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 Immediate Management and Resuscitation, the ability to provide prompt resuscitation of hypovolemia and blood administration is an absolute requirement for acceptable obstetrical care.
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.)
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 (General Considerations). 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. 27, Third Stage of Labor). 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 Uterine Inversion.
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. 27, Third Stage of Labor). 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.
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.
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 abnormalities predispose 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. 6, Abnormalities of the Placenta). During examination for lacerations and causes of atony, the uterus is massaged and uterotonic agents are administered.
There are several compounds that prompt the postpartum uterus to contract (Chap. 27, Management of the Third Stage). 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. 65, Management During Pregnancy). 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 (Amnionic-Fluid Embolism). 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. 27, Management of the Third Stage).
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:
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.
Immediately mobilize the emergent-care obstetrical team to the delivery room and call for whole blood or packed red cells.
Request urgent help from the anesthesia team.
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.
Begin volume resuscitation with rapid intravenous infusion of crystalloid (Immediate Management and Resuscitation).
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.
Thoroughly inspect the cervix and vagina again for lacerations that may have escaped attention.
If the woman is still unstable or if there is persistent hemorrhage, then blood transfusions are given (Immediate Management and Resuscitation).
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.
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.
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 Adjunctive Surgical Procedures to Treat Hemorrhage.
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:
Fundal placental implantation,
Delayed-onset or inadequate uterine contractility after delivery of the fetus, that is, uterine atony,
Cord traction applied before placental separation, and
Abnormally adhered placentation such as with the accrete syndromes (Maternal and Perinatal Outcomes).
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.
Maternal death from exsanguination caused by uterine inversion associated with a fundal placenta accreta during a home delivery.
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:
Immediate assistance is summoned, including obstetrical and anesthesia personnel.
Blood is brought to the delivery suite in case it may be needed.
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.
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.
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.
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.
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 (Risk Factors). 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.
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.
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.
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 Internal Iliac Artery Ligation can be used to prevent another inversion (Matsubara, 2009; Mondal, 2012). Occasionally, chronic puerperal uterine inversion may become apparent weeks after delivery.
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.
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 (“Fourth Stage” of Labor).
The levator ani muscles, described in Chapter 2 (Superficial Space of the Anterior Triangle), 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.
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.
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.
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.
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 Adjunctive Surgical Procedures to Treat Hemorrhage may be necessary to obtain hemostasis. For example, Lichtenberg (2003) described successful angiographic embolization for a high cervical tear after failed surgical repair.
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).
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.
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.
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.
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.
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 Angiographic Embolization 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).
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 (Uterine Rupture), 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 41-3Some Causes of Uterine Rupture ||Download (.pdf) TABLE 41-3 Some Causes of Uterine Rupture
|Preexisting Uterine Injury or Anomaly ||Uterine Injury or Abnormality Incurred in Current Pregnancy |
|Surgery involving the myometrium: |
Cesarean delivery or hysterotomy
Previously repaired uterine rupture
Myomectomy incision through or to the endometrium
Deep cornual resection of interstitial fallopian tube
Coincidental uterine trauma:
Abortion with instrumentation—sharp or suction curette, sounds
Sharp or blunt trauma—assaults, vehicular accidents, bullets, knives
Silent rupture in previous pregnancy
Pregnancy in undeveloped uterine horn
Defective connective tissue—Marfan or Ehlers-Danlos syndrome
|Before delivery: |
Persistent, intense, spontaneous contractions
Labor stimulation—oxytocin or prostaglandins
Intraamnionic instillation—saline or prostaglandins
Perforation by internal uterine pressure catheter
External trauma—sharp or blunt
Uterine overdistention—hydramnios, multifetal pregnancy
Internal version second twin
Difficult forceps delivery
Rapid tumultuous labor and delivery
Fetal anomaly distending lower segment
Vigorous uterine pressure during delivery
Difficult manual removal of placenta
Placental accrete syndromes
Gestational trophoblastic neoplasia
Sacculation of entrapped retroverted uterus
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.
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.
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).
The varied clinical presentations of uterine rupture and its management are discussed in detail in Chapter 31 (Uterine Rupture).
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. 47, Management of Trauma). 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.
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. 6-3, Maternal Blood Flow Disruption). 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.
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 (Hypovolemic Shock).
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.
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.
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. 47-11, Management of Trauma). 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. 24-13, Sinusoidal Heart Rate). Traumatic abruption is considered in more detail in Chapter 47 (Placental Injuries—Abruption or Tear).
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).
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. 35, Causes of Fetal Death).
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.
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 41-4Risk Factors for Placental Abruption ||Download (.pdf) TABLE 41-4 Risk Factors for Placental Abruption
|Risk Factor ||Relative Risk |
|Prior abruption ||10–50 |
|Increased age and parity ||1.3–2.3 |
|Preeclampsia ||2.1–4.0 |
|Chronic hypertension ||1.8–3.0 |
|Chorioamnionitis ||3.0 |
|Preterm ruptured membranes ||2.4–4.9 |
|Multifetal gestation ||2.1 |
|Low birthweight ||14.0 |
|Hydramnios ||2.0 |
|Cigarette smoking ||1.4–1.9 |
|Thrombophilias ||3–7 |
|Cocaine use ||NA |
|Uterine leiomyoma ||NA |
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).
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.
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 (Thrombophilias) and 59 (Antibodies against Natural Anticoagulants).
Especially if located near the mucosal surface behind the placental implantation site, uterine myomas can predispose to abortion or later to placental abruption (Chaps. 18, Cervical Insufficiency and 63, Pregnancy Complications).
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.
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.
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. 53, Acute Kidney Injury).
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 Pregnancy Outcomes.
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.
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).
Previously known as acute renal failure, acute kidney injury is a general term describing renal dysfunction from many causes (Chap. 53, Acute Kidney Injury). 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).
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 (Sheehan Syndrome).
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.
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.
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 Hypovolemic Shock, 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.
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.
If the fetus has died, then vaginal delivery is usually preferred. As reviewed on General Considerations, 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 Chronic Abruption, 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.
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.
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.
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.
Total placenta previa showing that copious hemorrhage could be anticipated with any cervical dilatation.
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 (Knots, Strictures, and Loops).
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.
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).
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.
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 (Placenta Accrete Syndromes). 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.
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 Risk Factors. 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 (Risk Factors).
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 (Placenta Accrete Syndromes). 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.
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 Blood Loss Estimation, 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 41-24B and 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.
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.
Transvaginal sonogram of a posterior 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 (Management).
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 (Management).
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 Internal Iliac Artery Ligation. Finally, pelvic artery embolization as described on Angiographic Embolization 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 (Peripartum Hysterectomy).
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.
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).
Placenta accrete syndromes. A. Placenta accreta. B. Placenta increta. C. Placenta percreta.
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. 31, Complications with Multiple Repeat Cesarean Deliveries). 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 41-2. In 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.
These are similar in many aspects to those for placenta previa (Incidence and Associated Factors). 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.
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. 14, MSAFP Elevation). 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.
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 (Cesarean Scar Pregnancy).
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.
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.
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 (Placental Site Involution), 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).
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 41-5Selected Maternal Outcomes in Women with Accrete Syndromes Identified Prenatally and Delivered in Tertiary-Care Units ||Download (.pdf) TABLE 41-5 Selected Maternal Outcomes in Women with Accrete Syndromes Identified Prenatally and Delivered in Tertiary-Care Units
|Outcomea ||San Diegob n = 62 ||Utahc n = 60 ||Torontod n = 33 |
|Gestational age (wk) ||33.9 ± 1.1 ||34 (17–41) ||∼ 32 (19–39) |
|Operating time (min) ||194 ± 1.6 ||NS ||107 (68–334) |
|Transfusions ||∼ 75% ||70% || |
| RBC (units) ||4.7 ± 2.2 ||≥ 4 (30%) ||3.5 (0–20) |
| FFP (units) ||4.1 ± 2.3 ||NS ||NS |
|Surgical outcomes || || || |
| Bladder injury ||14 (23%) ||22 (37%) ||10 (30%) |
| Ureteral injury ||5 (8%) ||4 (7%) ||0 |
|Postoperative || || || |
| ICU admission ||43 (72%) ||18 (30%) ||5 (15%) |
| LOS (days) ||7.4 ± 1.8 ||4 (3–13%) ||5 (2–13) |
| Readmission ||NS ||7 (12%) ||1 (3%) |
| Reoperation ||NS ||5 (8%) ||0 |
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 Angiographic Embolization, preoperative arterial catheterization may be beneficial (Desai, 2012).
There is some evidence that women with accrete syndromes have an increased risks for recurrence, uterine rupture, hysterectomy, and previa (Eshkoli, 2013).