Williams Manual of Pregnancy Complications, 23 ed.

CHAPTER 25. Placental Abruption

Placental abruption (or abruptio placentae) is defined as the premature separation of the normally implanted placenta. Placental abruption complicates approximately 1 in 200 deliveries. Some of the bleeding of placental abruption usually insinuates itself between the membranes and uterus, and then escapes through the cervix, causing external hemorrhage (Figure 25-1). Less often, the blood does not escape externally but is retained between the detached placenta and the uterus, leading to concealed hemorrhage (Figure 25-2). Placental abruption may be total or partial (Figure 25-3). Placental abruption with concealed hemorrhage carries with it much greater maternal hazards, not only because of the possibility of consumptive coagulopathy (see following discussion), but also because the extent of the hemorrhage may not be appreciated.


FIGURE 25-1 Hemorrhage from premature placental abruption. External hemorrhage: The placenta has detached peripherally, and the membranes between the placenta and cervical canal are detached from the underlying deciduas. This allows blood egress through the vagina. Concealed hemorrhage: The periphery of the placenta and the membranes are still adhered and blood remains within the uterus. Partial placenta previa: There is placental separation and external hemorrhage. (Reproduced, with permission, from Cunningham FG, Leveno KJ, Bloom SL, et al (eds). Williams Obstetrics. 23rd ed. New York, NY: McGraw-Hill; 2010.)


FIGURE 25-2 Total placental abruption with concealed hemorrhage and fetal death. (Reproduced, with permission, from Cunningham FG, Leveno KJ, Bloom SL, et al (eds). Williams Obstetrics. 23rd ed. New York, NY: McGraw-Hill; 2010.)


FIGURE 25-3 Partial placental abruption with adhered clot. (Reproduced, with permission, from Cunningham FG, Leveno KJ, Bloom SL, et al (eds). Williams Obstetrics. 23rd ed. New York, NY: McGraw-Hill; 2010.)

The primary cause of placental abruption is unknown, but there are several associated conditions. Some of these are listed in Table 25-1. By far the most commonly associated condition is some type of hypertension. This includes preeclampsia, gestational hypertension, or chronic hypertension. In cases of placental abruption so severe as to kill the fetus, maternal hypertension is apparent in about half of the women. Such hypertension may not be readily apparent until the depleted intravascular volume due to hemorrhage is adequately refilled. The incidence of placental abruption is increased as much as threefold in women with chronic hypertension and fourfold with severe preeclampsia.

TABLE 25-1. Risk Factors for Abruptio Placentae



Women with a history of a prior placental abruption have approximately a tenfold increased risk of recurrence in a subsequent pregnancy. Management of the subsequent pregnancy is made difficult in that the placental separation may occur suddenly at any time, even remote from term. In the majority of cases, fetal well-being is normal beforehand, and thus currently available methods of fetal evaluation are usually not predictive.


Bleeding with placental abruption is almost always maternal. In nontraumatic placental abruption, evidence for fetomaternal hemorrhage occurs in approximately 20 percent of cases and typically involves less than 10 mL. Significant fetal bleeding is more likely to be seen with traumatic abruption. In this circumstance, fetal bleeding results from a tear or fracture in the placenta rather than from the placental separation itself.


The more common signs and symptoms associated with placental abruption are listed in Table 25-2. It is emphasized, however, that the signs and symptoms with abruptio placentae can vary considerably. For example, external bleeding can be profuse, yet placental separation may not be so extensive as to compromise the fetus directly. Rarely, there may be no external bleeding but the placenta may be completely sheared off and the fetus dead.

TABLE 25-2. Signs and Symptoms in Women with Abruptio Placentae


In severe cases of placental abruption, the diagnosis is generally obvious. Milder and more common forms of abruption are difficult to recognize with certainty, and the diagnosis is often made by exclusion. Therefore, with vaginal bleeding complicating a viable pregnancy, it often becomes necessary to rule out placenta previa and other causes of bleeding by clinical inspection and ultrasound evaluation. It has long been taught, perhaps with some justification, that painful uterine bleeding means abruptio placentae, whereas painless uterine bleeding is indicative of placenta previa (see Chapter 26). Unfortunately, the differential diagnosis is not that simple. Labor accompanying placenta previa may cause pain suggestive of abruptio placentae. On the other hand, abruptio placentae may mimic normal or preterm labor, or it may cause no pain at all. The latter is more likely with a posteriorly implanted placenta. There are neither laboratory tests nor diagnostic methods that accurately detect lesser degrees of placental separation.

Consumptive Coagulopathy

One of the most common causes of clinically significant consumptive coagulopathy in obstetrics is placental abruption. Overt hypofibrinogenemia (less than 150 mg/dL) along with elevated levels of fibrin degradation products, D dimer, and variable decreases in other coagulation factors is found in about 30 percent of women with placental abruption severe enough to kill the fetus. At the outset, severe hypofibrinogenemia may or may not be accompanied by overt thrombocytopenia. After repeated blood transfusions, however, thrombocytopenia is common because stored blood is platelet poor. Such severe coagulation defects are seen less commonly in those cases in which the fetus survives.

Renal Failure

Acute renal failure due to profound blood loss may complicate placental abruption. Fortunately, reversible acute tubular necrosis accounts for three-fourths of cases of renal failure due to abruption. Even when placental abruption is complicated by severe intravascular coagulation and hemorrhage, prompt and vigorous treatment with blood and crystalloid solution will often prevent clinically significant renal dysfunction.

Couvelaire Uterus

Placental abruption may be complicated by widespread extravasation of blood into the uterine musculature and beneath the uterine serosa (Figure 25-4). This so-called uteroplacental apoplexy, first described by Couvelaire in the early 1900s, is now frequently called Couvelaire uterus. Such effusions of blood are also occasionally seen beneath the tubal serosa, in the connective tissue of the broad ligaments, and in the substance of the ovaries, as well as free in the peritoneal cavity. These myometrial hemorrhages seldom interfere with uterine contractions sufficiently to produce severe postpartum hemorrhage and are not an indication for hysterectomy.


FIGURE 25-4 Couvelaire uterus with 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. (Reproduced, with permission, from Cunningham FG, Leveno KJ, Bloom SL, et al (eds). Williams Obstetrics. 23rd ed. New York, NY: McGraw-Hill; 2010. Courtesy of Dr. Allison Smith.)


Treatment for placental abruption will vary depending upon gestational age and the status of the mother and fetus. With a live and mature fetus, and if vaginal delivery is not imminent, emergency cesarean delivery is preferred. With massive external bleeding, intensive resuscitation with blood plus crystalloid and prompt delivery to control the hemorrhage are lifesaving for the mother and, it is hoped, for the fetus (see Chapter 29). If the diagnosis is uncertain and the fetus is alive but without evidence of fetal compromise, very close observation, with facilities for immediate intervention, can be practiced.


When the fetus is dead or previable, there is no evidence that establishing an arbitrary time limit for delivery is necessary. Instead, maternal outcome depends upon the diligence with which adequate fluid and blood replacement therapy is pursued, rather than upon the interval to delivery.

If placental separation is so severe that the fetus is dead, vaginal delivery is preferred unless hemorrhage is so brisk that it cannot be successfully managed even by vigorous blood replacement or there are other obstetrical complications that prevent vaginal delivery. Serious coagulation defects are likely to prove especially troublesome with cesarean delivery. The abdominal and uterine incisions are prone to bleed excessively when coagulation is impaired. Hemostasis at the placental implantation site depends primarily upon myometrial contraction. Therefore, with vaginal delivery, stimulation of the myometrium pharmacologically and by uterine massage will cause these vessels to be constricted so that serious hemorrhage is avoided even though coagulation defects persist. Moreover, bleeding that does occur is shed through the vagina.

For further reading in Williams Obstetrics, 23rd ed.,

see Chapter 35, “Obstetrical Hemorrhage.”