtained by suturing the cervix after bringing it into view at the vulva as depicted in Figure 41-10. While cervical lacerations are repaired, associated vaginal lacerations may be tamponaded with gauze packs to arrest their bleeding. Because hemorrhage usually comes from the upper angle of the wound, the first suture using absorbable material is placed in tissue above the angle. Subsequently, either interrupted or continuous locking sutures are placed outward toward the operator. If lacerations extend to involve the lateral vaginal sulcus, then attempts to restore the normal cervical appearance may lead to subsequent stenosis.


FIGURE 41-10 Repair of cervical laceration with appropriate surgical exposure. Continuous absorbable sutures are placed beginning at the upper angle of the laceration.

Most cervical lacerations are successfully repaired using sutures. However, if there is uterine involvement and continued hemorrhage, some of the methods described on page 818 may be necessary to obtain hemostasis. For example, Lichtenberg (2003) described successful angiographic embolization for a high cervical tear after failed surgical repair.

image Puerperal Hematomas

Pelvic hematomas can have several anatomical manifestations following childbirth. They are most often associated with a laceration, episiotomy, or an operative delivery. However, they may develop following rupture of a blood vessel without associated lacerations (Nelson, 2012; Propst, 1998; Ridgway, 1995). In some cases, they are quickly apparent, but in others, hemorrhage may be delayed. Occasionally, they are associated with an underlying coagulopathy. Faulty clotting may be acquired, such as with consumptive coagulopathy from placental abruption or fatty liver failure, or may stem from a congenital bleeding disorder such as von Willebrand disease.

One classification of puerperal hematomas includes vulvar, vulvovaginal, paravaginal, and retroperitoneal hematomas. Vulvar hematomas may involve the vestibular bulb or branches of the pudendal artery, which are the inferior rectal, perineal, and clitoral arteries (Fig. 41-11). Paravaginal hematomas may involve the descending branch of the uterine artery (Zahn, 1990). In some cases, a torn vessel lies above the pelvic fascia, and a supralevator hematoma develops. These can extend into the upper portion of the vaginal canal and may almost occlude its lumen. Continued bleeding may dissect retroperitoneally to form a mass palpable above the inguinal ligament. Finally, it may even dissect up behind the ascending colon to the hepatic flexure at the lower margin of the diaphragm (Rafi, 2010).


FIGURE 41-11 Schematic showing types of puerperal hematoma. A. Coronal view showing supralevator and anterior perineal triangle hematomas on the right. B. Perineal view shows anterior perineal triangle anatomy and an ischioanal fossa hematoma on the left.

Vulvovaginal Hematomas

These may develop rapidly and frequently cause excruciating pain, as did the one shown in Figure 41-12. If bleeding ceases, then small- to moderate-sized hematomas may be absorbed. However, we have encountered a few that rebled up to 2 weeks postpartum. In others, the tissues overlying the hematoma may rupture from pressure necrosis. At this time, profuse hemorrhage may follow, but in other cases, the hematoma drains in the form of large clots and old blood. In those that involve the paravaginal space and extend above the levator sling, retroperitoneal bleeding may be massive and occasionally fatal.


FIGURE 41-12 Left-sided anterior perineal triangle hematoma associated with a vaginal laceration following spontaneous delivery in a woman with consumptive coagulopathy from acute fatty liver of pregnancy.

Diagnosis. A vulvar hematoma is readily diagnosed by severe perineal pain. A tense, fluctuant, and tender swelling of varying size rapidly develops and is eventually covered by discolored skin. A paravaginal hematoma may escape detection temporarily. However, symptoms of pelvic pressure, pain, or inability to void should prompt evaluation with discovery of a round, fluctuant mass encroaching on the vaginal lumen. When there is a supralevator extension, the hematoma extends upward in the paravaginal space and between the leaves of the broad ligament. The hematoma may escape detection until it can be felt on abdominal palpation or until hypovolemia develops. Imaging with sonography or computed tomographic (CT) scanning can be useful to assess hematoma location and extent. As discussed, supralevator hematomas are particularly worrisome because they can lead to hypovolemic shock and death.

Management. Vulvovaginal hematomas are managed according to their size, duration since delivery, and expansion. In general, smaller vulvar hematomas identified after the woman leaves the delivery room may be treated expectantly (Propst, 1998). But, if pain is severe or the hematoma continues to enlarge, then surgical exploration is preferable. An incision is made at the point of maximal distention, blood and clots are evacuated, and bleeding points ligated. The cavity may then be obliterated with absorbable mattress sutures. Often, no sites of bleeding are identified. Nonetheless, the evacuated hematoma cavity is surgically closed, and the vagina is packed for 12 to 24 hours. Supralevator hematomas are more difficult to treat. Although some can be evacuated by vulvar or vaginal incisions, laparotomy is advisable if there is continued hemorrhage.

Blood loss with large puerperal hematomas is nearly always considerably more than the clinical estimate. Hypovolemia is common, and transfusions are frequently required when surgical repair is necessary.

Angiographic embolization as described on page 820 has become popular for management of some puerperal hematomas. Embolization can be used primarily, or more likely secondarily, if surgical attempts at hemostasis have failed or if the hematoma is difficult to access surgically (Distefano, 2013; Ojala, 2005). The use of a Bakri balloon for a paracervical hematoma has also been described (Grönvall, 2013).

image Rupture of the Uterus

Uterine rupture may be primary, defined as occurring in a previously intact or unscarred uterus, or may be secondary and associated with a preexisting myometrial incision, injury, or anomaly. Some of the etiologies associated with uterine rupture are presented in Table 41-3. Importantly, the contribution of each of these underlying causes has changed remarkably during the past 50 years. Specifically, before 1960, when the cesarean delivery rate was much lower than it is currently and when women of great parity were numerous, primary uterine rupture predominated. As the incidence of cesarean delivery increased and especially as a subsequent trial of labor in these women became prevalent through the 1990s, uterine rupture through the cesarean hysterotomy scar became preeminent. As discussed in detail in Chapter 31 (p. 617), along with diminished enthusiasm for trial of labor in women with prior cesarean delivery, the two types of rupture likely now have equivalent incidences. Indeed, in a 2006 study of 41 cases of uterine rupture from the Hospital Corporation of America, half were in women with a prior cesarean delivery (Porreco, 2009).

TABLE 41-3. Some Causes of Uterine Rupture


Predisposing Factors and Causes

In addition to the prior cesarean hysterotomy incision already discussed, risks for uterine rupture include other previous operations or manipulations that traumatize the myometrium. Examples are uterine curettage or perforation, endometrial ablation, myomectomy, or hysteroscopy (Kieser, 2002; Pelosi, 1997). In the study by Porreco and colleagues (2009) cited earlier, seven of 21 women without a prior cesarean delivery had undergone prior uterine surgery.

In developed countries, the incidence of rupture was cited by Getahun and associates (2012) as 1 in 4800 deliveries. The frequency of primary rupture approximates 1 in 10,000 to 15,000 births (Miller, 1997; Porreco, 2009). One reason is a decreased incidence of women of great parity (Maymon, 1991; Miller, 1997). Another is that excessive or inappropriate uterine stimulation with oxytocin—previously a frequent cause—has mostly disappeared. Anecdotally, however, we have encountered primary uterine rupture in a disparate number of women in whom labor was induced with prostaglandin E1.

Pathogenesis. Rupture of the previously intact uterus during labor most often involves the thinned-out lower uterine segment. When the rent is in the immediate vicinity of the cervix, it frequently extends transversely or obliquely. When the rent is in the portion of the uterus adjacent to the broad ligament, the tear is usually longitudinal. Although these tears develop primarily in the lower uterine segment, it is not unusual for them to extend upward into the active segment or downward through the cervix and into the vagina (Fig. 41-13). In some cases, the bladder may also be lacerated (Rachagan, 1991). If the rupture is of sufficient size, the uterine contents will usually escape into the peritoneal cavity. If the presenting fetal part is firmly engaged, however, then only a portion of the fetus may be extruded from the uterus. Fetal prognosis is largely dependent on the degree of placental separation and magnitude of maternal hemorrhage and hypovolemia. In some cases, the overlying peritoneum remains intact, and this usually is accompanied by hemorrhage that extends into the broad ligament to cause a large retroperitoneal hematoma with extensive blood loss.


FIGURE 41-13 Supracervical hysterectomy specimen showing uterine rupture during spontaneous labor with a vertical tear at the left lateral edge of lower uterine segment.

Occasionally, there is an inherent weakness in the myometrium in which the rupture takes place. Some examples include anatomical anomalies, adenomyosis, and connective-tissue defects such as Ehlers-Danlos syndrome (Arici, 2013; Nikolaou, 2013).

Management and Outcomes. The varied clinical presentations of uterine rupture and its management are discussed in detail in Chapter 31 (p. 617).

In the most recent maternal mortality statistics from the Centers for Disease Control and Prevention, uterine rupture accounted for 14 percent of deaths caused by hemorrhage (Berg, 2010). Maternal morbidity includes hysterectomy that may be necessary to control hemorrhage. There is also considerably increased perinatal morbidity and mortality associated with uterine rupture. A major concern is that surviving infants develop severe neurological impairment (Porreco, 2009).

Traumatic Uterine Rupture

Although the distended pregnant uterus is surprisingly resistant to blunt trauma, pregnant women sustaining such trauma to the abdomen should be watched carefully for signs of a ruptured uterus (Chap. 47p. 954). Even so, blunt trauma is more likely to cause placental abruption as described subsequently. In a study by Miller and Paul (1996), trauma accounted for only three cases of uterine rupture in more than 150 women. Other causes of traumatic rupture that are uncommon today are those due to internal podalic version and extraction, difficult forceps delivery, breech extraction, and unusual fetal enlargement such as with hydrocephaly.

image Placental Abruption

Separation of the placenta—either partially or totally—from its implantation site before delivery is described by the Latin term abruptio placentae. Literally translated, this refers to “rending asunder of the placenta,” which denotes a sudden accident that is a clinical characteristic of most cases. In the purest sense, the cumbersome—and thus seldom used—term premature separation of the normally implanted placenta is most descriptive because it excludes separation of a placenta previa implanted over the internal cervical os.


Placental abruption is initiated by hemorrhage into the decidua basalis. The decidua then splits, leaving a thin layer adhered to the myometrium. Consequently, the process begins as a decidual hematoma and expands to cause separation and compression of the adjacent placenta. Inciting causes of many cases are not known, however, several have been posited. The phenomenon of impaired trophoblastic invasion with subsequent atherosis is related in some cases of preeclampsia and abruption (Brosens, 2011). Inflammation or infection may be contributory. Nath and colleagues (2007) found histological evidence of inflammation to be more common in prematurely separated placentas. Papio species of baboons develop abruptio placentae similar to humans, and up to half of prematurely separated placentas in these animals demonstrate neutrophilic infiltration (Schenone, 2012; Schlabritz-Loutsevich, 2013a,b).

Abruption likely begins with rupture of a decidual spiral artery to cause a retroplacental hematoma. This can expand to disrupt more vessels and extend placental separation (Fig. 6-3p. 119). In the early stages of placental abruption, there may be no clinical symptoms. If there is no further separation, the abruption is discovered on examination of the freshly delivered placenta, as a circumscribed depression on the maternal surface. These usually measure a few centimeters in diameter and are covered by dark, clotted blood. Because several minutes are required for these anatomical changes to materialize, a very recently separated placenta may appear totally normal at delivery. Our experiences are like those of Benirschke and associates (2012) in that the “age” of the retroplacental clot cannot be determined exactly. In the example shown in Figure 41-14, a large dark clot is well formed, it has depressed the placental bulk, and it likely is at least several hours old.


FIGURE 41-14 Partial placental abruption with a dark adhered clot.

Even with continued bleeding and placental separation, placental abruption can still be either total or partial (Fig. 41-15). With either, bleeding typically insinuates itself between the membranes and uterus, ultimately escaping through the cervix to cause external hemorrhage. Less often, the blood is retained between the detached placenta and the uterus, leading to concealed hemorrhage and delayed diagnosis (Chang, 2001). The delay translates into much greater maternal and fetal hazards. With concealed hemorrhage, the likelihood of consumptive coagulopathy also is greater. This is because increased pressure within the intervillous space caused by the expanding retroplacental clot forces more placental thromboplastin into the maternal circulation (p. 797).


FIGURE 41-15 Schematic of placental abruption. Shown to left is a total placental abruption with concealed hemorrhage. To the right is a partial abruption with blood and clots dissecting between membranes and decidua to the internal cervical os and then externally into the vagina.

Chronic Abruption. Some cases of chronic placental separation begin early in pregnancy. Dugoff and coworkers (2004) observed an association between some abnormally elevated maternal serum aneuploidy markers and subsequent abruption. Ananth (2006) and Weiss (2004) and their associates have also correlated first- and second-trimester bleeding with third-trimester placental abruption. In some cases of a chronic abruption, subsequent oligohydramnios develops—chronic abruption-oligohydramnios sequence—CAOS (Elliott, 1998). Even later in pregnancy, hemorrhage with retroplacental hematoma formation is occasionally arrested completely without delivery. These women may have abnormally elevated serum levels of alpha-fetoprotein (Ngai, 2012). We documented a chronic abruption in a woman with suggestive findings by labeling her red cells with radiochromium. Her symptoms abated, and at delivery 3 weeks later, a 400-mL clot found within the uterus contained no radiochromium, whereas peripheral blood at that time did. Thus, red cells in the clot had accumulated before they were labeled with the radioisotope 3 weeks before delivery.

Traumatic Abruption. External trauma—usually from motor vehicle accidents or aggravated assault—can cause placental separation. The frequency of abruption caused by trauma varies and may be dependent on whether these women are cared for in a major trauma unit. Kettel (1988) and Stafford (1988) and their coworkers have appropriately stressed that abruption can be caused by relatively minor trauma. The clinical presentation and sequelae of these abruptions are somewhat different from spontaneous cases. For example, associated fetomaternal hemorrhage, while seldom clinically significant with most spontaneous abruptions, is more common with trauma because of concomitant placental tears or “fractures” (Fig. 47-11p. 954). Fetal bleeding that averaged 12 mL was noted in a third of women with a traumatic abruption reported by Pearlman (1990). In eight women cared for at Parkland Hospital, we found fetal-to-maternal hemorrhage of 80 to 100 mL in three of eight cases of traumatic placental abruption (Stettler, 1992). Importantly, in some cases of trauma, a nonreassuring fetal heart rate tracing may not be accompanied by other evidence of placental separation. A sinusoidal tracing is one example (Fig. 24-13p. 482). Traumatic abruption is considered in more detail in Chapter 47 (p. 953).

Fetal-to-Maternal Hemorrhage. Most blood in the retroplacental hematoma in a nontraumatic placental abruption is maternal. This is because hemorrhage is caused by separation within the maternal decidua, and placental villi are usually initially intact. In 78 women at Parkland Hospital with a nontraumatic placental abruption, fetal-to-maternal hemorrhage was documented in only 20 percent—and all of these had < 10 mL fetal blood loss (Stettler, 1992). As discussed above, significant fetal bleeding is much more likely with a traumatic abruption that results from a concomitant placental tear.


The reported incidence of placental abruption varies because of different criteria used. That said, its frequency averages 0.5 percent or 1 in 200 deliveries. In the National Center for Health Statistics database of 15 million deliveries, Salihu and colleagues (2005) reported an incidence of 0.6 percent or 1 in 165 births. From the National Hospital Discharge Summary database from 1999 through 2001, the incidence of placental abruption was found to be 1 percent (Ananth, 2005). From a Maternal-Fetal Medicine Units Network study of approximately 10,000 nulliparous women, the incidence was 0.6 percent (Roberts, 2010). In nearly 366,000 deliveries at Parkland Hospital from 1988 through 2012, the incidence of placental abruption averaged 0.35 percent or 1 in 290 (Fig. 41-16).


FIGURE 41-16 Frequency of placental abruption and placenta previa by maternal age in 365,700 deliveries at Parkland Hospital from 1988 through 2012. (Data courtesy of Dr. Don McIntire.)

According to Ananth (2001b, 2005), the frequency of placental abruption has increased in this country from 0.8 percent in 1981 to 1.0 percent in 2001. Most of this increase was in black women. At Parkland Hospital, however, both the incidence and severity have decreased. With placental abruption so extensive as to kill the fetus, the incidence was 0.24 percent or 1 in 420 births from 1956 through 1967 (Pritchard, 1967). As the number of high-parity women giving birth decreased along with improved availability of prenatal care and emergency transportation, the frequency of abruption causing fetal death decreased to 0.12 percent or 1 in 830 births through 1989. Thereafter and through 2003, it decreased further to 0.06 percent or 1 in 1600, and most recently through 2012, it declined to 0.048 percent or 1 in 2060.

Perinatal Morbidity and Mortality

Major fetal congenital anomalies have an increased association with placental abruption (Riihimäki, 2013). Overall, perinatal outcomes are influenced by gestational age, and the frequency of placental abruption increases across the third trimester up to term. As seen in Figure 41-17, more than half of the placental abruptions at Parkland Hospital developed at ≥ 37 weeks. Perinatal mortality and morbidity, however, are more common with earlier abruptions. Perinatal deaths caused by abruptions can be assessed by their contribution to mortality or as an actual mortality ratio. Looked at the first way, although the rates of fetal death have declined, the contribution of abruption as a cause of stillbirths remains prominent because other causes have also decreased. For example, since the early 1990s, 10 to 12 percent of all third-trimester stillbirths at Parkland Hospital have been the consequence of placental abruption. This is similar to the rate reported by Fretts and Usher (1997) for the Royal Victoria Hospital in Montreal during the 18-year period ending in 1995 (Chap. 35p. 662).


Figure 41-17 Frequency of placental abruption by gestational age.

Looked at the other way, several investigators have documented high perinatal mortality rates caused by placental abruption. Salihu and colleagues (2005) analyzed more than 15 million singleton births in the United States between 1995 and 1998. The perinatal mortality rate associated with placental abruption was 119 per 1000 births compared with 8 per 1000 for the general obstetrical population. They emphasized that the high rate was due not just to placental abruption, but also to the associated increases in preterm delivery and fetal-growth restriction. Of the two, preterm birth has been reported to be the most important (Nath, 2008).

Perinatal morbidity—often severe—is common in survivors. An early study by Abdella and associates (1984) documented significant neurological deficits within the first year of life in 15 percent of survivors. Two subsequent studies by Matsuda and coworkers (2003, 2013) reported that 20 percent of survivors developed cerebral palsy. These observations are similar to ours from Parkland Hospital. Notably, 20 percent of liveborn neonates of women with an abruption had severe acidemia, defined by a pH < 7.0 or base deficit of ≥ 12 mmol/L. Importantly, 15 percent of liveborn neonates subsequently died.

Predisposing Factors

Demographic Factors. Several predisposing factors may increase the risk for placental abruption, and some are listed in Table 41-4. First, the incidence of abruption increases with maternal age (see Fig. 41-16). In the First- and Second-Trimester Evaluation of Risk (FASTER) trial, women older than 40 years were 2.3 times more likely to experience abruption compared with those 35 years or younger (Cleary-Goldman, 2005). There are conflicting data regarding women of great parity (Pritchard, 1991; Toohey, 1995). Race or ethnicity also appears to be important. In almost 366,000 deliveries at Parkland Hospital, abruption severe enough to kill the fetus was most common in African-American and white women—1 in 200—less so in Asian women—1 in 300—and least in Latin-American women—1 in 350 (Pritchard, 1991). A familial association was found in an analysis of a Norwegian population-based registry that included almost 378,000 sisters with more than 767,000 pregnancies (Rasmussen, 2009). If a woman had a severe abruption, then the risk for her sister was doubled, and the heritability risk was estimated to be 16 percent. The control group of their sisters-in-law had a risk similar to that for the general obstetrical population.

TABLE 41-4. Risk Factors for Placental Abruption


Hypertension and Preeclampsia. Some form of hypertension is the most frequent condition associated with placental abruption. This includes gestational hypertension, preeclampsia, chronic hypertension, or a combination thereof. In the report by Pritchard and colleagues (1991) that described 408 women with placental abruption and fetal demise cared for at Parkland Hospital, hypertension was apparent in half once hypovolemia was corrected. Half of these women—a fourth of all 408—had chronic hypertension. Looked at another way, a Network study reported that 1.5 percent of pregnant women with chronic hypertension suffered placental abruption (Sibai, 1998). Risk estimates by Zetterstrom and associates (2005) included a twofold increased incidence of abruption in women with chronic hypertension compared with normotensive women—an incidence of 1.1 versus 0.5 percent.

Chronic hypertension with superimposed preeclampsia or fetal-growth restriction confers an ever greater increased risk (Ananth, 2007). Even so, the severity of hypertension does not necessarily correlate with abruption incidence (Zetterstrom, 2005). The long-term effects of these associations are apparent from the significantly increased cardiovascular mortality risk in affected women (Pariente, 2013). Observations from the Magpie Trial Collaborative Group (2002) suggest that women with preeclampsia given magnesium sulfate may have a reduced risk for abruption.

Preterm Prematurely Ruptured Membranes. There is no doubt that there is a substantially increased risk for abruption when the membranes rupture before term. Major and colleagues (1995) reported that 5 percent of 756 women with ruptured membranes between 20 and 36 weeks developed an abruption. Kramer and coworkers (1997) found an incidence of 3.1 percent if membranes were ruptured for longer than 24 hours. Ananth and associates (2004) reported that the threefold risk of abruption with preterm rupture was further increased with infection. This same group has suggested that inflammation and infection as well as preterm delivery may be the primary causes leading to abruption (Nath, 2007, 2008).

Cigarette Smoking. Given other vascular diseases caused by smoking, it is not surprising that studies from the Collaborative Perinatal Project linked this to an increased risk for abruption (Misra, 1999; Naeye, 1980). Results of metaanalyses of 1.6 million pregnancies included a twofold risk for abruption in smokers (Ananth, 1999b). This risk increased to five- to eightfold if smokers had chronic hypertension, severe preeclampsia, or both. Similar findings have been reported by Mortensen (2001), Hogberg (2007), Kaminsky (2007), and all their coworkers.

Cocaine Abuse. Women who use cocaine can have an alarming frequency of placental abruption. Bingol and colleagues (1987) described 50 women who abused cocaine during pregnancy—eight had a stillbirth caused by placental abruption. In a systematic review, Addis and associates (2001) reported that placental abruption was more common in women who used cocaine than in those who did not.

Lupus Anticoagulant and Thrombophilias. Women affected by some of these have higher associated rates of thromboembolic disorders during pregnancy. However, the link with placental abruption is less clear (American College of Obstetricians and Gynecologists, 2012a, 2013a). Lupus anticoagulant is associated with maternal floor infarction of the placenta, but is less so with typical abruptions. There is no convincing evidence that thrombophilias—for example, factor V Leiden or prothrombin gene mutation—are associated with placental abruption. These have been reviewed by Kenny and coworkers (2014) and are discussed further in Chapters 52 (p. 1029) and 59 (p. 1174).

Uterine Leiomyomas. Especially if located near the mucosal surface behind the placental implantation site, uterine myomas can predispose to abortion or later to placental abruption (Chaps. 18p. 360 and 63p. 1225).

Recurrent Abruption. Because many of the predisposing factors are chronic and therefore repetitive, it would be reasonable to conclude that placental abruption would have a high recurrence rate. In fact, the woman who has suffered an abruption—especially one that caused fetal death—has an extraordinarily high risk for recurrence. In these women, Pritchard and associates (1970) identified a recurrence rate of 12 percent—and half of these caused another fetal death. Furuhashi and colleagues (2002) reported a 22-percent recurrence rate—half recurred at a gestational age 1 to 3 weeks earlier than the first abruption. Looked at a second way, Tikkanen and coworkers (2006) found that of 114 parous women who experienced an abruption, 9 percent had a prior abruption. A third perspective is provided by a population-based study of 767,000 pregnancies completed by Rasmussen and Irgens (2009). They reported a 6.5-fold increased risk for recurrence of a “mild” abruption and 11.5-fold risk for a “severe” abruption. For women who had two severe abruptions, the risk for a third was increased 50-fold.

Management of a pregnancy subsequent to an abruption is difficult because another separation may suddenly occur, even remote from term. In many of these recurrences, fetal well-being is almost always reassuring beforehand. Thus, antepartum fetal testing is usually not predictive (Toivonen, 2002).

Clinical Findings and Diagnosis

Most women with a placental abruption have sudden-onset abdominal pain, vaginal bleeding, and uterine tenderness. In a prospective study, Hurd and colleagues (1983) reported that 78 percent with placental abruption had vaginal bleeding, 66 percent had uterine tenderness or back pain, and 60 percent had a nonreassuring fetal status. Other findings included frequent contractions and persistent hypertonus. In a fifth of these women, preterm labor was diagnosed, and abruption was not suspected until fetal distress or death ensued.

Importantly, the signs and symptoms of placental abruption can vary considerably. In some women, external bleeding can be profuse, yet placental separation may not be so extensive as to compromise the fetus. In others, there may be no external bleeding, but the placenta is sufficiently sheared off that the fetus is dead—a concealed abruption. In one unusual case, a multiparous woman cared for at Parkland Hospital presented with a nosebleed. She had no abdominal or uterine pain, tenderness, or vaginal bleeding. Her fetus was dead, however, and her blood did not clot. The plasma fibrinogen level was 25 mg/dL. Labor was induced, and a total abruption was confirmed at delivery.

Differential Diagnosis. With severe placental abruption, the diagnosis generally is obvious. From the previous discussion, it follows that less severe, more common forms of abruption cannot always be recognized with certainty. Thus, the diagnosis is one of exclusion. Unfortunately, there are no laboratory tests or other diagnostic methods to accurately confirm lesser degrees of placental separation. Sonography has limited use because the placenta and fresh clots may have similar imaging characteristics. In an early study, Sholl (1987) confirmed the clinical diagnosis with sonography in only 25 percent of women. In a later study, Glantz and Purnell (2002) reported only 24-percent sensitivity in 149 consecutive women with a suspected placental abruption. Importantly, negative findings with sonographic examination do not exclude placental abruption. Conversely, magnetic resonance (MR) imaging is highly sensitive for placental abruption, and if knowledge of this would change management, then it should be considered (Masselli, 2011).

With abruption, intravascular coagulation is almost universal. Thus, elevated serum levels of D-dimers may be suggestive, but this has not been adequately tested. Ngai and associates (2012) have provided preliminary data that serum levels of alpha-fetoprotein > 280 μg/L have a positive-predictive value of 97 percent.

Thus, in the woman with vaginal bleeding and a live fetus, it is often necessary to exclude placenta previa and other causes of bleeding by clinical and sonographic evaluation. It has long been taught—perhaps with some justification—that painful uterine bleeding signifies placental abruption, whereas painless uterine bleeding is indicative of placenta previa. The differential diagnosis is usually not this straightforward, and labor accompanying previa may cause pain suggestive of placental abruption. On the other hand, pain from abruption may mimic normal labor, or it may be painless, especially with a posterior placenta. At times, the cause of the vaginal bleeding remains obscure even after delivery.

Hypovolemic Shock. Placental abruption is one of several notable obstetrical entities that may be complicated by massive and sometimes torrential hemorrhage. Hypovolemic shock is caused by maternal blood loss. In an earlier report from Parkland Hospital, Pritchard and Brekken (1967) described 141 women with abruption so severe as to kill the fetus. Blood loss in these women often amounted to at least half of their pregnant blood volume. Importantly, massive blood loss and shock can develop with a concealed abruption. Prompt treatment of hypotension with crystalloid and blood infusion will restore vital signs to normal and reverse oliguria from inadequate renal perfusion. In the past, placental abruption was an all-too-common cause of acute kidney injury requiring dialysis (Chap. 53p. 1063).

Consumptive Coagulopathy. Obstetrical events—mainly placental abruption and amnionic-fluid embolism—led to the initial recognition of defibrination syndrome, which is currently referred to as consumptive coagulopathy or disseminated intravascular coagulation. The major mechanism causing procoagulant consumption is intravascular activation of clotting. Abruption is the most common cause of clinically significant consumptive coagulopathy in obstetrics—and indeed, probably in all of medicine. There are significant amounts of procoagulants in the retroplacental clots, but these cannot account for all missing fibrinogen (Pritchard, 1967). We and others have observed that the levels of fibrin degradation products are higher in serum from peripheral blood compared with that found in serum from blood contained in the uterine cavity (Bonnar, 1969). The reverse would be anticipated in the absence of significant intravascular coagulation.

An important consequence of intravascular coagulation is the activation of plasminogen to plasmin, which lyses fibrin microemboli to maintain microcirculatory patency. With placental abruption severe enough to kill the fetus, there are always pathological levels of fibrinogen–fibrin degradation products and D-dimers in maternal serum.

Most women with placental abruption will have some degree of intravascular coagulation. However, in a third of those with an abruption severe enough to kill the fetus, the plasma fibrinogen level will be < 150 mg/dL. These clinically significant levels may cause troublesome surgical bleeding. Elevated serum levels of fibrinogen-fibrin degradation products, including D-dimers, are also found, but their quantification is not clinically useful. Serum levels of several other coagulation factors are also variably decreased. Thrombocytopenia, sometimes profound, may accompany severe hypofibrinogenemia initially and becomes common after repeated blood transfusions.

Consumptive coagulopathy is more likely with a concealed abruption because intrauterine pressure is higher, thus forcing more thromboplastin into the large veins draining the implantation site. With a partial abruption and a live fetus, severe coagulation defects are seen less commonly. Our experience has been that if serious coagulopathy develops, it is usually evident by the time abruption symptoms appear. Disseminated intravascular coagulation is discussed in more detail on page 808.

Couvelaire Uterus. At the time of cesarean delivery, it is not uncommon to find widespread extravasation of blood into the uterine musculature and beneath the serosa (Fig. 41-18). It is named after Couvelaire, who in the early 1900s termed it uteroplacental apoplexy. Effusions of blood are also seen beneath the tubal serosa, between the leaves of the broad ligaments, in the substance of the ovaries, and free in the peritoneal cavity. These myometrial hemorrhages seldom cause uterine atony, and alone they are not an indication for hysterectomy.


FIGURE 41-18 Couvelaire uterus from total placental abruption after cesarean delivery. Blood markedly infiltrates the myometrium to reach the serosa, especially at the cornua. It gives the myometrium a bluish-purple tone as shown. After the hysterotomy incision was closed, the uterus remained well contracted despite extensive extravasation of blood into the uterine wall. The small serosal leiomyoma seen on the lower anterior uterine surface is an incidental finding. (Courtesy of Dr. Angela Fields Walker).

Acute Kidney Injury. Previously known as acute renal failure, acute kidney injury is a general term describing renal dysfunction from many causes (Chap. 53p. 1063). In obstetrics, it is most commonly seen in cases of severe placental abruption in which treatment of hypovolemia is delayed or incomplete. Even whenabruption is complicated by severe intravascular coagulation, however, prompt and vigorous treatment of hemorrhage with blood and crystalloid solution usually prevents clinically significant renal dysfunction. It is unclear what contributory role abruption occupies in the increasing incidence of obstetric-related acute kidney injury in this country (Bateman, 2010; Kuklina, 2009). Undoubtedly, the risk for renal injury with abruption is magnified when preeclampsia coexists (Drakeley, 2002; Hauth, 1999). Currently, most cases of acute kidney injury are reversible and not so severe as to require dialysis. That said, irreversible acute cortical necrosis encountered in pregnancy is most often associated with abruption. In past years, a third of all patients admitted to renal units for chronic dialysis were women who had suffered an abruption (Grünfeld, 1987; Lindheimer, 2007).

Sheehan Syndrome. Rarely, severe intrapartum or early postpartum hemorrhage is followed by pituitary failure—Sheehan syndrome. The exact pathogenesis is not well understood, especially since endocrine abnormalities are infrequent even in women who suffer catastrophic hemorrhage. Findings include failure of lactation, amenorrhea, breast atrophy, loss of pubic and axillary hair, hypothyroidism, and adrenal cortical insufficiency. In some women, there may be varying degrees of anterior pituitary necrosis and impaired secretion of one or more trophic hormones (Matsuwaki, 2014; Robalo, 2012). The syndrome is discussed further in Chapter 58 (p. 1163).


Treatment of the woman with a placental abruption varies depending primarily on her clinical condition, the gestational age, and the amount of associated hemorrhage. With a living viable-size fetus and with vaginal delivery not imminent, emergency cesarean delivery is chosen by most. In some women, fetal compromise will be evident (Figs. 41-19 and 41-20). When evaluating fetal status, sonographic confirmation of fetal heart activity may be necessary because sometimes an electrode applied directly to a dead fetus will provide misleading information by recording the maternal heart rate. If the fetus has died or if it is not considered mature enough to live outside the uterus, then vaginal delivery is preferable. In either case, prompt and intensive resuscitation with blood plus crystalloid is begun to replace blood lost from retroplacental and external hemorrhage. These measures are lifesaving for the mother and hopefully for her fetus. If the diagnosis of abruption is uncertain and the fetus is alive and without evidence of compromise, then close observation may be warranted provided that immediate intervention is available.


FIGURE 41-19 Placental abruption with fetal compromise. Lower panel: Uterine hypertonus with a baseline pressure of 20 to 25 mm Hg and frequent contractions peaking at approximately 75 mm Hg. Upper panel: The fetal heart rate demonstrates baseline bradycardia with repetitive late decelerations.


FIGURE 41-20 Intrapartum placental abruption with acute onset of fetal compromise prompted emergent cesarean delivery. An infant with 1- and 5-minute Apgar scores of 4 and 7, respectively, was delivered.

A major hazard to cesarean delivery is imposed by clinically significant consumptive coagulopathy. As discussed on page 797, this likelihood is lessened if the fetus is still alive—and thus the abruption “less severe.” Preparations include assessment of coagulability—especially fibrinogen content—and plans for blood and component replacement.

Cesarean Delivery. The compromised fetus is usually best served by cesarean delivery, and the speed of response is an important factor in perinatal outcomes (see Fig. 41-20). Kayani and coworkers (2003) studied this relationship in 33 singleton pregnancies with a clinically overt placental abruption and fetal bradycardia. Of the 22 neurologically intact survivors, 15 were delivered within a 20-minute decision-to-delivery interval. However, eight of 11 infants who died or developed cerebral palsy were delivered with an interval > 20 minutes.

Vaginal Delivery. If the fetus has died, then vaginal delivery is usually preferred. As reviewed on page 780, hemostasis at the placental implantation site depends primarily on myometrial contraction and not blood coagulability. Thus, after vaginal delivery, uterotonic agents and uterine massage are used to stimulate myometrial contractions. Fibers compress placental site vessels and prompt hemostasis even if coagulation is defective.

There are exceptions for which vaginal delivery may not be preferable even if the fetus is dead. For example, in some cases, hemorrhage is so brisk that it cannot be successfully managed even by vigorous blood replacement. Obstetrical complications that prohibit vaginal delivery such as a term fetus with a transverse lie are another example. Women with a prior high-risk hysterotomy incision, that is, a prior vertical or classical cesarean delivery, pose a complex situation.

Labor with extensive placental abruption tends to be rapid because the uterus is usually persistently hypertonic. This can magnify fetal compromise (see Fig. 41-19). In some cases, baseline intraamnionic pressures reach 50 mm Hg or higher, and rhythmic increases reach more than 100 mm Hg with contractions.

Early amniotomy has long been championed in the management of placental abruption. This ostensibly achieves better spiral artery compression that might decrease implantation site bleeding and reduce thromboplastin infusion into the maternal vascular system. Although evidence supporting this theory is lacking, membrane rupture may hasten delivery. However, if the fetus is small, the intact sac may be more efficient in promoting cervical dilatation. If rhythmic uterine contractions are not superimposed on baseline hypertonus, then oxytocin is given in standard doses. There are no data indicating that oxytocin enhances thromboplastin escape into the maternal circulation to worsen coagulopathy (Clark, 1995; Pritchard, 1967).

In the past, some had set arbitrary time limits to permit vaginal delivery. Instead, experiences indicate that maternal outcome depends on the diligence with which adequate fluid and blood replacement therapy are pursued rather than on the interval to delivery. Observations from Parkland Hospital described by Pritchard and Brekken (1967) are similar to those from the University of Virginia reported by Brame and associates (1968). Specifically, women with severe abruption who were transfused during 18 hours or more before delivery had similar outcomes to those in whom delivery was accomplished sooner.

Expectant Management with Preterm Fetus. Delaying delivery may prove beneficial when the fetus is immature. Bond and colleagues (1989) expectantly managed 43 women with placental abruption before 35 weeks’ gestation, and 31 of them were given tocolytic therapy. The mean interval-to-delivery for all 43 was approximately 12 days. Cesarean delivery was performed in 75 percent, and there were no stillbirths. As discussed on page 794, women with a very early abruption frequently develop chronic abruption-oligohydramnios sequence—CAOS. In one report, Elliott and coworkers (1998) described four women with an abruption at a mean gestation of 20 weeks who developed oligohydramnios and delivered at an average gestational age of 28 weeks. In a description of 256 women with an abruption ≤ 28 weeks, Sabourin and colleagues (2012) reported that a mean of 1.6 weeks was gained. Of the group, 65 percent were delivered < 29 weeks, and half of all women underwent emergent cesarean delivery.

Unfortunately, even continuous fetal heart rate monitoring does not guarantee universally good outcomes. For example, a normal tracing may precede sudden further separation with instant fetal compromise as shown in Figure 41-20. In some of these, if the separation is sufficient, the fetus will die before it can be delivered. Tocolysis is advocated by some for suspected abruption if the fetus does not display compromise. One drawback reported in the early study by Hurd (1983) was that abruption went unrecognized for dangerously long periods if tocolysis was initiated. Subsequent studies were more optimistic and observed that tocolysis improved outcomes in a highly selected cohort of women with preterm pregnancies (Bond, 1989; Combs, 1992; Sholl, 1987). In another study, Towers and coworkers (1999) administered magnesium sulfate, terbutaline, or both to 95 of 131 women with abruption diagnosed before 36 weeks. The perinatal mortality rate was 5 percent in both groups with or without tocolysis. We are of the view that until a randomized trial is done, a clinically evident abruption contraindicates tocolytic therapy. This does not preclude magnesium sulfate given for severe gestational hypertension.

image Placenta Previa

The Latin previa means going before—and in this sense, the placenta goes before the fetus into the birth canal. In obstetrics, placenta previa describes a placenta that is implanted somewhere in the lower uterine segment, either over or very near the internal cervical os. Because these anatomical relationships cannot always be precisely defined, and because they frequently change across pregnancy, terminology can sometimes be confusing.

Placental Migration

With the frequent use of sonography in obstetrics, the term placental migration was used to describe the apparent movement of the placenta away from the internal os (King, 1973). Obviously, the placenta does not move per se, and the mechanism of apparent movement is not completely understood. To begin with, migration is clearly a misnomer, because decidual invasion by chorionic villi on either side of the cervical os persists. Several explanations are likely additive. First, apparent movement of the low-lying placenta relative to the internal os is related to the imprecision of two-dimensional sonography in defining this relationship. Second, there is differential growth of the lower and upper uterine segments as pregnancy progresses. With greater upper uterine blood flow, placental growth more likely will be toward the fundus—trophotropism. Many of those placentas that “migrate” most likely never were circumferentially implanted with true villous invasion that reached the internal cervical os. Finally, a low-lying placenta is less likely to “migrate” within a uterus with a prior cesarean hysterotomy scar. Of interest, at the time of delivery there are an equal number of anterior and posterior placentas (Young, 2013).

Placental migration has been quantified in several studies. Sanderson and Milton (1991) studied 4300 women at midpregnancy and found that 12 percent had a low-lying placenta. Of those not covering the internal os, previa did not persist, and none subsequently had placental hemorrhage. Conversely, approximately 40 percent of placentas that covered the os at midpregnancy continued to do so until delivery. Thus, placentas that lie close to but not over the internal os up to the early third trimester are unlikely to persist as a previa by term (Dashe, 2002; Laughon, 2005; Robinson, 2012). Still, Bohrer and associates (2012) reported that a second-trimester low-lying placenta was associated with antepartum admission for hemorrhage and increased blood loss at delivery.

The likelihood that placenta previa persists after being identified sonographically at given epochs before 28 weeks’ gestation is shown in Figure 41-21. Similar findings for twin pregnancies are reported until 23 weeks, after which the previa persistence rate is much higher (Kohari, 2012). A prior uterine incision also has an obvious effect. Stafford and coworkers (2010), but not Trudell and colleagues (2013), found that a previa and a third-trimester cervical length < 30 mm increased the risk for hemorrhage, uterine activity, and preterm birth. Friszer and associates (2013) showed that women admitted for bleeding had a greater chance of delivery by 7 days with the cervix < 25 mm, although Trudell and colleagues (2013) did not confirm this.


FIGURE 41-21 Likelihood of persistence of placenta previa or low-lying placenta at delivery. These are shown as a function of sonographic diagnosis at three pregnancy epochs of a previa or placental edges 1 to 5 mm from the cervical internal os. CD = cesarean delivery. (Data from Oyelese, 2006.)

As indicated and discussed subsequently, persistent previa is more common in women who have had a prior cesarean delivery. In the absence of any other indication, sonography need not be frequently repeated simply to document placental position. Moreover, restriction of activity is not necessary unless a previa persists beyond 28 weeks or if clinical findings such as bleeding or contractions develop before this time.


Terminology for placenta previa has been confusing. In a recent Fetal Imaging Workshop sponsored by the National Institutes of Health (Dashe, 2013), the following classification was recommended:

• Placenta previa—the internal os is covered partially or completely by placenta. In the past, these were further classified as either total or partial previa (Figs. 41-22 and 41-23).

• Low-lying placenta—implantation in the lower uterine segment is such that the placental edge does not reach the internal os and remains outside a 2-cm wide perimeter around the os. A previously used term, marginal previa, described a placenta that was at the edge of the internal os but did not overlie it.


FIGURE 41-22 Total placenta previa showing that copious hemorrhage could be anticipated with any cervical dilatation.


FIGURE 41-23 Second-trimester partial placenta previa. On speculum examination, the cervix is 3- to 4-cm dilated. The arrow points to mucus dripping from the cervix. (Photograph contributed by Dr. Rigoberto Santos.)

Clearly, the classification of some cases of previa will depend on cervical dilatation at the time of assessment (Dashe, 2013). For example, a low-lying placenta previa at 2-cm dilatation may become a partial placenta previa at 4-cm dilatation because the cervix has dilated to expose the placental edge (see Fig. 41-23). Conversely, a placenta previa that appears to be total before cervical dilatation may become partial at 4-cm dilatation because the cervical opening now extends beyond the edge of the placenta. Digital palpation in an attempt to ascertain these changing relations between the placental edge and internal os as the cervix dilates usually causes severe hemorrhage!

With both total and partial placenta previa, a certain degree of spontaneous placental separation is an inevitable consequence of lower uterine segment remodeling and cervical dilatation. Although this frequently causes bleeding, and thus technically constitutes a placental abruption, this term is usually not applied in these instances.

Somewhat but not always related is vasa previa, in which fetal vessels course through membranes and present at the cervical os (Bronsteen, 2013). This is discussed in Chapter 6 (p. 123).

Incidence and Associated Factors

Reported incidences for placenta previa average 0.3 percent or 1 case per 300 to 400 deliveries. It was reported to be almost 1 in 300 deliveries in the United States in 2003 (Martin, 2005). The frequency at Parkland Hospital from 1988 through 2012 was approximately 1 in 360 for nearly 366,000 births. Similar frequencies have been reported from Canada, England, and Israel, but it was only 1 in 700 deliveries from a Japanese study (Crane, 1999; Gurol-Urganci, 2011; Matsuda, 2011; Rosenberg, 2011). Except for the last study, these reported frequencies are remarkably similar considering the lack of precision in definition and classification discussed above.

Several factors increase the risk for placenta previa. One of these—multifetal gestation—seems intuitive because of the larger placental area. And indeed, the incidence of associated previa with twin pregnancy is increased by 30 to 40 percent compared with that of singletons (Ananth, 2003a; Weis, 2012). Many of the other associated factors are less intuitive.

Maternal Age. The frequency of placenta previa increases with maternal age (Biro, 2012). At Parkland Hospital, this incidence increased from a low rate of approximately 1 in 1660 for women 19 years or younger to almost 1 in 100 for women older than 35 (see Fig. 41-16). Coincidental with increasing maternal age in the United States and Australia, the overall incidence of previa has increased substantively (Frederiksen, 1999; Roberts, 2012). The FASTER Trial, which included more than 36,000 women, cited the frequency of previa to be 0.5 percent for women younger than 35 years compared with 1.1 percent in those older than 35 years (Cleary-Goldman, 2005).

Multiparity. The risk for previa increases with parity. The obvious effects of advancing maternal age and parity are confounding. Still, Babinszki and colleagues (1999) reported that the 2.2-percent incidence in women with parity of 5 or greater was increased significantly compared with that of women with lower parity.

Prior Cesarean Delivery. The cumulative risks for placenta previa that accrue with the increasing number of cesarean deliveries are extraordinary. In a Network study of 30,132 women undergoing cesarean delivery, Silver and associates (2006) reported an incidence of 1.3 percent for those with only one prior cesarean delivery, but it was 3.4 percent if there were six or more prior cesarean deliveries. In a retrospective cohort of nearly 400,000 women who were delivered of two consecutive singletons, those with a cesarean delivery for the first pregnancy had a significant 1.6-fold increased risk for previa in the second pregnancy (Gurol-Urganci, 2011). These same investigators reported a 1.5-fold increased risk from six similar population-based cohort studies. Gesteland (2004) and Gilliam (2002) and their coworkers calculated that the likelihood of previa was increased more than eightfold in women with parity greater than 4 and who had more than four prior cesarean deliveries.

Importantly, women with a prior uterine incision and placenta previa have an increased likelihood that cesarean hysterectomy will be necessary for hemostasis because of an associated accrete syndrome (p. 804). In the study by Frederiksen and colleagues (1999), 6 percent of women who had a primary cesarean delivery for previa required a hysterectomy. This rate was 25 percent for women with a previa undergoing repeat cesarean delivery.

Cigarette Smoking. The relative risk of placenta previa is increased at least twofold in women who smoke (Ananth, 2003a; Usta, 2005). It has been postulated that carbon monoxide hypoxemia causes compensatory placental hypertrophy and more surface area. Smoking may also be related to decidual vasculopathy that has been implicated in the genesis of previa.

Elevated Prenatal Screening MSAFP Levels. Women who have otherwise unexplained abnormally elevated prenatal screening levels of maternal serum alpha-fetoprotein (MSAFP) are at increased risk for previa and a host of other abnormalities as discussed on page 806. Moreover, women with a previa who also had a MSAFP level ≥ 2.0 MoM at 16 weeks’ gestation were at increased risk for late-pregnancy bleeding and preterm birth. Screening with MSAFP is considered in detail in Chapter 14 (p. 284).

Clinical Features

Painless bleeding is the most characteristic event with placenta previa. Bleeding usually does not appear until near the end of the second trimester or later, but it can begin even before midpregnancy. And undoubtedly, some late abortions are caused by an abnormally located placenta. Bleeding from a previa usually begins without warning and without pain or contractions in a woman who has had an uneventful prenatal course. This so-called sentinel bleed is rarely so profuse as to prove fatal. Usually it ceases, only to recur. In perhaps 10 percent of women, particularly those with a placenta implanted near but not over the cervical os, there is no bleeding until labor onset. Bleeding at this time varies from slight to profuse, and it may clinically mimic placental abruption.

A specific sequence of events leads to bleeding in cases in which the placenta is located over the internal os. First, the uterine body remodels to form the lower uterine segment. With this, the internal os dilates, and some of the implanted placenta inevitably separates. Bleeding that ensues is augmented by the inherent inability of myometrial fibers in the lower uterine segment to contract and thereby constrict avulsed vessels. Similarly, bleeding from the lower segment implantation site also frequently continues after placental delivery. Last, there may be lacerations in the friable cervix and lower segment. This may be especially problematic following manual removal of a somewhat adhered placenta.

Abnormally Implanted Placenta. A frequent and serious complication associated with placenta previa arises from its abnormally firm placental attachment. This is anticipated because of poorly developed decidua that lines the lower uterine segment. Biswas and coworkers (1999) performed placental bed biopsies in 50 women with a previa and in 50 control women. Trophoblastic giant-cell infiltration of spiral arterioles—rather than endovascular trophoblast—was found in half of previa specimens. However, only 20 percent from normally implanted placentas had these changes.

Placenta accrete syndromes arise from abnormal placental implantation and adherence and are classified according to the depth of placental ingrowth into the uterine wall. These include placenta accreta, increta, and percreta (p. 804). In a study of 514 cases of previa reported by Frederiksen and associates (1999), abnormal placental attachment was identified in 7 percent. As discussed above, previa overlying a prior cesarean incision conveys a particularly high risk for accreta.

Coagulation Defects. Placenta previa is rarely complicated by coagulopathy even when there is extensive implantation site separation (Wing, 1996b). Placental thromboplastin, which incites the intravascular coagulation seen with placental abruption, is presumed to readily escape through the cervical canal rather than be forced into the maternal circulation. The paucity of large myometrial veins in this area may also be protective.


Whenever there is uterine bleeding after midpregnancy, placenta previa or abruption should always be considered. In the Canadian Perinatal Network study discussed on page 783, placenta previa accounted for 21 percent of women admitted from 22 to 28 weeks’ gestation with vaginal bleeding (Sabourin, 2012). Previa should not be excluded until sonographic evaluation has clearly proved its absence. Diagnosis by clinical examination is done using the double set-up technique because it requires that a finger be passed through the cervix and the placenta palpated. A digital examination should not be performed unless delivery is planned. A cervical digital examination is done with the woman in an operating room and with preparations for immediate cesarean delivery. Even the gentlest examination can cause torrential hemorrhage. Fortunately, double set-up examination is rarely necessary because placental location can almost always be ascertained sonographically.

Sonographic Placental Localization. Quick and accurate localization can be accomplished using standard sonographic techniques (Dashe, 2013). In many cases, transabdominal sonography is confirmatory, as shown in Figure 41-24A, and an average accuracy of 96 percent has been reported (Laing, 1996). Imprecise results may be caused by bladder distention, so doubtful cases should be confirmed after bladder emptying. Moreover, sometimes a large fundal placenta is not appreciated to extend down to the internal cervical os. Transvaginal sonography is safe, and the results are superior as shown in Figures 41-24Band 41-25. In a comparative study by Farine and associates (1988), the internal os was visualized in all cases using transvaginal sonography but was seen in only 70 percent using transabdominal sonography. Transperineal sonography is also accurate to localize placenta previa (Hertzberg, 1992). In a study by Rani and colleagues (2007), placenta previa was correctly identified in 69 of 70 women and was confirmed at delivery. They reported the positive-predictive value to be 98 percent, whereas the negative-predictive value was 100 percent.


FIGURE 41-24 Total placenta previa. A. Transabdominal sonogram shows placenta (white arrowheads) covering the cervix (black arrows). B. Transvaginal sonogram shows placenta (arrows), lying between the cervix and fetal head.


FIGURE 41-25 Transvaginal sonogram of an anterior placenta previa at 36 weeks’ gestation. The placental margin (red arrow) extends downward toward the cervix. The internal os (yellow arrow) and cervical canal (short white arrows) are marked to show their relationship to the leading edge of the placenta.

Magnetic Resonance Imaging. Although several investigators have reported excellent results using MR imaging to visualize placental abnormalities, it is unlikely that this technique will replace sonography for routine evaluation anytime soon. That said, MR imaging has proved useful for evaluation of placenta accreta (p. 807).

Management of Placenta Previa

Women with a previa are managed depending on their individual clinical circumstances. The three factors that usually are considered include fetal age and thus maturity; labor; and bleeding and its severity.

If the fetus is preterm and there is no persistent active bleeding, management favors close observation in an obstetrical unit. Data are sparse regarding tocolytic administration for uterine contractions. Although good randomized trials are lacking, Bose and colleagues (2011) recommend that if tocolytics are given, they be limited to 48 hours of administration. We categorically recommend against their use in this setting. After bleeding has ceased for about 2 days and the fetus is judged to be healthy, the woman can usually be discharged home. Importantly, the woman and her family must fully appreciate the possibility of recurrent bleeding and be prepared for immediate transport back to the hospital. In other cases, prolonged hospitalization may be ideal.

In properly selected patients, there appear to be no benefits to inpatient compared with outpatient management (Mouer, 1994; Neilson, 2003). In a randomized study by Wing and colleagues (1996a), no differences in maternal or fetal morbidity were noted with either management method. This trial of inpatient versus home management included 53 women who had a bleeding previa at 24 to 36 weeks’ gestation. Of these 53 women, 60 percent had recurrent bleeding. Also, of all 53 women, half eventually required expeditious cesarean delivery. Home management is more economical. In one study, hospital stay length and costs for mother-infant care were reduced by half with outpatient management (Drost, 1994).

For women who are near term and who are not bleeding, plans are made for scheduled cesarean delivery. Timing is important to maximize fetal growth but to minimize the possibility of antepartum hemorrhage. A National Institutes of Health workshop concluded that women with a previa are best served by elective delivery at 36 to 37 completed weeks (Spong, 2011). With suspected placenta accrete syndromes, delivery was recommended at 34 to 35 completed weeks. At Parkland Hospital, we prefer to wait until 37 to 38 weeks before delivery (p. 807).


Practically all women with placenta previa undergo cesarean delivery. Many surgeons recommend a vertical skin incision. Cesarean delivery is emergently performed in more than half because of hemorrhage, for which about a fourth require blood transfusion (Boyle, 2009; Sabourin, 2012). Although a low transverse hysterotomy is usually possible, this may cause fetal bleeding if there is an anterior placenta and the placenta is cut through. In such cases, fetal delivery should be expeditious. Thus, a vertical uterine incision may be preferable in some instances. That said, even when the incision extends through the placenta, maternal or fetal outcomes are rarely compromised.

Following placental removal, there may be uncontrollable hemorrhage because of poorly contracted smooth muscle of the lower uterine segment. When hemostasis at the placental implantation site cannot be obtained by pressure, the implantation site can be oversewn with 0-chromic sutures. Cho and associates (1991) described interrupted 0-chromic sutures at 1-cm intervals to form a circle around the bleeding portion of the lower segment to control hemorrhage in all eight women in whom it was employed. Huissoud and coworkers (2012) also described use of circular sutures. Kayem (2011) and Penotti (2012) and their colleagues reported that only 2 of 33 women with a previa and no accreta who had anterior-posterior uterine compression sutures required hysterectomy. Kumru and associates (2013) reported success with the Bakri balloon in 22 of 25 cases. Diemert and coworkers (2012) described good results with combined use of a Bakri balloon and compression sutures. Albayrak and colleagues (2011) described Foley balloon tamponade. Druzin (1989) proposed tightly packing the lower uterine segment with gauze, and the pack was removed transvaginally 12 hours later. Law and coworkers (2010) reported successful use of hemostatic gel. Other methods include bilateral uterine or internal iliac artery ligation as described on page 819. Finally, pelvic artery embolization as described on page 820 has also gained acceptance.

If these more conservative methods fail and bleeding is brisk, then hysterectomy is necessary. Placenta previa—especially with abnormally adhered placental variations—currently is the most frequent indication for peripartum hysterectomy at Parkland Hospital and from other reports (Wong, 2011). It is not possible to accurately estimate the impact on hysterectomy from previa alone without considering the associated accrete syndromes. Again, for women whose placenta previa is implanted anteriorly at the site of a prior uterine incision, there is an increased likelihood of associated placenta accrete syndrome and need for hysterectomy. In a study of 318 peripartum hysterectomies from in the United Kingdom, 40 percent were done for abnormally implanted placentation (Knight, 2007). At Parkland Hospital, 44 percent of cesarean hysterectomies were done for bleeding placenta previa or placenta accrete syndrome. In an Australian study of emergency peripartum hysterectomy, 19 percent were done for placenta previa, and another 55 percent for a morbidly adhered placenta (Awan, 2011). The technique for peripartum hysterectomy is described in Chapter 30 (p. 599).

Maternal and Perinatal Outcomes

A marked reduction in maternal mortality rates from placenta previa was achieved during the last half of the 20th century. Still, as shown in Figure 41-2, placenta previa and coexistent accrete syndromes both contribute substantively to maternal morbidity and mortality. In one review, there was a threefold increased maternal mortality ratio of 30 per 100,000 for women with previa (Oyelese, 2006). In another report of 4693 maternal deaths in the United States, placenta previa and accrete syndromes accounted for 17 percent of deaths from hemorrhage (Berg, 2010).

The report from the Consortium on Safe Labor emphasizes the ongoing perinatal morbidity with placenta previa (Lai, 2012). Preterm delivery continues to be a major cause of perinatal death (NØrgaard, 2012). For the United States in 1997, Salihu and associates (2003) reported a threefold increased neonatal mortality rate with placenta previa that was caused primarily from preterm delivery. Ananth and colleagues (2003b) reported a comparably increased risk of neonatal death even for fetuses delivered at term. This is at least partially related to fetal anomalies, which are increased two- to threefold in pregnancies with placenta previa (Crane, 1999).

The association of fetal-growth restriction with placenta previa is likely minimal after controlling for gestational age (Crane, 1999). In a population-based cohort of more than 500,000 singleton births, Ananth and associates (2001a) found that most low-birthweight infants associated with placenta previa resulted from preterm birth. Harper and coworkers (2010) reported similar findings from a cohort of nearly 58,000 women who underwent routine second-trimester sonographic evaluation at their institution.

image Placenta Accrete Syndromes

These syndromes describe the abnormally implanted, invasive, or adhered placenta. Derivation of accrete comes from the Latin ac- + crescere—to grow from adhesion or coalescence, to adhere, or to become attached to (Benirschke, 2012). Accrete syndromes thus include any placental implantation with abnormally firm adherence to myometrium because of partial or total absence of the decidua basalis and imperfect development of the fibrinoid or Nitabuch layer. If the decidual spongy layer is lacking either partially or totally, then the physiological line of cleavage is absent, and some or all cotyledons are densely anchored. The surface area of the implantation site involved and the depth of trophoblastic tissue ingrowth are variable between women, but all affected placentas can potentially cause significant hemorrhage.

Accrete syndromes have evolved into one of the most serious problems in obstetrics. As subsequently discussed, the likelihood of placenta accrete syndrome is closely linked to prior uterine surgery. Thus, related to the increasing and current all-time high rate of cesarean delivery in the United States, the frequency of placenta accrete syndromes has reached seemingly epidemic proportions. And, at least until recently, there seems to be no consensus for management (Wright, 2013). To better codify some of the serious consequences associated with accrete syndromes, the American College of Obstetricians and Gynecologists (2012b) and the Society for Maternal-Fetal Medicine (2010) have taken the lead to address management problems. Accrete syndromes have also been the subject of recent reviews (Rao, 2012; Wortman, 2013a).


Microscopically, placental villi are anchored to muscle fibers rather than to decidual cells. Decidual deficiency then prevents normal placental separation after delivery. Intuitive thinking and now substantiated data suggest that accrete syndromes are not solely caused by an anatomical layer deficiency (Tantbirojn, 2008). Evidence indicates that the cytotrophoblasts may control decidual invasion through factors such as angiogenesis and growth expression (Cohen, 2010; Duzyj, 2013; Wehrum, 2011). Indeed, accrete syndrome tissue specimens have shown evidence for “hyperinvasiveness” compared with otherwise uncomplicated previa specimens (Pri-Paz, 2012). The distribution of large vessels is different than that seen with nonaccrete placentas (Chantraine, 2012). As described by Benirschke and colleagues (2012), there is an antecedent “constitutional endometrial defect” in most cases. The increased risk conveyed by previous uterine trauma—for example, cesarean delivery—may be partially explained by an increased vulnerability of the decidua to trophoblast invasion following incision into the decidua (Garmi, 2012).


Variants of placenta accrete syndrome are classified by the depth of trophoblastic growth (Fig. 41-26). Placenta accreta indicates that villi are attached to the myometrium. With placenta increta, villi actually invade the myometrium, and placenta percreta defines villi that penetrate through the myometrium and to or through the serosa. In clinical practice, these three variants are encountered in an approximate ratio of 80:15:5, respectively (Wong, 2008). In all three varieties, abnormal adherence may involve all lobules—total placenta accreta (Fig. 41-27). If all or part of a single lobule is abnormally attached, it is described as a focal placenta accreta. Histological diagnosis cannot be made from the placenta alone, and the uterus or curettings with myometrium are necessary for histopathological confirmation (Benirschke, 2012).


FIGURE 41-26 Placenta accrete syndromes. A. Placenta accreta. B. Placenta increta. C. Placenta percreta.


FIGURE 41-27 Photographs of accrete syndrome hysterectomy specimens. A. Cesarean hysterectomy specimen containing a total placenta previa with percreta involving the lower uterine segment and cervical canal. Black arrows show the invading line of the placenta through the myometrium. (Photograph courtesy of Dr. Thomas R. Dowd). B. Hysterectomy specimen containing a partial placenta previa with placenta percreta that invaded the lateral fundal region to cause hemoperitoneum.

Incidence and Associated Conditions

The increased frequency of accrete syndromes during the past 50 years stems from the liberalized use of cesarean delivery. In 1924, Polak and Phelan presented their data from Long Island College Hospital, which had one case of placenta accreta complicating 6000 deliveries. In a 1951 review, a maternal mortality rate of up to 65 percent was cited (McKeogh, 1951). In 1971, in the 14th edition of Williams Obstetrics, Hellman and Pritchard described placenta accreta as the subject of case reports. In a review several years later, Breen and coworkers (1977) cited a reported average incidence of 1 in 7000 deliveries.

Since these reports, however, the incidence of accrete syndromes has increased remarkably, in direct relationship to the increasing cesarean delivery rate (Chap. 31p. 618). The incidence of placenta accrete syndrome was cited as 1 in 2500 in the 1980s, and currently, the American College of Obstetricians and Gynecologists (2012b) cites it to be as high as 1 in 533 deliveries. Because of this increasing frequency, accrete syndromes are now one of the most serious problems in obstetrics. In addition to their significant contribution to maternal morbidity and mortality, accrete syndromes are a leading cause of intractable postpartum hemorrhage and emergency peripartum hysterectomy (Awan, 2011; Eller, 2011; Rossi, 2010). Their contribution as a cause of maternal deaths from hemorrhage is shown in Figure 41-2In their review of nearly 10,000 pregnancy-related maternal deaths in the United States, Berg and associates (2010) reported that 8 percent of deaths due to hemorrhage were caused by accrete syndromes.

Risk Factors

These are similar in many aspects to those for placenta previa (p. 801). That said, the two most important risk factors are an associated previa, a prior cesarean delivery, and more likely a combination of the two. In one study, an accrete placenta more likely followed emergency compared with elective cesarean delivery (Kamara, 2013). A classical hysterotomy incision has a higher risk for a subsequent accrete placenta (Gyamfi-Bannerman, 2012). Decidual formation may be defective over a previous hysterotomy scar, and it also may follow any type of myometrial trauma such as curettage (Benirschke, 2012). Myomectomy apparently confers a low risk (Gyamfi-Bannerman, 2012). In one study, 10 percent of women with a previa had an associated accrete placenta. In another study, almost half of women with a prior cesarean delivery had myometrial fibers seen microscopically adhered to the placenta (Hardardottir, 1996; Zaki, 1998). Findings from a Maternal-Fetal Medicine Units Network study by Silver and colleagues (2006) of women with one or more prior cesarean deliveries who also had a placenta previa are shown in Figure 41-28. The astonishing increase in frequency of associated accrete syndromes is apparent.


FIGURE 41-28 Frequency of accreta syndromes in women with 1 to 5 prior cesarean deliveries (CDs) now with a previa. (Data from Silver, 2006.)

Another risk factor became apparent with widespread use of MSAFP and human chorionic gonadotropin (hCG) screening for neural-tube defects and aneuploidies (Chap. 14p. 285). In a study reported by Hung (1999) of more than 9300 women screened at 14 to 22 weeks, the risk for accrete syndromes was increased eightfold with MSAFP levels > 2.5 MoM, and it was increased fourfold when maternal free β-hCG levels were > 2.5 MoM.

Cesarean-Scar Pregnancy. In some women with an accrete placenta, there may be adverse outcomes before fetal viability. One presentation generally referred to as a cesarean scar pregnancy clinically is similar to that of an ectopic pregnancy. Its frequency has been reported to be approximately 1 in 2000 pregnancies (Ash, 2007; Rotas, 2006). Timor-Tritsch (2012) provided a scholarly review of 751 such cases, and the subject is discussed in detail in Chapter 19 (p. 391).

Clinical Presentation and Diagnosis

In cases of first- and second-trimester accrete syndromes, there is usually hemorrhage that is the consequence of coexisting placenta previa. Such bleeding will usually prompt evaluation and management. In some women who do not have an associated previa, accreta may not be identified until third-stage labor when an adhered placenta is encountered.

Ideally, abnormal placental ingrowth is identified antepartum, usually by sonography (Chantraine, 2013; Tam Tam, 2012). For gray-scale transvaginal sonography, the American College of Obstetricians and Gynecologists (2012b) cites a sensitivity of 77 to 87 percent, specificity of 96 to 98 percent, and a positive- and negative-predictive value of 65 to 93 and 98 percent, respectively. Individual studies have reported similar findings (Chalubinski, 2013; Elhawary, 2013; Maher, 2013). Although controversial, at Parkland Hospital, we have found that the addition of Doppler color flow mapping is highly predictive of myometrial invasion (Fig. 41-29). This is suspected if the distance between the uterine serosa-bladder wall interface and the retroplacental vessels is < 1 mm and if there are large intraplacental lacunae (Twickler, 2000). Similarly, Cali and associates (2013) reported that hypervascularity of the uterine serosa-bladder wall interface had the highest positive- and negative-predictive values for placenta percreta.


FIGURE 41-29 Transvaginal sonogram of placental invasion with accrete syndrome. Retroplacental vessels (white arrows) invade the myometrium and obscure the bladder-serosal interface. Abnormal intraplacental venous lakes (black arrowheads) are commonly seen in this setting.

MR imaging can be used as an adjunct to sonography to define anatomy, degree of invasion, and possible ureteral or bladder involvement (Chalubinski, 2013; Palacios Jaraquemada, 2005). Lax and coworkers (2007) identified three MR imaging findings that suggested accreta. These include uterine bulging, heterogeneous signal intensity within the placenta, and dark intraplacental bands on T2-weighted imaging. Some suggest MR imaging when sonography results are inconclusive or there is a posterior previa (American College of Obstetricians and Gynecologists, 2012b; Elhawary, 2013).


Preoperative assessment should begin at the time of recognition during prenatal care (Fitzpatrick, 2014; Sentilhes, 2013). A major decision concerns the ideal institution for delivery. Exigencies to be considered are appropriate surgical, anesthesia, and blood banking capabilities. An obstetrical surgeon or gynecological oncologist as well as surgical, urological, and interventional radiological consultants should all be available (Eller, 2011; Stafford, 2008). The American College of Obstetricians and Gynecologists (2012b) and the Society for Maternal-Fetal Medicine (2010) recommend planned delivery in a tertiary-care facility. In some of these, especially designed teams have been assembled and are on call (Walker, 2013). Women who refuse blood or its derivatives pose especially difficult management decisions (Barth, 2011). If possible, delivery is best scheduled for peak availability of all resources and team members. However, emergency contingent plans should also be in place.

Timing of Delivery. To accomplish scheduled surgical intervention, preterm delivery is necessary and justified given the serious adverse maternal consequences of emergency cesarean delivery. The American College of Obstetricians and Gynecologists (2012b) recommends individualization of delivery timing. It cites a decision-analysis study that justifies elective delivery without fetal lung maturity testing after 34 completed weeks (Robinson, 2010). The results of two recent surveys indicate that most practitioners do not deliver these women until 36 weeks or later (Esakoff, 2012; Wright, 2013). At Parkland Hospital, we generally schedule these procedures after 36 completed weeks but are prepared also to manage them in nonelective situations.

Preoperative Arterial Catheterization. There has been enthusiasm for placement of intraarterial catheters to mitigate blood loss and to enhance surgical visibility. Balloon-tipped catheters advanced into the internal iliac arteries are inflated after delivery to occlude pelvic blood flow to aid placental removal and hysterectomy (Ballas, 2012; Desai, 2012). Alternatively, the catheters can be used to embolize bleeding arterial sites. Others have concluded that these procedures offer borderline efficacy and have serious risks (Sentilhes, 2009; Yu, 2009). Complications have included thromboses of the common and left iliac arteries (Bishop, 2011; Greenberg, 2007). At this time, we agree with the American College of Obstetricians and Gynecologists (2012b) that a firm recommendation cannot be made for or against their use.

Cesarean Delivery and Hysterectomy. Before commencing with delivery, the risk of hysterectomy to prevent exsanguination should be estimated. Confirmation of a percreta or increta almost always mandates hysterectomy. However, some of these abnormal placentations, especially if partial, may be amenable to placental delivery with hemostatic suture placement. Because the scope of invasion may not be apparent before delivery of the fetus, we usually attempt to create a wide bladder flap before making the hysterotomy incision. The round ligaments are divided, and the lateral edges of the peritoneal reflection are dissected downward. If possible, these incisions are extended to encircle the entire placental implantation site that visibly occupies the prevesical space and posterior bladder wall. Following this, a classical hysterotomy incision is made to avoid the placenta and profuse hemorrhage before fetal delivery. Some advocate a transverse fundal incision if the placenta occupies the entire anterior wall (Kotsuji, 2013).

After fetal delivery, the extent of placental invasion is assessed without attempts at manual placental removal. In a report from the United Kingdom, attempts for partial or total placental removal prior to hysterectomy were associated with twice as much blood loss (Fitzpatrick, 2014). Generally speaking, with obvious percreta or increta, hysterectomy is usually the best course, and the placenta is left in situ. As discussed in Chapter 36 (p. 670), a focal partial accreta may avulse easily and later emerge as a placental polyp (Benirschke, 2012). With more extensive placental ingrowth—even with total accreta—there may be little or no bleeding until manual placental removal is attempted. Unless there is spontaneous separation with bleeding that mandates emergency hysterectomy, the operation begins after full assessment is made. With bleeding, successful treatment depends on immediate blood replacement therapy and other measures that include uterine or internal iliac artery ligation, balloon occlusion, or embolization. Various case reports have described argon beam coagulation and hemostatic combat gauze (Karam, 2003; Schmid, 2012).

Leaving the Placenta in Situ. In a few cases, after the fetus has been delivered, it may be possible to trim the umbilical cord and repair the hysterotomy incision but leave the placenta in situ. This may be wise for women in whom abnormal placentation was not suspected before cesarean delivery and in whom uterine closure stops bleeding. After this, she can be transferred to a higher-level facility for definitive management. Another consideration is the woman with a strong desire for fertility and who has received extensive counseling. In some cases, the placenta spontaneously resorbs. In others, a subsequent hysterectomy—either planned or prompted by bleeding or infection—is performed weeks postpartum when blood loss might be lessened (Hays, 2008; Kayem, 2002; Lee, 2008; Timmermans, 2007). Of 26 women treated this way, 21 percent ultimately required hysterectomy. Of the remainder, most required additional medical and surgical interventions for bleeding and infection (Bretelle, 2007). Evidence that treatment with methotrexate aids resorption is lacking. We agree with the American College of Obstetricians and Gynecologists (2012b) that this method of management is seldom indicated. For women in whom the placenta is left in situ, serial serum β-hCG measurements are not informative, and serial sonographic or MR imaging is recommended (Timmermans, 2007; Worley, 2008).

Pregnancy Outcomes

Reports describing outcomes with accrete syndromes have limited numbers of patients. That said, two large series provide data from which some basic observations can be made. First, these syndromes can have disastrous outcomes for both mother and fetus. Although the depth of placental invasion does not correspond with perinatal outcome, it is of paramount maternal significance (Seet, 2012). Shown in Table 41-5 are outcomes from three reports of women from tertiary-care hospitals and in whom the diagnosis of accrete placenta was made preoperatively. Despite these advantages, a litany of complications included hemorrhage, urinary tract injury, ICU admission, and secondary surgical procedures. These reports chronicled outcomes in a second cohort of women in whom care was not given at a tertiary-care facility or in whom the diagnosis of accrete placenta was not made until delivery, or both. In these cohorts, morbidity was higher, and there was one maternal death.

TABLE 41-5. Selected Maternal Outcomes in Women with Accrete Syndromes Identified Prenatally and Delivered in Tertiary-Care Units


Second, in the Utah experiences, attempts at placental removal increased morbidity significantly—67 versus 36 percent—compared with no attempts at removal before hysterectomy. They also found that preoperative bilateral ureteral stenting reduced morbidity. However, no benefits accrued from internal iliac artery ligation (Eller, 2011; Po, 2012). Our management at Parkland Hospital is similar, however, the final decision for hysterectomy is not made until assessment at delivery. Also, we do not routinely perform preoperative ureteral stent placement. We have at times inserted stents transvesically if indicated intraoperatively. As discussed on page 820, preoperative arterial catheterization may be beneficial (Desai, 2012).

Subsequent Pregnancy

There is some evidence that women with accrete syndromes have an increased risks for recurrence, uterine rupture, hysterectomy, and previa (Eshkoli, 2013).


Obstetrical syndromes commonly termed consumptive coagulopathy or disseminated intravascular coagulation (DIC) were described in the 1901 report by DeLee in which “temporary hemophilia” developed with placental abruption or with a long-dead macerated fetus. In ensuing decades, similar—but frequently less intense—coagulopathic syndromes have been described for almost all areas of medicine (Levi, 2010b; Montagnana, 2010).

image Disseminated Intravascular Coagulation in Pregnancy

Because of many definitions used and its variable severity, citing an accurate incidence for consumptive coagulopathy is not possible in pregnant women. For example, as will be discussed, some degree of significant coagulopathy is found with most cases of placental abruption and amnionic-fluid embolism. Other instances in which frequently occurring but insignificant degrees of coagulation activation can be found include sepsis, thrombotic microangiopathies, acute kidney injury, and preeclampsia and HELLP (hemolysis, elevated liver enzyme levels, low platelet count) syndromes (Rattray, 2012; Su, 2012). Although profound consumptive coagulopathy can be associated with fatty liver disease of pregnancy, diminished hepatic synthesis of procoagulants makes a significant contribution (Nelson, 2013).

When consumptive coagulopathy is severe, the likelihood of maternal and perinatal morbidity and mortality is increased. Rattray and colleagues (2012) described 49 cases from Nova Scotia during a 30-year period. Antecedent causes included placental abruption, obstetrical hemorrhage, preeclampsia and HELLP syndromes, acute fatty liver, sepsis, and amnionic-fluid embolism. Of these, 59 percent received blood transfusions, 18 percent underwent hysterectomy, 6 percent were dialyzed, and there were three maternal deaths. The perinatal mortality rate was 30 percent.

Pregnancy-Induced Coagulation Changes

Several changes in coagulation and fibrinolysis can be documented during normal pregnancy. Some of these include appreciable increases in the plasma concentrations of factors I (fibrinogen), VII, VIII, IX, and X. A partial list of these normal values can be found in the Appendix (p. 1288) and in Chapter 4 (p. 57). At the same time, plasminogen levels are increased considerably, but levels of plasminogen activator inhibitor-1 and -2 (PAI-1 and PAI-2) also increase. Thus, plasmin activity usually decreases until after delivery (Hale, 2012; Hui, 2012). The mean platelet count decreases by 10 percent during pregnancy, and there is increased platelet activation (Kenny, 2014).

The net results of these changes include increased levels of fibrinopeptide A, β-thromboglobulin, platelet factor 4, and fibrinogen-fibrin degradation products, which includes d-dimers. Along with decreased concentrations of anticoagulant protein S, hypercoagulability, and decreased fibrinolysis, there is augmented—yet compensated—intravascular coagulation that may function to maintain the uteroplacental interface.

image Pathological Activation of Coagulation

Normal coagulation and fibrinolysis can be pathologically activated via two pathways. The extrinsic pathway is active by thromboplastin from tissue destruction, whereas the intrinsic pathway is initiated by collagen and other tissue components that become exposed with loss of endothelial integrity (Fig. 41-30). Tissue factor III is an integral membrane protein. It is released by endothelial cells to complex with factor VII, which in turn activates tenase (factor IX) and prothrombinase (factor X) complexes. Uncontrolled thrombin generation converts fibrinogen to fibrin, which polymerizes to deposit in small vessels of virtually every organ system. This seldom causes organ failure, because these vessels are protected by enhanced fibrinolysis stimulated by fibrin monomers released by coagulation. These monomers combine with tissue plasminogen activator and plasminogen to release plasmin, which lyses fibrinogen and fibrin monomers and polymers. The products form a series of fibrinogen-fibrin derivatives that are measured by immunoassay. These are the fibrin degradation products or fibrin-split products, which include d-dimers (see Fig. 41-30). There may also be evidence for microangiopathic hemolysis from mechanical trauma to the red cell membrane by fibrin strands in small vessels. This is likely a contributing cause of hemolysis in women with preeclampsia and HELLP syndromes (Pritchard, 1976a).


FIGURE 41-30 Mechanisms of coagulation and fibrinolysis.

The pathologically activated cycle of coagulation and fibrinolysis becomes clinically important when coagulation factors and platelets are sufficiently depleted to cause bleeding—hence, consumptive coagulopathy. Several obstetrical conditions are accompanied by release of potent inciting factors for clinically significant consumptive coagulation. The best known and most common, and therefore most serious, results from thromboplastin release with placental abruption. Also, unique to obstetrics is the immediate and profound coagulation factor depletion that can follow entry of amnionic fluid into the maternal circulation. This causes activation of factor X by abundant mucin in fetal squames. Other causes include activation by release of endotoxins from gram-negative bacteria and exotoxins from gram-positive bacteria.

image Diagnosis

The International Society on Thrombosis and Haemostasis has promulgated a DIC score to aid identification and prognosis prediction (Taylor, 2001). This algorithm, shown in Table 41-6, has not been applied in obstetrical conditions but can serve as a rough guideline to identify a pregnant woman with consumptive coagulopathy. Again, although not including obstetrical patients, the Prowess Trial evaluated 840 subjects with severe sepsis. The mortality rate increased from approximately 25 percent with a DIC score of 3 to 70 percent with a score of 7 (Dhainaut, 2004).

TABLE 41-6. Algorithm for Diagnosis of Overt Disseminated Intravascular Coagulation—“DIC Score”a


Evaluation and Management

Obstetrical causes of consumptive coagulopathy are almost always due to an identifiable, underlying pathological process that must be eliminated to halt ongoing defibrination. Thus, prompt identification and removal of the source of the coagulopathy is given priority. With surgical incisions or extensive lacerations accompanied by severe hemorrhage, rapid replacement of procoagulants is usually indicated. Vigorous restoration and maintenance of the circulation to treat hypovolemia cannot be overemphasized. With adequate perfusion, activated coagulation factors, fibrin, and fibrin degradation products are promptly removed by the reticuloendothelial system, along with restoration of hepatic and endothelial synthesis of procoagulants.

Some treatments for intravascular coagulation have been conceived by armchair theorists and are mentioned here only to be condemned. For example, in years past, some recommended heparin administration to block consumption of procoagulants. Others recommended epsilon-aminocaproic acid to inhibit fibrinolysis by blocking plasminogen conversion to plasmin. The dangers of giving heparin to an actively bleeding woman are obvious. Fibrinolysis inhibition is probably not quite as dangerous, but any putative benefits remain unproven.

Identification of Defective Hemostasis. Bioassay is an excellent method to detect or suspect clinically significant coagulopathy. Excessive bleeding at sites of modest trauma characterizes defective hemostasis. Examples include persistent bleeding from venipuncture sites, nicks from shaving the perineum or abdomen, trauma from bladder catheterization, and spontaneous bleeding from the gums, nose, or gastrointestinal tract. Purpuric areas at pressure sites such as sphygmomanometer cuffs or tourniquets suggest significant thrombocytopenia. As discussed, any surgical procedure provides the ultimate bioassay and elicits generalized oozing from the skin, subcutaneous and fascial tissues, the retroperitoneal space, the episiotomy, or incisions and dissections for cesarean delivery or hysterectomy.

Fibrinogen and Degradation Products. In late pregnancy, plasma fibrinogen levels typically have increased to 300 to 600 mg/dL. Even with severe consumptive coagulopathy, levels may sometimes be high enough to protect against clinically significant hypofibrinogenemia. For example, defibrination caused by a placental abruption might lower an initial fibrinogen level of 600 mg/dL to 250 mg/dL. Although this would indicate massive fibrinogen consumption, there are still adequate levels to promote clinical coagulation—usually about 150 mg/dL. If serious hypofibrinogenemia—less than 50 mg/dL—is present, the clot formed from whole blood in a glass tube may initially be soft but not necessarily remarkably reduced in volume. Then, over the next half hour or so, as platelet-induced clot retraction develops, the clot becomes quite small. When many of the erythrocytes are extruded, the volume of liquid in the tube clearly exceeds that of clot.

Fibrinolysis cleaves fibrin and fibrinogen into various fibrin degradation products that are detected by several sensitive test systems. There are many fragment types, and monoclonal antibodies in assay kits usually measure d-dimers specific for that assay. These values are always abnormally high with clinically significant consumptive coagulopathy. At least in obstetrical disorders, quantification has not been correlated with outcomes, although “moderate” to “strong” increases constitute part of the diagnostic algorithm shown in Table 41-6.


Seriously low platelet concentrations are likely if petechiae are abundant or if clotted blood fails to retract within an hour or so. Confirmation is provided by a platelet count. If there is associated severe preeclampsia syndrome, there may also be qualitative platelet dysfunction (Chap. 40p. 738).

Prothrombin and Partial Thromboplastin Times

Prolongation of these standard coagulation tests may result from appreciable reductions in procoagulants essential for generating thrombin, from very low fibrinogen concentrations, or from appreciable amounts of circulating fibrinogen-fibrin degradation products. Prolongation of the prothrombin time and partial thromboplastin time need not be the consequence of consumptive coagulopathy.

image Placental Abruption

This is the most common cause of severe consumptive coagulopathy in obstetrics and is discussed on page 793.

image Preeclampsia Syndrome

Endothelial activation or injury is a hallmark of preeclampsia, eclampsia, and HELLP syndrome. In general, the clinical severity of preeclampsia is directly correlated with thrombocytopenia and fibrinogen-fibrin degradation products (Levi, 2010b; Kenny, 2014). That said, intravascular coagulation is seldom clinically worrisome. Delivery reverses these changes, and treatment until then is supportive. These syndromes are discussed in detail in Chapter 40.

image Fetal Death and Delayed Delivery

Consumptive coagulopathy associated with prolonged retention of a dead fetus is unusual today because fetal death can be easily confirmed and there are highly effective methods for labor induction. Currently, the syndrome is only occasionally encountered when there is one dead twin fetus and an ongoing pregnancy. With singleton pregnancies, if the dead fetus is undelivered, most women enter spontaneous labor within 2 weeks. Gross disruption of maternal coagulation rarely develops before 4 weeks (Pritchard, 1959, 1973). After 1 month, however, almost a fourth will develop consumptive coagulopathy.

The pathogenesis of coagulopathy appears to be mediated by thromboplastin released by the dead fetus and the placenta (Jimenez, 1968; Lerner, 1967). Typically, the fibrinogen concentration falls during 6 weeks or more to levels that are normal for nonpregnant adults, but in some cases, this declines to < 100 mg/dL. Simultaneously, fibrin degradation product and d-dimer levels become elevated in serum, and moderate thrombocytopenia develops (Pritchard, 1973). If enough time elapses to seal the placental-decidual interface, these coagulation defects may correct spontaneously before evacuation (Pritchard, 1959).

Discordant Fetal Death in Multifetal Gestation

Obvious coagulation derangement occasionally develops in a multifetal pregnancy in which there is at least one fetal death and survival of another (Chescheir, 1988; Landy, 1989). This situation is uncommon, and in one study of 22 such pregnancies, none developed a coagulopathy (Petersen, 1999). Most cases are seen in monochorionic twins with shared circulations, which are described in Chapter 45 (p. 904). The course in such a woman cared for at Parkland Hospital is shown in Figure 41-31. In this case, the coagulopathy ceased spontaneously, and the surviving healthy twin was delivered near term. The placenta of the long-dead fetus was filled with fibrin.


FIGURE 41-31 A. Following the confirmed death of one twin at 28 weeks’ gestation, serial studies demonstrated decreasing plasma fibrinogen concentrations and elevated serum fibrin-degradation products that reached a nadir 4 weeks later. After this, fibrinogen concentrations increased and fibrin degradation product levels decreased in mirror-like fashion. B. When delivered at 36 weeks, the fibrin-filled placenta (clear arrow) of the long-dead fetus (asterisk) is apparent. The liveborn cotwin was healthy and had normal coagulation studies and a normal-appearing placenta (blue arrow).

image Amnionic-Fluid Embolism

This uniquely obstetrical syndrome was described in 1941 by Steiner and Lushbaugh and became classically characterized by the abrupt onset of hypotension, hypoxia, and severe consumptive coagulopathy. Even so, amnionic-fluid embolism has great individual variation in its clinical manifestation. For example, only one of these three clinical hallmarks predominates in some affected women.

Despite variations in the reported incidence of this uncommon but extremely important complication, many reports describe a similar frequency. A study that included 3 million births in the United States cited an estimated frequency of 7.7 cases per 100,000 births (Abenhaim, 2008). The United Kingdom Obstetric Surveillance System reported an incidence of 2.0 per 100,000 births (Knight, 2010). And review of more than 4 million births in Canada yielded an incidence of 2.5 per 100,000 births (Kramer, 2012). Another review of data from five high-resource countries cites frequencies from 1.9 to 6.1 per 100,000 deliveries. The case-fatality rates in all of these studies ranged from 11 to 43 percent. From another perspective, amnionic-fluid embolism was the cause of 10 to 15 percent of all pregnancy-related deaths in the United States and Canada (Berg, 2003; 2010; Clark, 2008; Kramer, 2012).

Predisposing conditions are rapid labor, meconium-stained amnionic fluid, and tears into uterine and other large pelvic veins. Other risk factors commonly cited include older maternal age; postterm pregnancy; labor induction or augmentation; eclampsia; cesarean, forceps, or vacuum delivery; placental abruption or previa; and hydramnios (Knight, 2010, 2012; Kramer, 2012). The association of uterine hypertonus appears to be the effect rather than the causeof amnionic-fluid embolism. This is likely because uterine blood flow ceases when intrauterine pressures exceed 35 to 40 mm Hg. Thus, a hypertonic contraction would be the least likely circumstance for amnionic fluid and other debris to enter uterine veins (Clark, 1995). Because of this, there is also no association between this disorder and hypertonus from oxytocin.

In obvious cases of amnionic-fluid embolism, the clinical picture is unquestionably dramatic. The classic example is that of a woman in the late stages of labor or immediately postpartum who begins gasping for air and then rapidly suffers seizures or cardiorespiratory arrest complicated by massive hemorrhage from consumptive coagulopathy. It has become apparent that there is a variation in the clinical manifestations of this condition. For example, we and others have managed several women in whom otherwise uncomplicated vaginal or cesarean delivery was followed by severe acute consumptive coagulopathy without overt cardiorespiratory difficulties. In those women, consumptive coagulopathy appears to be the forme fruste of amnionic-fluid embolism (Kramer, 2012; Porter, 1996).


Some amnionic fluid commonly enters the maternal circulation at the time of normal delivery through a minor breach in the physiological barrier between maternal and fetal compartments. Thus, it is fortunate that infused amnionic fluid is generally innocuous, even in large amounts (Adamsons, 1971; Stolte, 1967). At delivery, squames, other cellular elements of fetal origin, and trophoblasts can be identified in maternal peripheral blood (Clark, 1986; Lee, 1986). These are presumed to enter venous channels from the placental implantation site or from small lacerations that inevitably develop in the lower uterine segment or cervix with delivery. Although these events are usually innocuous, amnionic fluid constituents in some women initiate a complex series of pathophysiological sequelae shown in Table 41-7. The wide range of clinical manifestations underscores the subjective nature of diagnosis of many of these women.

TABLE 41-7. Clinical Findings in 204 Women with Amnionic-Fluid Embolism


Considering the wide spectrum of cardiovascular pathophysiological aberrations and sometimes profound coagulopathy, one can reasonably conclude that amnionic fluid and its constituents have a multitude of actions. For example, tissue factor in amnionic fluid presumably activates factor X to incite coagulation (Ecker, 2012; Levi, 2013). Others that have been described include endothelin-1 expressed by fetal squames, phosphatidylserine expressed by amnion, and complement activators (Khong, 1998; Zhou, 2009). An anaphylactoid reaction with complement activation has been postulated because serum levels of tryptase and histamine are also elevated (Benson, 2001; Clark, 1995).


Animal studies in primates and goats have provided important insights into central hemodynamic aberrations caused by amnionic fluid infused intravenously (Adamsons, 1971; Hankins, 1993). In general, evidence for fetal debris embolization and toxicity increases with the volume infused and the amount of meconium contamination (Hankins, 2002). If a response is evoked, its initial phase consists of pulmonary and systemic hypertension. A similar response was reported in a woman in whom transesophageal echocardiography was performed within minutes of collapse. Findings included a massively dilated akinetic right ventricle and a small, vigorously contracting, cavity-obliterated left ventricle (Stanten, 2003). Profound oxygen desaturation is often seen in the initial phase, and this is the cause of neurological injury in most survivors (Harvey, 1996). All of these observations are consistent with failure to transfer blood from the right to the left heart because of severe and unrelenting pulmonary vasoconstriction. This initial phase is probably followed by decreased systemic vascular resistance and diminished cardiac output (Clark, 1988). Women who survive beyond these first two phases invariably have a consumptive coagulopathy and usually lung and brain injury.

Postmortem Findings. Histopathological findings may be dramatic in fatal cases of amnionic-fluid embolism such as the one shown in Figure 41-32. The detection of such debris, however, may require special staining, and even then, it may not be seen. In one study, fetal elements were detected in 75 percent of autopsies and in 50 percent of specimens prepared from concentrated buffy coat aspirates taken antemortem from a pulmonary artery catheter (Clark, 1995). Several other studies, however, have demonstrated that fetal squamous cells, trophoblasts, and other debris of fetal origin may commonly be found in the central circulation of women with conditions other than amnionic-fluid embolism. Thus, the diagnosis is generally made by identifying clinically characteristic signs and symptoms and excluding other causes.


FIGURE 41-32 Fatal amnionic-fluid embolism. A. Lung findings at autopsy: fetal squames (arrows) packed into a small pulmonary artery. Most of the empty spaces within the vessel were demonstrated by special lipid stains to be filled with vernix caseosa. B. Laboratory findings from the same woman demonstrated acute defibrination with decreased levels of fibrinogen and platelets along with increased levels of fibrinogen-fibrin degradation products.

Management and Clinical Outcomes

Immediate resuscitative actions are necessary to interdict the high mortality rate. As discussed, the initial period of systemic and pulmonary hypertension that frequently heralds amnionic-fluid embolism is transient. Tracheal intubation, cardiopulmonary resuscitation, and other supportive measures must be instituted without delay. Treatment is directed at oxygenation and support of the failing myocardium, along with circulatory support that includes rapid blood and component replacement. That said, there are no data indicating that any type of intervention improves maternal or fetal prognosis. In undelivered women undergoing cardiopulmonary resuscitation, consideration should be given to emergency cesarean delivery to perhaps optimize these efforts and improve newborn outcome. Decision making for perimortem cesarean delivery is more complex in a woman who is hemodynamically unstable but who has not suffered cardiac arrest (Chap. 47p. 956).

Most reports describe dismal outcomes with amnionic-fluid embolism. However, this is likely influenced by underdiagnosis and reporting biases that favor the most severe cases, which are recognized but also have the greatest mortality rates. Several reports are illustrative. From a California database of 1.1 million deliveries, there was a 60-percent mortality rate with amnionic-fluid embolism (Gilbert, 1999). In a report from the Suzhou region of China, 90 percent of mothers died (Weiwen, 2000). This latter report emphasizes that death can be amazingly rapid because 12 of the 34 women who died did so within 30 minutes. The mortality rate was less dismal in the largest study from a Canadian database. Of 120 women with an amnionic-fluid embolism, only a fourth died. In many reports, survivors commonly have profound neurological impairment. Clark (1995) observed that only 8 percent of women who lived despite cardiac arrest survived neurologically intact.

As perhaps expected, perinatal outcomes are also poor and are inversely related to the maternal cardiac arrest-to-delivery interval. Even so, neonatal survival rate is 70 percent, but unfortunately, up to half of survivors suffer residual neurological impairment. In the Canadian study, 28 percent of infants were considered to be asphyxiated at birth (Kramer, 2012).

image Sepsis Syndrome

Various infections that are accompanied by endo- or exotoxin release can result in sepsis syndrome in pregnant women. Although a feature of this syndrome includes activation of coagulation, seldom does sepsis alone cause massive procoagulant consumption. Escherichia coli bacteremia is frequently seen with antepartum pyelonephritis and puerperal infections, however, accompanying consumptive coagulopathy is usually not severe. Some notable exceptions are septicemia associated with puerperal infection or septic abortion caused by exotoxins released from infecting organisms such as group A Streptococcus pyogenes, Staphylococcus aureus, or Clostridium perfringens or sordellii. Treatment of sepsis syndrome and septic shock is discussed in Chapter 47 (p. 946).

Purpura Fulminans

This severe—often lethal—form of consumptive coagulopathy is caused by microthrombi in small blood vessels leading to skin necrosis and sometimes vasculitis. Debridement of large areas of skin over the extremities and buttocks frequently requires treatment in a burn unit. Purpura fulminans usually complicates sepsis in women with heterozygous protein C deficiency and low protein C serum levels (Levi, 2010b). Recall that homozygous protein C deficiency results in fatal neonatal purpura fulminans (Chap. 52p. 1031).

image Abortion

Septic abortion—especially associated with the organisms discussed above—can incite coagulation and worsen hemorrhage, especially with midtrimester abortions. Indeed, sepsis syndrome accompanied by intravascular coagulation accounts for 25 percent of abortion-related deaths (Saraiya, 1999). In the past, especially with illegal abortions, infections with Clostridium perfringens were a frequent cause of intense intravascular hemolysis at Parkland Hospital (Pritchard, 1971). More recently, however, septic abortions from infection with Clostridium sordellii have emerged as important causes (Chap 18p. 357).

Second-trimester induced abortions can stimulate intravascular coagulation even in the absence of sepsis. Ben-Ami and associates (2012) described a 1.6-percent incidence in 1249 late second-trimester pregnancies terminated by dilatation and evacuation. Two thirds were done for fetal demise, which may have been contributory to coagulopathy. Another source of intense coagulation is from instillation of hypertonic solutions to effect midtrimester abortions. These are not commonly performed currently for pregnancy terminations (Chap. 18p. 369). The mechanism is thought to initiate coagulation by thromboplastin release into maternal circulation from placenta, fetus, and the decidua by the necrobiotic effect of the hypertonic solutions (Burkman, 1977).


One of the most crucial elements of obstetrical hemorrhage management is recognition of its severity. As discussed on page 781, visual estimation of blood loss, especially when excessive, is notoriously inaccurate, and true blood loss is often two to three times the clinical estimates. Consider also that in obstetrics, part and sometimes even all of the lost blood may be concealed. Estimation is further complicated in that peripartum hemorrhage—when most severe cases are encountered—also includes the pregnancy-induced increased blood volume. If pregnancy hypervolemia is not a factor, then following blood loss of 1000 mL, the hematocrit typically falls only 3 to 5 volume percent within an hour. The hematocrit nadir depends on the speed of resuscitation using infused intravenous crystalloids. Recall that with abnormally increased acute blood loss, the real-time hematocrit is at its maximum whenever measured in the delivery, operating, or recovery room.

A prudent rule is that any time blood loss is considered more than average by an experienced team member, then the hematocrit is determined and plans are made for close observation for physiological deterioration. Urine output is one of the most important “vital signs” with which to monitor the woman with obstetrical hemorrhage. Renal blood flow is especially sensitive to changes in blood volume. Unless diuretic agents are given—and these are seldom indicated with active bleeding—accurately measured urine flow reflects renal perfusion, which in turn reflects perfusion of other vital organs. Urine flow of at least 30 mL, and preferably 60 mL, per hour or more should be maintained. With potentially serious hemorrhage, an indwelling bladder catheter is inserted to measure hourly urine flow.

image Hypovolemic Shock

Shock from hemorrhage evolves through several stages. Early in the course of massive bleeding, there are decreases in mean arterial pressure, stroke volume, cardiac output, central venous pressure, and pulmonary capillary wedge pressure. Increases in arteriovenous oxygen content difference reflect a relative increase in tissue oxygen extraction, although overall oxygen consumption falls.

Blood flow to capillary beds in various organs is controlled by arterioles. These are resistance vessels that are partially controlled by the central nervous system. However, approximately 70 percent of total blood volume is contained in venules, which are passive resistance vessels controlled by humoral factors. Catecholamine release during hemorrhage causes a generalized increase in venular tone that provides an autotransfusion from this capacitance reservoir (Barber, 1999). This is accompanied by compensatory increases in heart rate, systemic and pulmonary vascular resistance, and myocardial contractility. In addition, there is redistribution of cardiac output and blood volume by selective, centrally mediated arteriolar constriction or relaxation—autoregulation. Thus, although perfusion to the kidneys, splanchnic beds, muscles, skin, and uterus is diminished, relatively more blood flow is maintained to the heart, brain, and adrenal glands.

When the blood volume deficit exceeds approximately 25 percent, compensatory mechanisms usually are inadequate to maintain cardiac output and blood pressure. Importantly, additional small losses of blood will now cause rapid clinical deterioration. Following an initial increased total oxygen extraction by maternal tissue, maldistribution of blood flow results in local tissue hypoxia and metabolic acidosis. This creates a vicious cycle of vasoconstriction, organ ischemia, and cellular death. Another important clinical effect of hemorrhage is activation of lymphocytes and monocytes, which in turn cause endothelial cell activation and platelet aggregation. These cause release of vasoactive mediators with small vessel occlusion and further impairment of microcirculatory perfusion. Other common obstetrical syndromes—preeclampsia and sepsis—also lead to loss of capillary endothelial integrity, additional loss of intravascular volume into the extracellular space, and platelet aggregation (Chaps. 40, p. 734 and 47p. 947).

The pathophysiological events just described lead to the important but often overlooked extracellular fluid and electrolyte shifts involved in both the genesis and successful treatment of hypovolemic shock. These include changes in the cellular transport of various ions such as sodium and water into skeletal muscle and potassium loss. Replacement of extracellular fluid and intravascular volume are both necessary. Survival is enhanced in acute hemorrhagic shock if blood plus crystalloid solution is given compared with blood transfusions alone.

image Immediate Management and Resuscitation

Whenever there is suggestion of excessive blood loss in a pregnant woman, steps are simultaneously taken to identify the source of bleeding and to begin resuscitation. If she is undelivered, restoration of blood volume is beneficial to mother and fetus, and it also prepares for emergent delivery. If she is postpartum, it is essential to immediately identify uterine atony, retained placental fragments, or genital tract lacerations. At least one and preferably more large-bore intravenous infusion systems are established promptly with rapid administration of crystalloid solutions, while blood is made available. An operating room, surgical team, and anesthesia providers are assembled immediately. Specific management of hemorrhage is further dependent on its etiology. For example, antepartum bleeding from placenta previa is approached somewhat differently than that from postpartum atony.

Fluid Resuscitation

It cannot be overemphasized that treatment of serious hemorrhage demands prompt and adequate refilling of the intravascular compartment with crystalloid solutions. These rapidly equilibrate into the extravascular space, and only 20 percent of crystalloid remains intravascularly in critically ill patients after 1 hour (Zuckerbraun, 2010). Because of this, initial fluid is infused in a volume three times the estimated blood loss.

Resuscitation of hypovolemic shock with colloid versus crystalloid solutions is debated. In a Cochrane review of resuscitation of nonpregnant critically ill patients, Perel and Roberts (2007) found equivalent benefits but concluded that colloid solutions were more expensive. Similar results were found in the Saline versus Albumin Fluid Evaluation (SAFE) randomized trial of almost 7000 nonpregnant patients (Finfer, 2004). We concur with Zuckerbraun and colleagues (2010) that acute volume resuscitation is preferably done with crystalloid and blood.

Blood Replacement

There is considerable debate regarding the hematocrit level or hemoglobin concentration that mandates blood transfusion. Cardiac output does not substantively decrease until the hemoglobin concentration falls to approximately 7 g/dL or hematocrit of 20 volume percent. At this level the Society of Thoracic Surgeons (2011) recommends consideration for red-cell transfusions. Also, Military Combat Trauma Units in Iraq used a target hematocrit of 21 volume percent (Barbieri, 2007). In general, with ongoing obstetrical hemorrhage, we recommend rapid blood infusion when the hematocrit is < 25 volume percent. This decision is dependent on whether the fetus has been delivered, surgery is imminent or ongoing operative blood loss is expected, or acute hypoxia, vascular collapse, or other factors are present.

Scant clinical data elucidate these issues. In a study from the Canadian Critical Care Trials Group, nonpregnant patients were randomly assigned to restrictive red cell transfusions to maintain hemoglobin concentration > 7 g/dL or to liberal transfusions to maintain the hemoglobin level at 10 to 12 g/dL. The 30-day mortality rate was similar—19 versus 23 percent in the restrictive versus liberal groups, respectively (Hebert, 1999). In a subanalysis of patients who were less ill, the 30-day mortality rate was significantly lower in the restrictive group—9 versus 26 percent. In a study of women who had suffered postpartum hemorrhage and who were now isovolemic and not actively bleeding, there were no benefits of red cell transfusions when the hematocrit was between 18 and 25 volume percent (Morrison, 1991). The number of units transfused in a given woman to reach a target hematocrit depends on her body mass and on expectations of additional blood loss.

Blood Component Products. Contents and effects of transfusion of various blood components are shown in Table 41-8Compatible whole blood is ideal for treatment of hypovolemia from catastrophic hemorrhage. It has a shelf life of 40 days, and 70 percent of the transfused red cells function for at least 24 hours following transfusion. One unit raises the hematocrit by 3 to 4 volume percent. Whole blood replaces many coagulation factors—which is important in obstetrics—especially fibrinogen—and its plasma treats hypovolemia. A collateral derivative is that women with severe hemorrhage are resuscitated with fewer blood donor exposures than with packed red cells and components (Shaz, 2009).

TABLE 41-8. Blood Products Commonly Transfused in Obstetrical Hemorrhage


There are reports that support the preferable use of whole blood for massive hemorrhage, including our experiences at Parkland Hospital (Alexander, 2009; Hernandez, 2012). Of more than 66,000 deliveries, women with obstetrical hemorrhage treated with whole blood had significantly decreased incidences of renal failure, acute respiratory distress syndrome, pulmonary edema, hypofibrinogenemia, ICU admissions, and maternal death compared with those given packed red cells and component therapy. Freshly donated whole blood has also been used successfully for life-threatening massive hemorrhage at combat support hospitals in Iraq (Spinella, 2008).

It is problematic that in most institutions today, whole blood is rarely available. Thus, most women with obstetrical hemorrhage and ongoing massive blood loss are given packed red cells and crystalloid in 2:1 or 3:1 proportions. In these instances, there are no data to support a 1:1 red cell:plasma transfusion ratio. Many institutions use massive transfusion protocols designed to anticipate all facets of obstetrical hemorrhage defined as massive. These “recipes” commonly contain a combination of red cells, plasma, cryoprecipitate, and platelets (Pacheco, 2011; Shields, 2011). If time permits, we usually prefer to await results of emergently performed hematological laboratory assessments to treat deficiencies of fibrinogen or platelets. If time does not permit this, however, the massive transfusion protocol is activated.

Dilutional Coagulopathy. A major drawback of treatment for massive hemorrhage with crystalloid solutions and packed red blood cells is depletion of platelets and clotting factors. As discussed on page 808, this can lead to a dilutional coagulopathy clinically indistinguishable from disseminated intravascular coagulation (Hossain, 2013). In some cases, impaired hemostasis further contributes to blood loss.

Thrombocytopenia is the most frequent coagulation defect found with blood loss and multiple transfusions (Counts, 1979). In addition, packed red cells have very small amounts of soluble clotting factors, and stored whole blood is deficient in platelets and in factors V, VIII, and XI. Massive replacement with red cells only and without factor replacement can also cause hypofibrinogenemia and prolongation of the prothrombin and partial thromboplastin times. Because many causes of obstetrical hemorrhage also cause consumptive coagulopathy, the distinction between dilutional and consumptive coagulopathy can be confusing. Fortunately, treatment for both is similar.

A few studies have assessed the relationship between massive transfusion and resultant coagulopathy in civilian trauma units and military combat hospitals (Bochicchio, 2008; Borgman, 2007; Gonzalez, 2007; Johansson, 2007). Patients undergoing massive transfusion—defined as 10 or more units of blood—had much higher survival rates as the ratio of plasma to red cell units was near 1.4, that is, one unit of plasma given for each 1.4 units of packed red cells. By way of contrast, the highest mortality group had a 1:8 ratio. Most of these studies found that component replacement is rarely necessary with acute replacement of 5 to 10 units of packed red cells.

From the foregoing, when red cell replacement exceeds five units or so, a reasonable practice is to evaluate the platelet count, clotting studies, and plasma fibrinogen concentration. In the woman with obstetrical hemorrhage, the platelet count should be maintained above 50,000/μL by the infusion of platelet concentrates. A fibrinogen level < 100 mg/dL or a sufficiently prolonged prothrombin or partial thromboplastin time in a woman with surgical bleeding is an indication for replacement. Fresh-frozen plasma is administered in doses of 10 to 15 mL/kg, or alternatively, cryoprecipitate is infused (see Table 41-8).

Type and Screen versus Crossmatch. A blood type and antibody screen should be performed for any woman at significant risk for hemorrhage. Screening involves mixing maternal serum with standard reagent red cells that carry antigens to which most of the common clinically significant antibodies react. Crossmatching involves the use of actual donor erythrocytes rather than the standardized red cells. Clinical results show that the type-and-screen procedure is amazingly efficient. Indeed, only 0.03 to 0.07 percent of patients identified to have no antibodies are subsequently found to have antibodies by crossmatch (Boral, 1979). Importantly, administration of screened blood rarely results in adverse clinical sequelae.

Packed Red Blood Cells. One unit of packed erythrocytes is derived from one unit of whole blood to have a hematocrit of 55 to 80 volume percent, depending on the length of gentle centrifugation. Thus one unit contains the same volume of erythrocytes as one whole blood unit. It will increase the hematocrit by 3 to 4 volume percent depending on patient size. Packed red blood cell and crystalloid infusion are the mainstays of transfusion therapy for most cases of obstetrical hemorrhage.

Platelets. With operative delivery or with lacerations, platelet transfusions are considered with ongoing obstetrical hemorrhage when the platelet count falls below 50,000/μL (Kenny, 2014). In the nonsurgical patient, bleeding is rarely encountered if the platelet count is 10,000/μL or higher (Murphy, 2010). The preferable source of platelets is a bag obtained by single-donor apheresis. This is the equivalent of six units from six individual donors. Depending on maternal size, each single-donor apheresis bag raises the platelet count by approximately 20,000/μL (Schlicter, 2010). If these bags are not available, then individual-donor platelet units are used. One unit contains about 5.5 × 1010platelets, and six to eight such units are generally transfused.

Importantly, the donor plasma in platelet units must be compatible with recipient erythrocytes. Further, because some red blood cells are invariably transfused along with the platelets, only units from D-negative donors should be given to D-negative recipients. If necessary, however, adverse sequelae are unlikely. For example, transfusion of ABO-nonidentical platelets in nonpregnant patients undergoing cardiovascular surgery had no clinical effects (Lin, 2002).

Fresh-Frozen Plasma. This component is prepared by separating plasma from whole blood and then freezing it. Approximately 30 minutes are required for frozen plasma to thaw. It is a source of all stable and labile clotting factors, including fibrinogen. Thus, it is often used for treatment of women with consumptive or dilutional coagulopathy. Plasma is not appropriate for use as a volume expander in the absence of specific clotting factor deficiencies. It should be considered in a bleeding woman with a fibrinogen level < 100 mg/dL or with an abnormal prothrombin or partial thromboplastin time.

An alternative to frozen plasma is liquid plasma (LQP). This never-frozen plasma is stored at 1 to 6ºC for up to 26 days, and in vitro, it appears to be superior to thawed plasma (Matijevic, 2013).

Cryoprecipitate and Fibrinogen Concentrate. Each unit of cryoprecipitate is prepared from one unit of fresh-frozen plasma. Each 10- to 15-mL unit contains at least 200 mg of fibrinogen, factor VIII:C, factor VIII:von Willebrand factor, factor XIII, and fibronectin (American Association of Blood Banks, 2002). It is usually given as a “pool” or “bag” using an aliquot of fibrinogen concentrate taken from 8 to 120 donors. Cryoprecipitate is an ideal source of fibrinogen when levels are dangerously low and there is oozing from surgical incisions. Another alternative is virus-inactivated fibrinogen concentrate. Each gram of this raises the plasma fibrinogen level approximately 40 mg/dL (Ahmed, 2012; Kikuchi, 2013). Either is used to replace fibrinogen. However, there are no advantages to these compared with fresh-frozen plasma for general clotting factor replacement. Exceptions are general factor deficiency replacement for women in whom volume overload may be a problem—an unusual situation in obstetrics—and for those with a specific factor deficiency.

Recombinant Activated Factor VII (rFVIIa). This synthetic vitamin K-dependent protein is available as NovoSeven. It binds to exposed tissue factor at the site of injury to generate thrombin that activates platelets and the coagulation cascade. Since its introduction, rFVIIa has been used to help control hemorrhage from surgery, trauma, and many other causes (Mannucci, 2007). More than three fourths of Level I trauma centers include it in their massive transfusion protocols (Pacheco, 2011). It is included in the massive transfusion protocol at Parkland Hospital.

One major concern with rFVIIa use is arterial—and to a lesser degree venous—thrombosis. In a review of 35 randomized trials with nearly 4500 subjects, arterial thromboembolism developed in 55 percent (Levi, 2010a). A second concern is that it was found to be only marginally effective in most of these studies (Pacheco, 2011). In obstetrics, recombinant FVIIa has also been used to control severe hemorrhage in women with and without hemophilia (Alfirevic, 2007; Franchini, 2007). It has been used with uterine atony, lacerations, and placental abruption or previa. In approximately a third of cases, hysterectomy was required. Importantly, rFVIIa will not be effective if the plasma fibrinogen level is < 50 mg/dL or the platelet count is < 30,000/μL.

Topical Hemostatic Agents. Several agents can be used to control persistent oozing. These were recently reviewed by dos Santos and Menzin (2012). In general, these are rarely used in obstetrical hemorrhage.

Autologous Transfusion. Patient phlebotomy and autologous blood storage for transfusion has been disappointing. Exceptions are women with a rare blood type or with unusual antibodies. In one report, three fourths of women who began such a program in the third trimester donated only one unit (McVay, 1989). This is further complicated in that the need for transfusion cannot be predicted (Reyal, 2004). For these and other reasons, most have concluded that autologous transfusions are not cost effective (Etchason, 1995; Pacheco, 2011, 2013).

Cell Salvage. To accomplish autotransfusion, blood lost intraoperatively into the surgical field is aspirated and filtered. The red cells are then collected into containers with concentrations similar to packed red cells and are infused as such. Intraoperative blood salvage with reinfusion is considered to be safe in obstetrical patients (Pacheco, 2011; Rainaldi, 1998). That said, Allam and associates (2008) reported the lack of prospective trials but also found no reports of serious complications.

Complications with Transfusions. During the past several decades, substantial advances have been achieved in blood transfusion safety. Although many risks are avoided or mitigated, the most serious known risks that remain include errors leading to ABO-incompatible blood transfusion, transfusion-related acute lung injury (TRALI), and bacterial and viral transmission (Lerner, 2010).

The transfusion of an incompatible blood component may result in acute hemolysis. If severe, this can cause disseminated intravascular coagulation, acute kidney injury, and death. Preventable errors responsible for most of such reactions frequently include mislabeling of a specimen or transfusing an incorrect patient. Although the rate of such errors in the United States has been estimated to be 1 in 14,000 units, these are likely underreported (Lerner, 2010; Linden, 2001). A transfusion reaction is characterized by fever, hypotension, tachycardia, dyspnea, chest or back pain, flushing, severe anxiety, and hemoglobinuria. Immediate supportive measures include stopping the transfusion, treating hypotension and hyperkalemia, provoking diuresis, and alkalinizing the urine. Assays for urine and plasma hemoglobin concentration and an antibody screen help confirm the diagnosis.

The syndrome of transfusion-related acute lung injury (TRALI) can be a life-threatening complication. It is characterized by severe dyspnea, hypoxia, and noncardiogenic pulmonary edema that develop within 6 hours of transfusion (Triulzi, 2009). TRALI is estimated to complicate at least 1 in 5000 transfusions. Although the pathogenesis is incompletely understood, injury to the pulmonary capillaries may arise from anti-human leukocyte antigen (HLA) antibodies in donor plasma (Lerner, 2010; Schubert, 2013). These antibodies bind to leukocytes that aggregate in pulmonary capillaries and release inflammatory mediators. A delayed form of TRALI syndrome has been reported to have an onset 6 to 72 hours following transfusion (Marik, 2008). Management is with supportive therapy that may include mechanical ventilation (Chap. 47p. 944).

Bacterial infection from transfusion of a contaminated blood component is unusual because bacterial growth is discouraged by refrigeration. The most often implicated contaminant of red cells include Yersinia, Pseudomonas, Serratia, Acinetobacter, and Escherichia species. The more important risk is from bacterial contamination of platelets, which are stored at room temperature. Current estimates are that 1 in 1000 to 2000 platelet units are contaminated. Death from transfusion-related sepsis is 1 per 17,000 for single-door platelets and 1 per 61,000 for apheresis-donor packs (Lerner, 2010).

Risks from many transfusion-related viral infections have been curtailed. Fortunately, the most feared infection—HIV—is the least common. With current screening methods using nucleic acid amplification, the risk of HIV or hepatitis C virus infection in screened blood is estimated to be 1 case per 1 to 2 million units transfused (Stramer, 2004). The risk for HIV-2 infection is less.

Other viral infections include hepatitis B transmission, which is estimated to be < 1 per 100,000 transfused units (Jackson, 2003). Choosing donors who have been vaccinated will lower this incidence. Because of its high prevalence, cytomegalovirus-infected leukocytes are necessarily often transfused. Thus, precautions are taken for immunosuppressed recipients, keeping in mind that this includes the fetus (Chap. 15p. 310). Finally, there are slight risks for transmitting West Nile virus, human T-lymphotropic virus Type I, and parvovirus B19 (American Association of Blood Banks, 2013).

Red Cell Substitutes. Use of these artificial carriers of oxygen has been abandoned (Ness, 2007; Spiess, 2009). Three that have been studied include perfluorocarbons, liposome-encapsulated hemoglobin, and hemoglobin-based oxygen carriers.

image Adjunctive Surgical Procedures to Treat Hemorrhage

Uterine Artery Ligation

Several surgical procedures may be helpful to arrest of obstetrical hemorrhage. Of these, the technique for unilateral or bilateral uterine artery ligation is used primarily for lacerations at the lateral part of a hysterotomy incision (Fig. 41-33). In our experiences, this procedure is less helpful for hemorrhage from uterine atony.


FIGURE 41-33 Uterine artery ligation. The suture goes through the lateral uterine wall anteriorly, curves around posteriorly, then re-enters anteriorly. When tied, it encompasses the uterine artery.

Uterine Compression Sutures. Almost 20 years ago a surgical technique to arrest hemorrhage for severe postpartum atony was introduced by B-Lynch and coworkers (1997). The procedure involves placement of a No. 2-chromic suture to compress the anterior and posterior uterine walls together. Because they give the appearance of suspenders, they are also called braces (Fig. 41-34). Several modifications of the B-Lynch technique have been described (Cho, 2000; Hayman, 2002; Matsubara, 2013b; Nelson, 2007). Indications vary for its application, and this will affect the success rate. For example, B-Lynch (2005) cited 948 cases with only seven failures. Conversely, Kayem and associates (2011) described 211 women in whom compression sutures were employed. The overall failure rate of 25 percent did not differ between B-Lynch sutures and their modifications. Our experiences at Parkland Hospital are not nearly so successful. The technique has been effective in perhaps half of cases in which it is used.


FIGURE 41-34 Uterine compression suture or “brace.” The B-Lynch suture technique is illustrated from an anterior view of the uterus in Figures AB, and D and a posterior view in Figure C. The numbers denote the sequential path of the suture and are shown in more than one figure. Step 1. Beginning below the incision, the needle pierces the lower uterine segment to enter the uterine cavity. Step 2. The needle exits the cavity above the incision. The suture then loops up and around the fundus to the posterior uterine surface. Step 3. The needle pierces the posterior uterine wall to reenter the uterine cavity. The suture then traverses from left to right within the cavity. Step 4. The needle exits the uterine cavity through the posterior uterine wall. From the back of the uterus, the suture loops up and around the fundus to the front of the uterus. Step 5. The needle pierces the myometrium above the incision to reenter the uterine cavity. Step 6. The needle exits below the incision and the sutures at points 1 and 6 are tied below the incision. The hysterotomy incision is then closed in the usual fashion.

There are complications with compression sutures, and some are unique (Matsubara, 2013b). Their precise frequency is unknown, but it is likely low. The most common involve variations of uterine ischemic necrosis with peritonitis (Gottlieb, 2008; Joshi, 2004; Ochoa, 2002; Treloar, 2006). Total uterine necrosis was described by Friederich and associates (2007) in a woman in whom B-Lynch sutures were placed along with bilateral ligation of uterine, uteroovarian, and round ligament arteries. In most cases, subsequent pregnancies are uneventful if compression sutures are placed. A few women, however, with B-Lynch or Cho sutures have been reported to have defects in the uterine wall (Akoury, 2008; An, 2013). Another long-term complication is uterine cavity synechiae, which may develop in 20 to 50 percent of these women by 3 months (Alouini, 2011; Ibrahim, 2013; Poujade, 2011).

Internal Iliac Artery Ligation

Ligation of one or both internal iliac arteries has been used for many years to reduce hemorrhage from pelvic vessels (Allahbadia, 1993; Joshi, 2007). Drawbacks are that the procedure may be technically difficult and is only successful half of the time (American College of Obstetricians and Gynecologists, 2012b). It is not particularly helpful to abate hemorrhage with postpartum atony (Clark, 1985; Joshi, 2007).

Adequate exposure is obtained by opening the peritoneum over the common iliac artery and dissecting down to the bifurcation of the external and internal iliac arteries (Fig. 41-35). Branches distal to the external iliac arteries are palpated to verify pulsations at or below the inguinal area. Ligation of the internal iliac artery 5 cm distal to the common iliac bifurcation will usually avoid the posterior division branches (Bleich, 2007). The areolar sheath of the artery is incised longitudinally, and a right-angle clamp is carefully passed just beneath the artery from lateral to medial. Care must be taken not to perforate contiguous large veins, especially the internal iliac vein. Suture—usually nonabsorbable—is passed under the artery with a clamp, and the vessel is then securely ligated.


FIGURE 41-35 Ligation of the right internal iliac artery. A. The peritoneum covering the right iliac vessels is opened and reflected. B. Unembalmed cadaveric dissection shows the right-angle clamp passing underneath the anterior division of the internal iliac artery just distal to its posterior division. (Photograph contributed by Dr. Marlene Corton.)

Following ligation, pulsations in and distal to the external iliac artery are again confirmed. If not, pulsations must be identified after arterial hypotension has been successfully treated to ensure that the artery has not been compromised. The most important mechanism of action with internal iliac artery ligation is an 85-percent reduction in pulse pressure in those arteries distal to the ligation (Burchell, 1968). This converts an arterial pressure system into one with pressures approaching those in the venous circulation. This creates vessels more amenable to hemostasis via pressure and clot formation.

Even bilateral internal iliac artery ligation does not appear to interfere with subsequent reproduction. Nizard and colleagues (2003) reported follow-up in 17 women who had bilateral artery ligation. From a total of 21 pregnancies, 13 were normal, three ended with miscarriage, three were terminated, and there were two ectopic pregnancies.

Angiographic Embolization

This tool is now used for many causes of intractable hemorrhage when surgical access is difficult. In more than 500 women reported, embolization was 90-percent effective (Bodner, 2006; Lee, 2012; Poujade, 2012; Sentilhes, 2009). Rouse (2013) recently reviewed the subject and concluded that embolization can be used to arrest refractory postpartum hemorrhage. However, the author cautioned that the procedure is less effective with placenta percreta or with concurrent coagulopathy. Other reports have been less enthusiastic, and the American College of Obstetricians and Gynecologists (2012b) describes its efficacy as “unclear.” Fertility is not impaired, and many subsequent successful pregnancies have been reported (Chauleur, 2008; Fiori, 2009; Kolomeyevskaya, 2009). There are limited data describing its antepartum use. Embolization in a 20-week pregnant woman was reported for a large lower uterine segment arteriovenous malformation (Rebarber, 2009). It has also been used for renal hemorrhage (Wortman, 2013b).

Complications of embolization are relatively uncommon, but they can be severe. Uterine ischemic necrosis has been described (Coulange, 2009; Katakam, 2009; Sentilhes, 2009). Uterine infection has been reported (Nakash, 2012). Finally, Al-Thunyan and coworkers (2012) described a woman with massive buttock necrosis and paraplegia following bilateral internal iliac artery embolization.

Preoperative Pelvic Arterial Catheter Placement

There are a few instances in which massive blood loss and difficult surgical dissection is anticipated. For these, investigators have described use of balloon-tipped catheters inserted into the iliac or uterine arteries preoperatively. Catheters can then be inflated or embolization performed to mitigate heavy blood loss if it develops (Desai, 2012; Matsubara, 2013a). These techniques are used more commonly in cases of accrete syndromes (p. 804), and they have also been described for abdominal pregnancy (Chap. 19p. 388). The reported success rates have been variable, and these techniques are not universally recommended (Angstmann, 2012; Pacheco, 2011, 2013; Zacharias, 2003). Again the American College of Obstetricians and Gynecologists (2012b) considers the use and efficacy of these techniques to be “unclear.” Adverse effects are uncommon, but postoperative iliac and popliteal artery thrombosis and stenosis have been reported (Greenberg, 2007; Hoffman, 2010; Sewell, 2006).

Pelvic Umbrella Pack

The umbrella or parachute pack was described by Logothetopulos (1926) to arrest intractable pelvic hemorrhage following hysterectomy. Although seldom used today, it can be lifesaving if all other measures have failed. The pack is constructed of a sterile x-ray cassette bag that is filled with gauze rolls knotted together to provide enough volume to fill the pelvis (Fig. 41-36). The pack is introduced transabdominally with the stalk exiting the vagina. Mild traction is applied by tying the stalk to a 1-liter fluid bag, which is hung over the foot of the bed. An indwelling urinary catheter is placed to prevent urinary obstruction and to monitor urinary output. Percutaneous pelvic drains can be placed to monitor ongoing bleeding within the peritoneal cavity. Broad-spectrum antimicrobials are given, and the umbrella pack is removed vaginally after 24 hours.


FIGURE 41-36 Assembly of a pelvic pressure pack to control hemorrhage. A sterile x-ray cassette cover drape (plastic bag) is filled with gauze rolls tied end-to-end. The length of gauze is then folded into a ball (A) and placed within the cassette bag in such a way that the gauze can be unwound eventually with traction on the tail (D). Intravenous tubing (E) is tied to the exiting part of the neck (C) and connected to a 1-liter bag or other suitable weight (F). Once in place, the gauze pack (A) fills the pelvis to tamponade vessels, and the narrow upper neck (B) passes to exit the vagina (C). The IV bag is suspended off the foot of the bed to sustain pressure of the gauze pack on bleeding sites.

Dildy and colleagues (2006) described use of the pelvic pack to arrest hemorrhage following hysterectomy in 11 women. These women were given seven to 77 units of red cells, and the pack successfully stopped bleeding in all but two women. Over the years, we have had mixed results with this technique, but we can recommend it as a “last-ditch” attempt when exsanguination is inevitable, especially in “low-resource” areas.


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