Obstetrical Hemorrhage

OVERVIEW, IMPLICATIONS, AND CLASSIFICATION CAUSES OF OBSTETRICAL HEMORRHAGE CONSUMPTIVE COAGULOPATHY MANAGEMENT OF HEMORRHAGE SURGICAL MANAGEMENT OF HEMORRHAGE

Obstetrics is bloody business. Although medical advances have dramatically reduced the dangers of childbirth, death from hemorrhage still remains a leading cause of maternal mortality.

Hemorrhage - is a leading reason for admission of pregnant women to intensive care units-is the single most important cause of maternal death worldwide.

OVERVIEW, IMPLICATIONS, AND CLASSIFICATION

Fatal hemorrhage is most likely in circumstances in which blood or components are not available immediately.

women who are Jehovahs Witnesses have a 44-fold increased risk of maternal death because of hemorrhage

Establishment and maintenance of facilities that allow prompt administration of blood are absolute requirements for acceptable obstetrical care.

Generally speaking, obstetrical hemorrhage may be

antepartum such as with placenta previa or placental abruption

postpartumfrom uterine atony or genitaltract lacerations - more commonly

Incidence and Predisposing Conditions

The exact incidence of obstetrical hemorrhage is not known because of its imprecise definition as well as difficulty in its recognition and thus its diagnosis.

One indicator is the number of women transfused, and this has likely decreased because of prevailingconservative attitudes towards blood replacement.

using discharge statistics, it is apparent that hemorrhage is underreported.

Table 35-1 lists the many clinical circumstances in which risk of hemorrhage is appreciably increased. It is apparent that serious hemorrhage may occur at any time throughout pregnancy and the puerperium. Although the timing of bleeding is widely used to classify obstetrical hemorrhage, the term third-trimester bleeding is imprecise, and its use is notrecommended.

One factor not generally considered as predisposing to exsanguination is the lack of adequate obstetrical and anesthetic services.

Antepartum Hemorrhage

Slight vaginal bleeding is common during active labor. This bloody show is the consequence of effacement and dilatation of the cervix, with tearing of small vessels.

Uterine bleeding, however, coming from above the cervix, is cause for concern. It may follow some separation of a placenta implanted in the immediate vicinity of the cervical canalplacenta previa. It may come from separation of a placenta located elsewhere in the uterine cavityplacental abruption. Rarely, there may be velamentousinsertion of the umbilical cord, and involved placentalvessels may overlie the cervixvasa previa.

In such cases, hemorrhage may follow laceration of these vessels at the time of membrane rupture. The source of uterine bleeding is not always identified. Inthat circumstance, antepartum bleeding typically begins with few, if any, symptoms and then stops.

At delivery no anatomical cause is identified. In many of these cases, bleeding likely is the consequence of slight marginal placental separation. A pregnancy with such bleeding remains at increased risk for a poor outcome even though the bleeding soon stops and placenta previa appears to have been excluded by sonography.

women with uterine bleeding between 14 and 26 weeks and found that a fourth had placental abruption or previa. Total fetal loss rates including abortions and perinatal deaths were 32 percent.

unexplained antepartum hemorrhage before34 weeks was associated with a 62-percent risk of delivery within 1 week when associated with uterine contractions and with a 13-percent risk even in the absence of contractions.

In pregnancies with hemorrhage after 26 weeks not explained by placental abruption or previa, adverse outcomes in a third.

For this reason, delivery should be considered in any woman at term with unexplained vaginal bleeding.

Postpartum Hemorrhage

Postpartum hemorrhage describes an event rather than a diagnosis, and when encountered, its etiology must be determined.

Common causes include: bleeding from the placental implantation site trauma to the genital tract and adjacent structures or both (Table 35-2).

Definition

Postpartum hemorrhage (traditional def)-loss of 500 mL of blood or more after completion of the third stage of labor. This is problematic because half of all women delivered vaginally shed that amount of blood or more whenlosses are measured quantitatively (Fig. 35-2).

Pritchard and associates (1962) used precise methods and found that approximately 5 percent of women delivering vaginally lost more than 1000 mL of blood. They also reported that estimated blood loss is commonly only approximately half theactual loss. Because of this, estimated blood loss in excess of 500 mL should call attention to mothers who are bleeding excessively.

Toledo and colleagues (2007) have shown that calibrated drape markings improve estimation accuracy. Still, as shown by the study of Sosa and associates (2009) cited above, even this technique underestimates blood loss when compared with more precise methods described by Pritchard and colleagues (1962).

The blood volume of a pregnant woman with normal pregnancy-induced hypervolemia usually increases by 30 to 60 percent.This amounts to 1500 to 2000 mL for an average-sized woman.The equation that determines this is shown in Table 35-3.

This computation was constructed by studying blood volumes and blood losses in more than 100 women using chromium-51 labeled erythrocytes. A normallypregnant woman tolerates, without any remarkable decrease in postpartum hematocrit, a blood loss at delivery that approaches the volume of blood that she added during pregnancy. Thus, if blood loss is less than the amount added by pregnancy, the hematocrit stays the same acutely and during the first several days. It eventually increases as normal plasma volume shrinks postpartum.

Any time the postpartum hematocrit is lower than one obtained on admission for delivery, blood loss can be estimated as the sum of the calculated pregnancy hypervolemia plus 500 mL for each 3 volumes percent drop in the hematocrit.

Late Postpartum Hemorrhage.-Bleeding after the first 24 hours

Hemostasis at the Placental Site.

Near term, it is estimated that at least 600 mL/min of blood flows through the intervillous space

This flow is carried by the spiral arterieswhich average 120 in numberand their accompanying veins. With separation of the placenta, these vessels are avulsed.

Hemostasis at the placental implantation site is achieved

First by contraction of the myometrium that compresses this formidable number of relativelylarge vessels (Fig. 2-14, p. 25).

FIGURE 2-14 The smooth muscle fibers compress traversingblood vessels when contracted.

This is followed by subsequent clotting and obliteration of their lumens. Thus, adhered pieces of placenta or large blood clots that prevent effective myometrial contraction can impair hemostasis at the implantation site.

It is therefore readily apparent that fatal postpartum hemorrhage can result from uterine atony despite normal coagulation.

Conversely, if the myometrium within and adjacent to the denuded implantation site contracts vigorously, fatal hemorrhage from the placental implantation site is unlikely even in circumstanceswhen coagulation may be severely impaired.

Clinical Characteristics.

Postpartum bleeding may begin before or after placental separation.Instead of sudden massive hemorrhage, there usually is steady bleeding. At any given instant, it appears to be only moderate, but may persist until serious hypovolemia develops.

Especially with hemorrhage after placental delivery, constant seepage can lead to enormous blood loss.The effects of hemorrhage depend to a considerable degree on the nonpregnant blood volume and the corresponding magnitude of pregnancy-induced hypervolemia.

A treacherous feature of postpartum hemorrhage is the failure of the pulse and blood pressure to undergo more than moderate alterations until large amounts of blood have been lost.

The normotensive woman initially may actually become somewhat hypertensive in response tohemorrhage. Moreover, the already hypertensive woman may be interpreted to be normotensive although remarkably hypovolemic. Accordingly, hypovolemia may not be recognized until very late.

The woman with severe preeclampsia or eclampsia does not have normally expanded blood volume. Thus, these women are very sensitive to, or even intolerant of, what may be considered normal blood loss When excessive hemorrhage is suspected in the woman with severe preeclampsia, efforts should be made immediately to identify those clinical and laboratory findings that would prompt vigorous crystalloid and blood administration to resuscitate hypovolemia.

In some women after delivery, blood may not escape vaginally but instead may collect within the uterine cavity, which can become distended by 1000 mL or more of blood.

In some, the attendant may massage a roll of abdominal fat mistaken for the postpartum uterus. Thus, observation of the uterus postpartum mustnot be left to an inexperienced person.

Diagnosis

Except possibly when intrauterine and intravaginal accumulation of blood is not recognized, or in some instances of uterine rupture with intraperitoneal bleeding, the diagnosis of postpartum hemorrhage should be obvious. The differentiation between bleeding from uterine atony and that from genital tract lacerations is tentatively determined by predisposing risk factorsand the condition of the uterus (see Table 35-2).

Bleeding from lacerations If bleeding persists despite a firm, well-contracted uterus Bright red blood also suggests arterial blood

To confirm that lacerations are a cause of bleeding, careful inspection of the vagina, cervix, and uterus is essential.

Sometimes bleeding may be caused by both atony and trauma, especially after major operative delivery. If easily accessible, such as with conduction analgesia, inspection of the cervix and vagina should be performed after every delivery to identify hemorrhage from lacerations. Palpation of the uterine cavity and inspection of the cervix and entire vagina is essential after internal podalic version and breech extraction. The same is true when unusual bleeding is identified during the second stage of labor.

CAUSES OF OBSTETRICAL HEMORRHAGE1) Placental Abruption2) Placenta Previa3) Third-Stage Bleeding4) Uterine Atony5) Inversion of the Uterus6) Genital Tract Lacerations7) Puerperal Hematomas8) Rupture of the Uterus

Placental Abruption

Placental abruptionAbruptio placentae,Accidental hemorrhage (Great Britain)

-Placental separation from its implantation site before delivery

Latin term abruptio placentae means rending asunder of the placenta and denotes a sudden accident, which is a clinical characteristic ofmost cases.

The cumbersome term premature separation of thenormally implanted placenta is most descriptive. It differentiates the placenta that separates prematurely but is implanted some distance beyond the cervical internal os from one that is implanted over the cervical internal osthat is, placenta previa.

The bleeding of placental abruption typically insinuates itself between the membranes and uterus, ultimately escaping through the cervix, causing external hemorrhage (Fig. 35-3).

Less often, the blood does not escape externally but is retained between the detached placenta and the uterus, leading to concealed hemorrhage (Fig. 35-3).

As shown in Figures 35-4 and 35-5, placental abruption may be total or partial. Concealed hemorrhage carries much greater maternal and fetal hazards. This is not only because of possible consumptive coagulopathy, but also because the extent of the hemorrhage is not readily appreciated, and the diagnosis typically is delayed.

Significance and Frequency

Abruption severity often depends on how quickly the woman is seen following symptom onset. With delay, the likelihood of extensive separation causing fetal death is increased remarkably.

The frequency with which placental abruption is diagnosed varies because of different criteria, but the reported frequency averages 1 in 200 deliveries.

Both incidence and severity have decreased over time. As the number of highparity women giving birth decreased and as availability of prenatal care and emergency transportation improved, the frequencyof abruption causing fetal death dropped.

Perinatal Morbidity and Mortality

Although the rates of fetal death from abruption have declined, they remain especially prominent as stillbirth rates from other causes have decreased.

Inc perinatal mortality low-birthweight perinates (also d/t preterm) increased serious adverse sequelae in infants who survive: significant neurological deficits within the first year of lifecerebral palsy

Etiology and Associated Factors

The primary cause of placental abruption is unknown, but several associated conditions are listed in Table 35-4.

Age, Parity, Race, and Familial Factors.

Age: >35 y/o

Parity: higher in women of great parity, Tooheydid not find this.

Race or ethnicity---important: African-American Caucasian women

Familial association. If a woman had a severeabruption, then the risk for her sister was doubled, and the heritability risk was estimated to be 16 %

Hypertension. The most common condition associated with placental abruption is some type of hypertensiongestational hypertension, preeclampsia, chronic hypertension, or combinations of these. In the

The severity of hypertension does not necessarily correlate with the incidence of abruption

Prematurely Ruptured Membranes and PretermDelivery.

There is no doubt that there is an increased incidenceof abruption when the membranes rupture before term.This risk was further increased with infection. has suggested that inflammation and infection may be the primary cause of placental abruption

They also reported a strong association with low birthweight principally due to perterm delivery, but not growth restriction.

Smoking. cigarette smoking is assoc w/ abruption twofold risk for abruption in smokers5 to 8 fold if w/ chronic hypertension severe preeclampsia

Cocaine.Women who used cocaine have an alarming frequency of placental abruption.stillbirths caused by placental abruption

Thrombophilias. Over the past decade, a number of inheritedor acquired thrombophilias have been associated with thromboembolic disorders during pregnancy.

Some of these disorders for example factor V Leiden or prothrombin gene mutation are associated with placental abruption and infarction as well as preeclampsia.

Traumatic Abruption.

In some cases of external trauma, usuallyassociated with motor vehicle accidents or physical violence, placental separation may follow.

However, as placental abruption incidence has declined over the years, traumatic abruptions have become relatively more common.

abruption can be caused by relatively minor trauma

Moreover, a nonreassuring fetal heart rate tracing is not always immediately associated with evidence of placental separation.

Leiomyomas.

These tumors, especially if located behind theplacental implantation site, predispose to abruption RETROPLACENTA

Recurrent AbruptionA woman who has suffered a placental abruptionespecially that caused fetal deathhas a high recurrence rate.

Management of a pregnancy subsequent to an abruption is thus difficult because another separation may suddenly recur, even remote from term. In many of these recurrences, fetal wellbeing is reassuring beforehand. Thus, antepartum fetal testing isusually not predictive.

PathologyPlacental abruption is initiated by hemorrhage into the decidua basalis. The decidua then splits, leaving a thin layer adhered to the myometrium. Consequently, the process in its earliest stages consists of the development of a decidual hematoma that leads to separation, compression, and ultimate destruction of the placenta adjacent to it. Histological evidence of inflammation more commonly in cases of placental abruption than in normal controls. inflammationinfectionmay be a contributor to causal pathways

In its early stage, there may be no clinical symptoms, and the separation is discovered upon examination of the freshly delivered placenta. In these cases, there is a circumscribed depression on the placentas maternal surface. It usually measures a few centimeters in diameter and is covered by dark, clotted blood.

Because several minutes are required for these anatomical changes to materialize, a very recently separated placenta may appear to be totally normal at delivery.

The age of the retroplacental clot cannot be determined exactly. In the example shown in Figure 35-5, a substantive-sized dark clot is well formed, it has depressed the placental bulk, and it likely is several hours old.

In some instances, a decidual spiral artery ruptures to cause a retroplacental hematoma, which as it expands, disrupts more vessels to separate more placenta (see Fig. 27-3, p. 579). The area of separation rapidly becomes more extensive and reaches the margin of the placenta. Because the uterus is still distended by the products of conception, it is unable to contract sufficiently to compress the torn vessels that supply the placental site. The escaping blood may dissect the membranes from the uterine wall and eventually appear externally or may be completely retained within the uterus (see Figs. 35-3 and 35-4).

Concealed Hemorrhage. Retained or concealed hemorrhage is likely when:

There is an effusion of blood behind the placenta, but its margins still remain adhered

The placenta is completely separated, yet the membranes retain their attachment to the uterine wall

Blood gains access to the amnionic cavity after breaking through the membranes

The fetal head is so closely applied to the lower uterine segment that blood cannot make its way past.

Most often, however, the membranes are gradually dissected off the uterine wall, and blood sooner or later escapes.

Chronic Placental Abruption. In some women, hemorrhage with retroplacental hematoma formation is somehow arrested completely without delivery. We have been able to document this phenomenon by labeling maternal red cells with chromium-51. In one case, red blood cells were concealed as a 400-mL clot, which was found within the uterus at delivery 3 weeks later. The clot contained no radiochromium, whereas peripheralblood at that time did. The blood in the clot thereforehad accumulated before the erythrocytes were labeled.

Some cases of abruption first develop very early in pregnancy. There is an association between abnormally elevated maternal serum markers in thefirst trimester and subsequent abruption. ..first and second-trimester bleeding with placental abruption in the third trimester.

Fetal-to-Maternal Hemorrhage.

Bleeding with placental abruption is almost always maternal. This is logical because the separation is within the maternal decidua.

In 78 women with a nontraumatic placental abruption, we found evidence of fetal to- maternal hemorrhage in 20 %. In all, the volume of fetalblood was less than 10 mL.

Conversely, significant fetal bleeding is much more likely with traumatic abruption. In this circumstance, fetal bleeding results from a tear or fracture in the placenta rather than from the placental separation itself.

Clinical DiagnosisThe signs and symptoms of placental abruption can vary considerably.

For example, external bleeding can be profuse, yetplacental separation may not be so extensive as to compromise the fetus.

Rarely, there may be no external bleeding, but the placenta may be completely sheared off and the fetus dead as the direct consequence.

In one unusual case, a multiparous woman near term presented to Parkland Hospital because of a nosebleed. There was no abdominal or uterine pain or tenderness and no vaginal bleeding, but her fetus was dead. Her blood did not clot, and the plasma fibrinogen level was 25 mg/dL. Labor was induced,and at delivery a total abruption with fresh clots was found.

vaginal bleeding - 78 % uterine tenderness or back pain - 66 % fetal distress - 60 % frequent uterine contractions uterine hypertonus

In 22 percent, preterm labor was initially diagnosed until subsequent fetal death or distress developed.

Sonography infrequently confirms the diagnosis of placental abruption at least acutely, because the placenta and fresh clot have similar sonographic appearances.Importantly, negative findings with sonographic examination do not exclude placental abruption.

Differential Diagnosis.

With severe placental abruption, the diagnosis generally is obvious. Milder and more common formsof abruption may be difficult to recognize with certainty, and the diagnosis is often made by exclusion. Unfortunately, neither laboratory tests nor diagnostic methods are available to detect lesser degrees of placental separation accurately.

Therefore, with vaginal bleeding in a pregnancy with a live fetus, it often becomes necessary to exclude placenta previa and other causes of bleeding by clinical and sonographic evaluation.

Clinically, it has long been taughtperhaps with some justification that

painful uterine bleeding signifies placental abruption

painless uterine bleeding signifies 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 vaginalbleeding remains obscure even after delivery.

Shock. It was once held that the shock sometimes seen with placental abruption was disproportionate to the amount of hemorrhage.

Supposedly, placental thromboplastin enters the maternal circulation and incites intravascular coagulation and other features of the amnionic fluid embolism syndrome (see p. 788).This rarely happens, and hypovolemic shock is instead directly due tomaternal blood loss.

women with abruption so severe as to kill the fetus, blood loss often amounted to at least half of the pregnant blood volume.

Conversely, neither hypotension nor anemia is obligatory even with extreme concealed hemorrhage. Oliguria from inadequate renal perfusion that is observed in these circumstances is responsiveto vigorous intravenous fluid and blood infusion.

Consumptive Coagulopathy. Placental abruption is one of the most common causes of clinically significant consumptive coagulopathy in obstetrics.

changes in coagulation factorshypofibrinogenemiaplasma levels 35 years old Multiparity: para 5 or greater Multifetal gestations Prior cesarean delivery

Smoked cigarettes - carbon monoxide hypoxemia caused compensatory placental hypertrophy

Unexplained elevated screening levels of maternal serum alpha-fetoprotein (MSAFP)

Prior uterine incision with a previa increases the likelihood that cesarean hysterectomy will be necessaryto control bleeding from a placenta accreta, increta, or percreta

FindingsPainless hemorrhage - the most characteristic event in placenta previa usually does not appear until near the end of thesecond trimester or after.

However, bleeding may begin earlier, and some abortions may result from such an abnormal location of the developing placenta.

With many previas, bleeding begins without warning andwithout pain in a woman who has had an uneventful prenatal course. Fortunately, the initial bleeding is rarely so profuse as to prove fatal. Usually it ceases, only to recur. In some women, particularly those with a placenta implanted near but not over the cervical os, bleeding does not appear until the onset of labor. Then, it may vary from slight to profuse and clinically may mimic placental abruption.

The cause of hemorrhage is reemphasized: When the placenta is located over the internal os, the formation of the lower uterine segment and the dilatation of the internal os result inevitably in tearing of placental attachments. The bleeding is augmented by the inherent inability of myometrial fibers of the lower uterine segment to contract and thereby constrict the avulsed vessels.

Hemorrhage from the implantation site in the lower uterine segment may continue after placental delivery because the lower uterine segment contracts poorly. Bleeding may also result from lacerations in the friable cervix and lower uterine segment, especially following manual removal of a somewhat adhered placenta.

Placenta Accreta, Increta, and Percreta. Placenta previa may be associated with placenta accreta or one of its more advanced forms, placenta increta or placenta percreta. Such abnormally firm attachment of the placenta might be anticipated because of poorly developed decidua in the lower uterine segment.

Coagulation Defects. In our experience, coagulopathy is rare with placenta previa, even when there is extensive separation from the implantation site.

Presumably thromboplastin, which incites intravascular coagulation that commonly characterizes placental abruption, readily escapes through the cervical canal rather than being forced into the maternal circulation.

DiagnosisPlacenta previa or abruption should always be suspected in women with uterine bleeding during the latter half of pregnancy.

The possibility of placenta previa should not be dismisseduntil sonographic evaluation has clearly proved its absence. The diagnosis can seldom be established firmly by clinical examination unless a finger is passed through the cervix and the placenta is palpated. Such digital cervical examination is never permissible unless the woman is in an operating room with all the preparations for immediate cesarean delivery even the gentlest digital examination can cause torrential hemorrhage. Furthermore, this type of examination should not be performed unless delivery is planned, for it may cause bleeding that necessitates immediate delivery. This double set-up examination is rarely necessary because placental location can almost always be ascertained by sonography.Sonographic Localization. The simplest, safest, and most accurate method of placental localization is provided by transabdominalsonography (Fig. 35-13A).

False-positive results are often a result of bladder distension. Therefore, scans in apparently positive casesshould be repeated after emptying the bladder.

An uncommon source of error has been identification of abundant placenta implanted in the uterine fundus but failure to appreciate that the placenta was large and extended downward all the way to the internal cervical os.

The use of transvaginal sonography has substantively improved diagnostic accuracy of placenta previa (Figs. 35-13B and 35-14). Although it may appear dangerous to introduce an ultrasound probe into the vagina in suspected cases, the technique has been shown to be safe

Transperineal sonography was reported accurate to localize placenta previa.

Magnetic Resonance (MR) Imaging. A number of investigators have used MR imaging to visualize placental abnormalities, including previa. Although there are many positive attributes to its use, it is unlikely that MR imaging will replace sonographic scanning for routine evaluation in the near future.

Placental Migration. Sanderson and Milton (1991) studied 4300 womenat 18 to 20 weeks and found that 12 percent of placentas were low lying. Of those not covering the internal os, previa did not persist and hemorrhage was not encountered. Conversely, of those covering the os at midpregnancy, approximately 40 percent persisted as a previa. Thus, placentas that lie close to the internal osbut not over itduring the second trimester or early third trimester are unlikely to persist as a previa by term.

As shown in Figure 35-15, the likelihood that placenta previa persists after being identified sonographically before 28 weeks is greater in women who have had a prior cesarean delivery

In the absence of any other abnormality, sonography need not be frequently repeated simply to follow placental position.

Restriction of activity is not necessary unless a previa persists beyond 28 weeks or becomes clinically apparent before that time.

The mechanism of apparent placental movement is notcompletely understood. That said, migration is clearly a misnomer because decidual invasion by chorionic villi on either side of the cervical os persists. The apparent movement of the low-lying placenta relative to the internal os probably results from inability to precisely define this relationship in a three dimensional manner using two-dimensional sonography in early pregnancy. This difficulty is coupled with differential growth of lower and upper myometrial segments as pregnancy progresses. Thus, those placentas that migrate most likely never had actual circumferential villus invasion that reached the internal cervical os in the first place.

Management of Placenta PreviaWomen with a previa may be considered in one of the following categories:

The fetus is preterm and there are no other indications for delivery The fetus is reasonably mature Labor has ensued Hemorrhage is so severe as to mandate delivery despite gestational age.

Management with a preterm fetus, but without persistent active uterine bleeding, consists of close observation. For some women, prolonged hospitalization may be ideal. However, a woman is usually discharged after bleeding has ceased and her fetus judged to be healthy. The woman and her family must fully appreciate the possibility of complications and be prepare to transport her to the hospital immediately. In properly selectedpatients, there appears to be no benefit to inpatient versus outpatient management of placenta previa

Importantly, there are no differences in maternal or fetal morbidity rates with outpatient versus inpatient observation.

DeliveryCesarean delivery is necessary in practically all women with placenta previa. Most often, a transverse uterine incision is possible. However, because fetal bleeding may result from a transverse incision into an anterior placenta, a vertical incision is sometimes employed. But, even when the incision extends through the placenta, maternal or fetal outcomes are rarely compromised.

Ward (2003) described an alternative surgical technique in which a cleavage plane is developed following the uterine incision. The operator undermines the placenta toward the closest edge until the membranes are palpable and they are then ruptured with the fetus delivered around the intact placenta. This approach has not yet been evaluated in controlled studies.

Because of the poorly contractile nature of the lower uterine segment, there may be uncontrollable hemorrhage following placental removal. When bleeding from the placental bed cannot be controlled by conservative means, other methods can be attempted.Oversewing the implantation site with 0-chromic suturesmay provide hemostasis. In some women, bilateral uterine or internal iliac artery ligation may provide hemostasis. Cho and colleagues (1991) described placinginterrupted 0-chromic sutures one centimeter apart and forming a sutured circle around the bleeding portion of the lower segment. This method controlled hemorrhage in all eight women in whom it was employed. Druzin (1989) described four cases in which the lower uterine segment was tightly packed with gauze that successfully arrested hemorrhage. The pack was removed transvaginally 12 hours later. Pelvic artery embolization as also has gained acceptance.

If such conservative methods fail, and bleeding is brisk, then hysterectomy is necessary For women whose placenta previa is implanted anteriorly in the site of a prior hysterotomy incision, there is an increased likelihood of associated placenta accreta and need for hysterectomy.

Maternal and Perinatal OutcomesPlacenta previa is an important cause of maternal morbidity and mortality.

Preterm delivery as a result of placenta previa is a major cause of perinatal death. Some of this risk appears related to fetal-growth restriction and limited prenatal care. And although suspected by some investigators, an association of increased congenital malformations and previa was not confirmed until relatively recently by Crane(1999).

Third-Stage BleedingSome bleeding is inevitable during the third stage of labor as the result of transient partial separation of the placenta. As the placenta separates, blood from the implantation site may escapeinto the vagina immediatelythe Duncan mechanism of placentalseparation. Alternately, it may be concealed behind theplacenta and membranes until the placenta is deliveredtheSchultze mechanism.In the presence of any external hemorrhage during the thirdstage, the uterus should be massaged if it is not contractedfirmly. If the signs of placental separation have appeared, expressionof the placenta should be attempted by manual fundalpressure as described in Chapter 17 (p. 398). Descent of theplacenta is indicated by the cord becoming slack. If bleedingcontinues, manual removal of the placenta may be necessary.Delivery of the placenta by cord traction, especially when the uterusis atonic, may cause uterine inversion. Prevention and managementof this complication are discussed in detail on page 780.Bleeding with Prolonged Third StageIn some cases, the placenta does not separate promptly. There isstill no definite answer to the question concerning the length of time that should elapse in the absence of bleeding before the placentais removed manually. Obstetrical tradition has set somewhatarbitrary limits on third-stage duration in attempts to defineabnormally retained placenta and thus, to reduce blood loss fromprolonged placental separation. Combs and Laros (1991) studied12,275 singleton vaginal deliveries and reported the medianthird-stage duration to be 6 minutes, and for 3.3 percent of thesewomen, it was more than 30 minutes. Several measures of hemorrhage,including curettage or transfusion, increased when thethird stage was approximately 30 minutes or longer. Prolongedthird-stage labor is discussed in Chapter 17 (p. 397).Technique of Manual Placental RemovalAdequate analgesia is mandatory, and aseptic surgical techniqueshould be used. After grasping the fundus through the abdominalwall with one hand, the other hand is introduced into the vaginaand passed into the uterus, along the umbilical cord. As soon asthe placenta is reached, its margin is located, and the border of thehand is insinuated between it and the uterine wall (Fig. 35-16).Then with the back of the hand in contact with the uterus, the placentais peeled off its uterine attachment by a motion similar tothat used in separating the leaves of a book. After its complete separation,the placenta should be grasped with the entire hand,which is then gradually withdrawn. Membranes are removed atthe same time by carefully teasing them from the decidua, usingring forceps to grasp them as necessary. Another method is to wipeout the uterine cavity with a laparotomy sponge.Management after Placental DeliveryThe fundus should always be palpated following either spontaneousor manual placental delivery to confirm that the uterus iswell contracted. If it is not firm, vigorous fundal massage is indicated.Most evidence suggests that uterine massage preventspostpartum hemorrhage from atony (Hofmeyr and associates,2008). Typically, 20 U of oxytocin in 1000 mL of lactatedRinger or normal saline proves effective when administered intravenouslyat approximately 10 mL/min200 mU of oxytocinper minutesimultaneously with effective uterine massage.Oxytocin should never be given as an undiluted bolusdose, because serious hypotension or cardiac arrhythmias mayoccur (see Chap. 17, p. 399). Uterine AtonyFailure of the uterus to contract properly following delivery isthe most common cause of obstetrical hemorrhage. In manywomen, uterine atony can at least be anticipated well in advanceof delivery (Table 35-2). Although risk factors are well known,the ability to identify which individual woman will experienceatony is limited. Rouse and colleagues (2006) studied 23,900women undergoing primary cesarean delivery and reported thathalf of those women experiencing atony had no risk factors.The overdistended uterus is prone to be hypotonic after delivery.Thus, women with a large fetus, multiple fetuses, or hydramniosare prone to uterine atony. The woman whose labor is characterizedby uterine activity that is either remarkably vigorous orbarely effective is also likely to bleed excessively from postpartumatony. Similarly, labor either initiated or augmented with oxytocicsis more likely to be followed by atony and hemorrhage.High parity may be a risk factor for uterine atony. Fuchs andcolleagues (1985) described outcomes of nearly 5800 womenpara 7 or greater. They reported that the 2.7-percent incidenceof postpartum hemorrhage was increased fourfold comparedwith that of the general obstetrical population. Babinszki andcolleagues (1999) reported the incidence of postpartum hemorrhageto be 0.3 percent in women of low parity, but it was 1.9percent in those para 4 or greater.Another risk is if the woman has had a prior postpartum hemorrhage.Finally, attempts to hasten placental delivery may incite atony. Constant kneading and squeezing of the uterus that alreadyis contracted likely impedes the physiological mechanism of placentaldetachment, causing incomplete placental separation and increasedblood loss.Retained Placental FragmentsImmediate postpartum hemorrhage is seldom caused by retainedplacental fragments, but a remaining piece of placenta is a commoncause of bleeding late in the puerperium. Inspection of theplacenta after delivery should be routine. If a portion is missing,the uterus should be explored and the fragment removed, particularlywith continuing postpartum bleeding. Retention of a succenturiatelobe is an occasional cause of postpartum hemorrhage(see Chap. 27, p. 577). The late bleeding that may result from aplacental polyp is discussed in Chapter 30 (p. 648).Uterotonic AgentsA number of compounds are used to cause the postpartumuterus to contract.Oxytocin. In most units, after placental delivery is accomplished,oxytocin is given intravenously or intramuscularly, asdescribed in Chapter 17 (p. 399). This or other oxytocics willprevent most cases of uterine atony.Ergot Derivatives. If oxytocin does not prove effective to reverseuterine atony, we usually administer 0.2 mg of methylergonovineintramuscularly. This may stimulate the uterus tocontract sufficiently to control hemorrhage. Any superiortherapeutic effects of ergot derivatives compared with those ofoxytocin are speculative. Importantly, if ergot agents are intravenouslyadministered, they may cause dangerous hypertension,especially in women with preeclampsia.Prostaglandin Analogs. The 15-methyl derivative ofprostaglandin F2_carboprost tromethaminehas been approvedsince the mid-1980s for treatment of uterine atony. Theinitial recommended dose is 250 _g (0.25 mg) given intramuscularly.This is repeated if necessary at 15- to 90-minute intervalsup to a maximum of eight doses. Oleen and Mariano(1990) studied its use for postpartum hemorrhage at 12 obstetricalunits. Arrest of bleeding was considered successful in 88percent of 237 women treated. Another 7 percent requiredother oxytocics for control of hemorrhage. The remaining5 percent required surgical intervention.Carboprost is associated with side effects in approximately20 percent of women (Oleen and Mariano, 1990). In descendingorder of frequency, these include diarrhea, hypertension,vomiting, fever, flushing, and tachycardia. We have encounteredserious hypertension in a few women so treated. AndHankins and colleagues (1988) observed that intramuscularcarboprost was followed within 15 minutes by arterial oxygendesaturation that averaged 10 percent. They concluded that thiswas due to pulmonary airway and vascular constriction.Rectally administered prostaglandin E2 20-mg suppositoriesare used for uterine atony but have not been studied in clinicaltrials. A few reports have suggested that synthetic prostaglandinE1 analogmisoprostol or Cytotecmay be effective for thetreatment of atony (Abdel-Aleem and associates, 2001; OBrienand colleagues, 1998). In a recent Cochrane review, however,Mousa and Alfirevic (2007) reported no benefit to misoprostolcompared with standard therapy with oxytocin and ergometrine.Only three studies met the stringent criteria for inclusion,and all dosing regimens were different.Misoprostol has also been evaluated for prophylaxis of postpartumhemorrhage. In a randomized trial, Derman and coworkers(2006) compared a 600-_g oral dose with placebogiven at delivery. Postpartum hemorrhage was significantly reducedfrom 12 to 6 percent, and severe hemorrhage from 1.2 to0.2 percent with misoprostol use. However, based on theirstudy of 325 women, Gerstenfeld and Wing (2001) concludedthat 400 _g of misoprostol administered rectally was no moreeffective than intravenous oxytocin in preventing postpartumhemorrhage. And in their systematic review, Villar and coworkers(2002) reported that oxytocin and ergot preparationsadministered during third-stage labor were more effective thanmisoprostol for prevention of postpartum hemorrhage.Bleeding Unresponsive to OxytocicsContinued bleeding after multiple administrations of oxytocicsmay be from unrecognized genital tract lacerations, including insome cases uterine rupture. Thus, if bleeding persists, no timeshould be lost in haphazard efforts to control hemorrhage, butthe following management steps should be initiated immediately:1. Initiate bimanual uterine compression, a simple procedurethat controls most uterine hemorrhage (Fig. 35-17). Thistechnique consists of massage of the posterior aspect of theuterus with a hand on the abdomen and massage throughthe vagina of the anterior uterine wall with the other handmade into a fist.2. Call for help! 3. Add a second large-bore intravenous catheter so that crystalloidwith oxytocin may be continued at the same timeblood is given.4. Begin blood transfusions. The blood group of every obstetricalpatient should be known, if possible, before labor, and anindirect Coombs test done to detect erythrocyte antibodies.If the latter is negative, then crossmatching of blood is notnecessary (see p. 793). In an extreme emergency, type O,D-negative universal donor blood is given.5. Explore the uterine cavity manually for retained placentalfragments or lacerations.6. Thoroughly inspect the cervix and vagina for lacerationsafter adequate exposure.7. Insert a Foley catheter to monitor urine output, which is agood measure of renal perfusion.8. Begin volume resuscitation as described subsequently onpage 791.Blood transfusion should be considered in any woman withpostpartum hemorrhage in whom abdominal uterine massageand oxytocic agents fail to control bleeding. With transfusionand simultaneous manual uterine compression and intravenousoxytocin, additional measures are rarely required.Surgical Management of Uterine AtonyWith intractable atony unresponsive to the above measures,surgical intervention can be lifesaving. In our experience,uterine artery ligationdiscussed on page 795is less helpfulfor hemorrhage from uterine atony compared with its use forhysterotomy extensions at cesarean delivery. It is also debatablewhether internal iliac artery ligation is beneficial for uterineatony (Clark and colleagues, 1985). From India, Joshi andco-workers (2007) described 36 women who had the procedurefor postpartum atonya third of those required hysterectomy.Our concern, in addition to an inherently highfailure rate, is that the procedure, discussed on page 796, istechnically difficult and consumes valuable time if hysterectomyis necessary.Uterine Compression Sutures. In 1997, B-Lynch and colleaguesdescribed a surgical technique for severe postpartumatony in which a pair of vertical brace, #2-chromic sutureswere secured around the uterus. When tightened and tied,they give the appearance of suspendersor bracesthat compressthe anterior and posterior walls together (Fig. 35-18).Price and B-Lynch (2005) summarized 17 reports in which 44of 46 procedures were successful. In another preliminary report,B-Lynch (2005) cited 948 cases with only seven failures.Our experiences are not nearly so successful, but the techniquecertainly is effective in some cases. A number of modificationsof the B-Lynch technique have been described (Bhal,2005; Cho, 2000; Ghezzi, 2007; Hayman, 2002; Pereira,2005, and all their colleagues).Reports of complications from compression sutures havebeen slowly emerging. At this time, their incidence is unknownbut is likely low. Uterine ischemic necrosis with peritonitis hasbeen described in several case reports (Gottlieb, 2008; Joshi,2004; Ochoa, 2002; Treloar, 2006, and all their colleagues). Thewomen described by Akoury and Sherman (2008) had oneB-Lynch suture and two Cho sutures and were found to haveone large triangular and two smaller defects in the uterine wall ina subsequent pregnancy. Total ischemic uterine necrosis developedin a woman described by Friederich and associates (2007).In addition to B-Lynch compression sutures, the woman alsohad bilateral ligation of uterine, uterovarian, and round ligamentarteries.Uterine PackingThis technique should be considered in women with refractorypostpartum hemorrhage related to uterine atony who wish topreserve fertility. Popular during the first half of the 20th century,uterine packing subsequently fell from favor because ofconcerns about concealed bleeding and infection (Hsu and coworkers,2003). Newer techniques, however, have allayed someof these concerns (Roman and Rebarber, 2003). In one technique,the tip of a 24F Foley catheter with a 30-mL balloon isguided into the uterine cavity and filled with 60 to 80 mL ofsaline. The open tip permits continuous drainage from theuterus. If bleeding subsides, the catheter is typically removed after12 to 24 hours. Alternatively, the uterus or pelvis may bepacked directly with gauze (Gilstrap, 2002). Placenta Accreta, Increta, and PercretaIn most instances, the placenta separates spontaneously fromits implantation site during the first few minutes after deliveryof the infant. Infrequently, detachment is delayed because theplacenta is unusually adhered to the implantation site. In thesecases, the decidua is scanty or absent, and the physiological lineof cleavage through the decidual spongy layer is lacking. As aconsequence, one or more placental lobules, also termed cotyledons,are firmly bound to the defective decidua basalis or evento the myometrium. When the placenta is densely anchored inthis fashion, the condition is called placenta accreta. Varyingdegrees of accreta cause significant morbidity and at times,mortality from severe hemorrhage, uterine perforation, andinfection.DefinitionsThe term placenta accreta is used to describe any implantationin which there is abnormally firm adherence to the uterine wall.As the consequence of partial or total absence of the deciduabasalis and imperfect development of the fibrinoid or Nitabuchlayer, placental villi are attached to the myometrium in placentaaccreta (Fig. 35-19A). With placenta increta, villi actually invadeinto the myometrium (Fig. 35-19B). Finally, with placentapercreta, villi penetrate through the myometrium (Fig.35-19C). The abnormal adherence may involve all lobulestotalplacenta accretaas was the case in Figure 35-20A. Or, it mayinvolve only a few to several lobulespartial placenta accretasuch as shown in Figure 35-20B. All or part of a single lobulemay be attachedfocal placenta accreta. According toBenirschke and colleagues (2006), histological diagnosis cannotbe made from the placenta alone, and the entire uterus or curettingswith myometrium are necessary for histopathological confirmation IncidenceOver the past few decades, the incidences of placenta accreta,increta, and percreta have increased. This is because of the increasingcesarean delivery rate (see Chap. 25, p. 544). TheAmerican College of Obstetricians and Gynecologists (2002)estimated that placenta accreta complicates 1 in 2500 deliveries.From their review, Stafford and Belfort (2008) cite the incidenceof approximately 1 in 2500 in the 1980s, 1 in 535 in2002, and 1:210 in 2006. For some time, it has been a leadingcause of intractable postpartum hemorrhage requiring emergencyperipartum hysterectomy (Zelop and colleagues, 1993).And as shown in Figure 35-1, various forms of accreta are a substantivecause of maternal deaths from hemorrhage.Associated ConditionsDecidual formation is commonly defective in the lower uterinesegment over a previous cesarean delivery scar or after uterinecurettage. In a review of 622 cases of placenta accreta collected between1945 and 1969, Fox (1972) reported that: (1) a third ofcases had placenta previa, (2) a fourth had a prior cesarean delivery, (3) nearly a fourth had previously undergone curettage, and (4) afourth were gravida 6 or more. Zaki and associates (1998) foundthat 10 percent of 112 consecutive cases of placenta previa had associatedaccreta. Hardardottir and colleagues (1996) observed thatalmost 50 percent of placentas in women with a prior cesareandelivery had adhered myometrial fibers detected microscopically.There are risk factors for placenta accreta that have come tolight with MSAFP screening for neural-tube defects and aneuploidies(see Chap. 13, p. 289). Hung and co-workers (1999)analyzed outcomes of more than 9300 women screened forDown syndrome at 14 to 22 weeks. They reported a 54-fold increasedrisk for accreta in women with placenta previa. The riskfor accreta was increased eightfold when MSAFP levels exceeded2.5 MoM; it was increased fourfold when maternal free_-hCG levels were greater than 2.5 MoM; and it was increasedthreefold when maternal age was 35 years or older.Clinical Course and DiagnosisIn the first trimester, as discussed in Chapter 10 (p. 253), abnormalmyometrial invasion may manifest as a cesarean scar pregnancy(Ash and associates, 2007). According to their review, Rotas andcolleagues (2006) reported this type of ectopic pregnancy to be increasingin frequency and cited an incidence of approximately 1 in2000 pregnancies. If pregnancy advances, placental villi at the siteof a previous cesarean scar may lead to uterine rupture before labor(Liang and co-workers, 2003). Antepartum hemorrhage with placentaaccreta is common and usually the consequence of coexistingplacenta previa. In many cases, placenta accreta is not identifieduntil third-stage labor. In this setting, an adhered placenta, asdescribed on page 775, is encountered.Perioperative EvaluationEfforts are ongoing to better identify placental ingrowth antepartum.Lam and colleagues (2004) found that sonographywas only 33-percent sensitive for detecting placenta accreta.With sonographic Doppler color flow mapping-such as shownin Figure 35-21, Twickler and colleagues (2000) reported thattwo factors were highly predictive of myometrial invasion: (1) adistance less than 1 mm between the uterine serosa-bladder interfaceand the retroplacental vessels, and (2) identification oflarge intraplacental lakes. These had a sensitivity of 100 percentand positive-predictive value of 78 percent. Chou and co-workers(2001) also described successful use of three-dimensional colorDoppler imaging for diagnosis of placenta percreta.Magnetic resonance (MR) imaging is used as an adjunct tosonography when there is strong clinical suspicion of an accreta.Warshak and colleagues (2006) described a two-step protocol inwhich MR imaging was used if sonography was inconclusive.They reported that 23 of 26 cases of placenta accreta were accuratelypredicted, and 14 of 14 were correctly excluded. Lax andco-workers (2007) identified three MR imaging findings thatsuggested accreta: (1) uterine bulging, (2) heterogeneous signalintensity within the placenta, and (3) presence of dark intraplacentalbands on T2-weighted imaging.Baxi and associates (2004) found that elevated serum Ddimerlevels may predict significant blood loss and morbidity inwomen with placenta accreta. This perhaps reflects trophoblasticinvasion into the myometrium and adjacent tissues.ManagementThorough preoperative assessment allows better planning. Exigenciesto be considered are appropriate surgical and bloodbanking facilities, as well as availability of gynecological oncological,surgical, or urological consultation (Bauer and Bonanno,2009; Stafford and Belfort, 2008). Transfer to a level IIIfacility should be considered (Worley and colleagues, 2008).Preoperative Arterial Catheter Placement. Experiencehas accrued with preoperative placement of pelvic arterialcatheters. Balloon-tipped catheters are placed before surgeryinto the internal iliac arteries and are inflated after the fetus isdelivered to decrease blood loss during placental delivery andhysterectomy, if indicated. Alternatively, the catheters can be injectedwith a substance to embolize the arterial sites. Yu and colleagues(2009) presented data from 11 women with abnormalplacentation during late gestation in whom uterine artery embolizationwas done after fetal but before placental delivery.They reported favorable outcomes. From France, Sentilhes andco-workers (2009) described successes in four of 17 women.Oyelese and Smulian (2006) reviewed the limited reported resultsin the literature and reached no firm conclusions concerningefficacy. Greenburg and colleagues (2007) described awoman who developed thrombolic occlusion of the commonand left iliac arteries and advise caution with embolization use.Delivery of the Placenta. Problems associated with deliveryof the placenta and subsequent developments vary appreciably,depending on the site of implantation, depth of myometrialpenetration, and number of lobules involved. It is likely that focalplacenta accreta with implantation in the upper uterine segmentdevelops more often than recognized. Either the involvedlobule is pulled off the myometrium with perhaps somewhatexcessive bleeding, or the lobule is torn from the placenta andadheres to the implantation site with increased bleeding, immediatelyor later. According to Benirschke and Kaufmann (2006), this may be one mechanism for formation of a so-called placentalpolyp (see Chap. 30, p. 648).With more extensive involvement, hemorrhage becomes profuseas delivery of the placenta is attempted. Successful treatmentdepends on immediate blood replacement therapy as subsequentlydescribed, and nearly always prompts hysterectomy. Thismay be aided by fully developing the bladder flap and dissecting itaround the percreta if possible prior to delivery. Other measures includeuterine or internal iliac artery ligation, balloon occlusion, orembolization as discussed above. Karam and colleagues (2003)described use of argon beam coagulation for hemostasis in awoman with placenta percreta and bladder invasion.With total placenta accreta, there may be very little or nobleeding, at least until manual placental removal is attempted.At times, traction on the umbilical cord inverts the uterus.Mostly, however, usual attempts at manual removal do not succeedbecause a cleavage plane between the placenta and uterinewall cannot be developed. In the past, conservative managementincluded manual removal of as much placenta as possiblefollowed by uterine packing. Unfortunately, 25 percent ofwomen managed conservatively died (Fox, 1972). Thus, thesafest treatment in this circumstance is hysterectomy.At cesarean delivery, another option for a woman who is notbleeding significantly is to leave the entire placenta in placewithout attempts to extract it and to close the cesarean hysterotomyincision. Leaving the placenta in situ has also been attemptedwith advanced gestational-age extrauterine pregnancies(Worley and associates, 2008). Currently, there is minimalexperience with this approach, and these are chronicled in casereports. Several scenarios have been described. In most,methotrexate was given at the time of surgery. In some, pelvicarterial embolization was also performed (Kayem and colleagues,2002; Lee and co-workers, 2008). In a few cases, theplacenta spontaneously resorbed (Henrich and co-workers,2002; Kayem and associates, 2002). Subsequent hysterectomyeither planned or prompted by bleeding or infectionis performed several weeks postpartum when blood loss may beless torrential (Hays, 2008; Lee, 2008; Nijman, 2002, and alltheir colleagues).Management Outcomes. Most reported outcomes with abnormalplacentation are retrospective observational studies oflimited size. These are usually reported to describe successeswith one particular management method such as some of theones cited above. Eller and co-workers (2009) reviewed outcomesin 76 cases of placenta accreta cared for at the Universityof Utah. They found that preoperative identification withscheduled cesarean hysterectomy without placental removal wasassociated with significantly reduced morbidity36 versus 67percentcompared with those of attempted placental removal.They also reported that preoperative bilateral ureteral stentingsignificantly reduced morbidity18 versus 55 percentcomparedwith no stenting. Finally, internal iliac artery ligation didnot lower morbidity. Although such a primary surgical approachcan be technically difficult in some cases, at ParklandHospital we have found this management to be preferable, exceptthat we do not routinely perform preoperative ureteralcatheterization, and instead, place such catheters transvesically during surgery if necessary. The use of preoperative arterialcatheterization as described may be useful in some cases.Leaving the placenta in situ may prevent massive hemorrhagerequiring hysterectomy with the goal of fertility preservation andpotential damage to pelvic structures. Timmermans and coworkers(2007) reviewed 48 publications from 1985 through2006 and described so-called conservative management in 60such women. Initially, the placenta was either only partially removedor left completely intact. Approximately half were treatedwith either adjuvant methotrexate or uterine artery embolization.The overall success ratedefined as fertility preventionwas 80 percent. The most common complication was vaginalbleeding in a third that began hours to 3 months postpartum. Athird of these15 percent of the whole grouprequired hysterectomyto arrest hemorrhage. Of 11 women with puerperalinfection, two required hysterectomy. Serial serum _-hCGmeasurements were not found to be predictive, and the authorsrecommend serial imaging with sonography or MR imaging. Inversion of the UterusComplete uterine inversion after delivery of the infant is almostalways the consequence of strong traction on an umbilical cordattached to a placenta implanted in the fundus (Fig. 35-22). Incompleteuterine inversion may also occur (Fig. 35-23). Contributingto uterine inversion is a sturdy cord that does notreadily break away from the placenta, combined with fundalpressure and a relaxed uterus, including the lower segment andcervix. Placenta accreta may be implicated as in the case inFigure 35-22, although uterine inversion can occur without afirmly adhered placenta.The incidence of uterine inversion varies, and in three reportstotaling approximately 116,500 deliveries, it averaged 1 in3000 (Achanna and colleagues, 2006; Baskett, 2002; Platt andDruzin, 1981). This is consistent with experiences from the obstetricalservice at Parkland Hospital, in which we encounterseveral cases annually among approximately 15,000 deliveries.Perhaps ironically, most are seen with low-risk deliveries.ManagementUterine inversion is most often associated with immediate lifethreateninghemorrhage. In the past, it was taught that shockwas disproportionate to blood loss, possibly mediated byparasympathetic stimulation caused by stretching of tissues.Careful evaluation of the need in many cases for transfusion oflarge volumes of blood, however, illustrates that blood loss is usually massive and greatly underestimated (Watsonand associates, 1980).Delay in treatment increases the mortality rate appreciably.It is imperative that a number of steps betaken urgently and simultaneously: Immediate assistance is summoned to includeanesthesia personnel and other physicians The recently inverted uterus with placenta alreadyseparated from it may often be replacedsimply by pushing up on the fundus with thepalm of the hand and fingers in the direction ofthe long axis of the vagina Adequate large-bore intravenous infusion systemsare established, and crystalloid and blood aregiven to treat hypovolemia If still attached, the placenta is not removed untilinfusion systems are operational, fluids are beinggiven, and a uterine-relaxing anesthetic such as ahalogenated inhalation agent has been administered.Other tocolytic drugs such as terbutaline,ritodrine, magnesium sulfate, and nitroglycerinhave been used successfully for uterine relaxationand repositioning (Hong and colleagues, 2006;You and Zahn, 2006). In the meantime, if theinverted uterus has prolapsed beyond the vagina,it is replaced within the vagina After removing the placenta, steady pressure withthe fist is applied to the inverted fundus in an attemptto push it up into the dilated cervix.Alternatively, two fingers are rigidly extended andare used to push the center of the fundus upward.Care is taken not to apply so much pressure asto perforate the uterus with the fingertips. As soonas the uterus is restored to its normal configuration,the tocolytic agent is stopped. An oxytocininfusion is begun while the operator maintainsthe fundus in its normal anatomical position.Initially, bimanual compression as shown in Figure35-17 aids in control of further hemorrhage until uterinetone is recovered. After the uterus is well contracted,the operator continues to monitor the uterus transvaginallyfor any evidence of subsequent inversion.Surgical InterventionMost often, the inverted uterus can be restored to itsnormal position by the techniques described. Occasionally,the uterus cannot be reinverted by vaginal manipulationbecause of a dense constriction ring(Kochenour, 2002). In this case, laparotomy is imperative.The configuration seen at surgery is shown in Figure 35-24.The fundus may be simultaneously pushed upward from belowand pulled from above. A deep traction suture well placed in theinverted fundus may be of aid. If the constriction ring still prohibitsreposition, it is carefully incised posteriorly to expose thefundus (Van Vugt and associates, 1981). A variant using tissue forcepsto grasp the top of the fundus has been described by Robsonand colleagues (2005). After replacement of the fundus, the anesthetic agent used to relax the myometrium is stopped, oxytocininfusion is begun, and the uterine incision is repaired. Genital Tract LacerationsPerineal LacerationsAll except the most superficial perineal lacerations are accompaniedby varying degrees of injury to the lower portion of thevagina. Such tears may reach sufficient depth to involve the analsphincter and may extend to varying depths through the vaginalwalls. Bilateral lacerations into the vagina are usually unequal inlength and separated by a tongue-shaped portion of vaginalmucosa.Vaginal LacerationsIsolated lacerations involving the middle or upper third of thevagina, but unassociated with lacerations of the perineum orcervix, are encountered less commonly. These are usually longitudinaland frequently result from injuries sustained during aforceps or vacuum delivery. However, they may even developwith spontaneous delivery. Such lacerations frequently extenddeep into the underlying tissues and may give rise to significanthemorrhage, which usually is controlled by appropriate suturing.They may be missed unless thorough inspection of the uppervagina is performed. Bleeding while the uterus is firmly contractedis strong evidence of genital tract laceration, retainedplacental fragments, or both.Lacerations of the anterior vaginal wall in close proximity tothe urethra are relatively common. They are often superficial withlittle to no bleeding, and repair is usually not indicated. If such lacerationsare large enough to require extensive repair, difficulty invoiding can be anticipated, and an indwelling catheter is placed.Injuries to Levator Ani MusclesThese result from overdistension of the birth canal (see Figs. 2-25 and 2-26, p. 33). Muscle fibers are separated, and diminutionin their tonicity may be sufficient to interfere with pelvicdiaphragm function. In such cases, pelvic relaxation may develop.If the injuries involve the pubococcygeus muscle, urinaryincontinence also may result (see Chap. 30, p. 649).Injuries to the CervixThe cervix is lacerated in more than half of all vaginal deliveries(Fahmy and associates, 1991). Most of these are less than 0.5cm, although deep cervical tears may extend to the upper thirdof the vagina. In rare instances, the cervix may be entirely orpartially avulsed from the vagina. Such colporrhexis may occurin the anterior, posterior, or lateral fornices. These injuriessometimes follow difficult forceps rotations or deliveries performedthrough an incompletely dilated cervix with the forcepsblades applied over the cervix. Rarely, cervical tears may reach toinvolve the lower uterine segment and uterine artery and its majorbranches, and even extend through the peritoneum. Theymay be totally unsuspected, but more often, they manifest asexcessive external hemorrhage or as hematomas.Extensive tears of the vaginal vault should be explored carefully.If there is question of peritoneal perforation or ofretroperitoneal or intraperitoneal hemorrhage, laparotomyshould be considered. With damage of this severity, intrauterineexploration for possible rupture is also indicated. Surgical repairis usually required, and effective analgesia or anesthesia, vigorousblood replacement, and capable assistance are mandatory.Cervical lacerations up to 2 cm must be regarded as inevitablein childbirth. Such tears heal rapidly and are rarely the source ofcomplications. In healing, they cause a significant change in theround shape of the external os, from circular before labor to appreciablywidened after delivery (see Fig. 2-12, p. 24). As theconsequence of such tears, there may be eversion with exposureof the mucus-producing endocervical epithelium.Occasionally, the edematous anterior lip of the cervix may becaught during labor and compressed between the fetal head andmaternal symphysis pubis. If ischemia is severe, the cervical lipmay necrose and separate. Rarely, the entire vaginal portionmay be avulsed from the rest of the cervixtermed annular orcircular detachment of the cervix.Diagnosis. A deep cervical tear should always be suspected inwomen with profuse hemorrhage during and after third-stage labor,particularly if the uterus is firmly contracted. Thorough examinationis necessary, and the flabby cervix often makes digitalexamination alone unsatisfactory. Thus, the extent of the injurycan be fully appreciated only after adequate exposure and visualinspection of the cervix. Visualization is best accomplished whenan assistant applies firm downward pressure on the uterus whilethe operator exerts traction on the lips of the cervix with ringforceps. Right-angle vaginal wall retractors are often helpful.In view of the frequency with which deep tears follow majoroperative vaginal deliveries, the cervix should be inspected routinelyat the conclusion of the third stage after all difficult deliveries,even if there is no bleeding.Management. Deep cervical tears usually require surgical repair.When the laceration is limited to the cervix, or even whenit extends somewhat into the vaginal fornix, satisfactory results are obtained by suturing the cervix after bringing it into view atthe vulva (Fig. 35-25). Because the hemorrhage usually comesfrom the upper angle of the wound, the first suture is placedproximal to the angle. Suturing proceeds outward toward theoperator. Associated vaginal lacerations may be tamponadedwith gauze packs to retard hemorrhage while cervical lacerationsare repaired. Either interrupted or running absorbable suturesare suitable. Overzealous suturing in an attempt to restore thenormal cervical appearance may lead to subsequent stenosisduring uterine involution. Alternatively, Lichtenberg (2003)described the successful use of angiographic embolization fortreatment of a high cervical tear after failed surgical repair. Puerperal HematomasIn a review of seven series, the incidence of puerperal hematomaswas found to vary from 1 in 300 to 1 in 1000 deliveries (Cunningham,2002). Nulliparity, episiotomy, and forceps deliveryare the most commonly associated risk factors (Propst andThorp, 1998; Ridgway, 1995). In other cases, hematomas maydevelop following rupture of a blood vessel without laceration ofsuperficial tissues. These may occur with spontaneous or operativedelivery, and hemorrhage may be delayed. Finally, coagulopathies,such as von Willebrand disease, are rarer causes.Puerperal hematomas may be classified as vulvar, vulvovaginal,paravaginal, or retroperitoneal. Vulvar hematomas most ofteninvolve branches of the pudendal artery, including the posteriorrectal, transverse perineal, or posterior labial artery (seeFig. 2-5, p. 20). Paravaginal hematomas may involve the descendingbranch of the uterine artery (Zahn and Yeomans,1990). Infrequently, a torn vessel lies above the pelvic fascia. Inthat event, the hematoma develops above it. In its early stages,the hematoma forms a rounded swelling that projects into theupper portion of the vaginal canal and may almost occlude itslumen. If the bleeding continues, it dissects retroperitoneally,and thus, may form a tumor palpable above the inguinal ligament.Alternatively, it may dissect upward, eventually reachingthe lower margin of the diaphragm.Vulvar HematomasThese hematomas, such as the one shown in Figure 35-26, andparticularly those that develop rapidly, may cause excruciatingpain. This often is the first symptom noticed. Moderate-sizedhematomas may be absorbed spontaneously. The tissues overlyingthe hematoma may rupture as a result of pressure necrosis,and profuse hemorrhage may follow. In others, the contents ofthe hematoma may be discharged in the form of large clots. In thesubperitoneal variety, extravasation of blood beneath the peritoneummay be massive and occasionally fatal. Some of thesedissect behind the ascending colon up to the hepatic flexure.Diagnosis. A vulvar hematoma is readily diagnosed by severeperineal pain and usually rapid appearance of a tense, fluctuant,and sensitive swelling of varying size covered by discolored skin.When the mass develops adjacent to the vagina, it may escapedetection temporarily. Symptoms of pressure, if not pain or inabilityto void, should prompt a vaginal examination with discoveryof a round, fluctuant mass encroaching on the lumen.When a hematoma extends upward between the folds of thebroad ligament, it may escape detection unless a portion of thehematoma can be felt on abdominal palpation or unless hypovolemiadevelops. These are worrisome because they can be fatal.Sonographic or CT imaging may be helpful to assess the locationand extent of these hematomas.Treatment. Smaller vulvar hematomas identified after leavingthe delivery room may be treated expectantly (Propst andThorp, 1998). But if pain is severe or the hematoma continues to enlarge, the best treatment is prompt incision and drainage.This is done at the point of maximal distension along with evacuationof blood and clots and ligation of bleeding points. Thecavity may then be obliterated with mattress sutures. Often, nosites of bleeding are identified after the hematoma has beendrained. In such cases, the cavity is surgically closed, and thevagina is packed for 12 to 24 hours. With hematomas of thegenital tract, blood loss is nearly always considerably morethan the clinical estimate. Hypovolemia and severe anemiashould be prevented by adequate blood replacement. Half ofwomen with hematomas requiring surgical repair also requiretransfusions (Zahn and Yeomans, 1990).Subperitoneal and supravaginal hematomas are more difficultto treat because of difficult surgical access. Some can beevacuated by vulvar or vaginal incision, but unless there is completehemostasis, laparotomy is advisable.Angiographic Embolization. This technique has becomepopular for management of intractable puerperal hematomas.Embolization can be used primarily or most often when hemostasisis not obtained by surgical methods. It is described furtheron page 797. Ojala and co-workers (2005) described threewomen with a vulvovaginal hematoma in which it was used. Rupture of the UterusUterine rupture may develop as a result of preexisting injury oranomaly, it may be associated with trauma, or it may complicatelabor in a previously unscarred uterus. A classification of the etiologyof uterine rupture is presented in Table 35-5.The most common cause of uterine rupture is separation of aprevious cesarean hysterotomy scar. With decreasing interest in atrial of labor following a prior cesarean delivery, rupture of anunscarred uterus may now be associated with up to half of casesof uterine rupture (Porrecco and co-workers, 2009). This is discussedin detail in Chapter 26 (p. 573). Other common predisposingfactors to uterine rupture are previous traumatizing operationsor manipulations such as curettage, perforation, ormyomectomy (Kieser and Baskett, 2002; Pelosi and Pelosi,1997). Excessive or inappropriate uterine stimulation with oxytocin,a previously frequent cause, has become uncommon.Mishra and colleagues (1995) described a 43-year-old womanwho suffered a ruptured vertical cesarean incision associatedwith inhaled crack cocaine that produced tetanic contractions.Morbidity and MortalityPrenatal morbidity and mortality rates can be substantive withrupture of a prior uterine incision during labor (see Chap. 26,p. 573). Rachagan and colleagues (1991) reported the fetalmortality rate to be almost 70 percent with either spontaneousor traumatic uterine rupture. In 24 women with uterine ruptureprincipally unassociated with prior incisions, Eden and associates(1986) reported one maternal death and a 46-percent perinatalloss rate. As discussed above, Porrecco and co-workers(2009) reported a 46-percent incidence of perinatal mortality orsevere morbidity in 37 women who suffered a uterine rupturewith a viable-aged fetus. Hysterectomy may be necessary tocontrol hemorrhage.Traumatic RuptureAlthough the uterus is surprisingly resistant to blunt trauma,pregnant women sustaining such trauma to the abdomenshould be watched carefully for signs of a ruptured uterus (see Chap. 42, p. 938) as well as a placental abruption, described onpage 761. Miller and Paul (1996) found that trauma accountedfor a ruptured uterus in only 3 of more than 150 women. In thepast, internal podalic version and extraction often caused traumaticrupture during delivery. Other causes of traumatic ruptureinclude difficult forceps delivery, unusual fetal enlargementsuch as hydrocephaly, and breech extraction.Spontaneous RuptureIn the study by Miller and Paul (1996), the incidence of spontaneousuterine rupture was only approximately 1 in 15,000 deliveries.The investigators also found that spontaneous rupture ismore likely in women of high parity (Miller and colleagues, 1997).Oxytocin stimulation of labor has been commonly associated withuterine rupture, especially in women of high parity (Fuchs and coworkers,1985; Rachagan and associates, 1991). Other uterotonicagents are also implicated. Uterine rupture has resulted from laborinduction with prostaglandin E2 gel or E1 vaginal tablets (Bennett,1997; Maymon and associates, 1991). For these reasons, all uterotonicagents should be given with great caution to induce or stimulatelabor in women of high parity. Similarly, in women of highparity, a trial of labor with suspected cephalopelvic disproportion,high cephalic presentation, or abnormal presentation, such as abrow, must be undertaken with caution.Pathological AnatomyRupture of the previously intact uterus at the time of labor mostoften involves the thinned-out lower uterine segment. The rent,when it is in the immediate vicinity of the cervix, frequently extendstransversely or obliquely. Usually, the tear is longitudinalwhen it occurs in the portion of the uterus adjacent to the broadligament (Fig. 35-27). Although developing primarily in thelower uterine segment, it is not unusual for the laceration to extendfurther upward into the body of the uterus or downwardthrough the cervix into the vagina. At times, the bladder mayalso be lacerated (Rachagan and colleagues, 1991). After completerupture, the uterine contents escape into the peritonealcavity. In cases in which the presenting part is firmly engaged,however, then only a portion of the fetus may be extruded fromthe uterus. In uterine rupture in which the peritoneum remainsintact, hemorrhage frequently extends into the broad ligament.This may result in a large retroperitoneal hematoma and exsanguination.Clinical Course and TreatmentA discussion of the various clinical presentations of uterine ruptureas well as treatment approaches is covered in detail inChapter 26 (p. 573).CONSUMPTIVE COAGULOPATHYIn 1901, DeLee reported that temporary hemophilia developedin a woman with a placental abruption and in anotherwith a long-dead macerated fetus. Observations that extensiveplacental abruption and other accidents of pregnancy were frequentlyassociated with hypofibrinogenemia stimulated interestin causes of intense intravascular coagulation. Although theseobservations were initially almost totally confined to obstetricalcases, subsequently they were made for almost all areas of medicine(Baglin, 1996). These syndromes are commonly termedconsumptive coagulopathy or disseminated intravascular coagulation(DIC). Pregnancy HypercoagulabilityPregnancy normally induces appreciable increases in the concentrationsof coagulation factors I (fibrinogen), VII, VIII,IX, and X (see Chap. 5, p. 116). Many of these are shown inthe Appendix. Other plasma factors and platelets do notchange so remarkably. Plasminogen levels are increased considerably,yet plasmin activity antepartum is normally decreasedcompared with that of nonpregnancy. At the sametime, in pregnancy, there does appear to be increased activationof platelet, clotting, and fibrinolytic mechanisms (Bakerand associates, 2009). Specifically, there are significant increasesin fibrinopeptide A, _-thromboglobulin, platelet factor4, and fibrinogen-fibrin degradation products. Gerbasiand colleagues (1990) concluded that this compensated, acceleratedintravascular coagulation may serve to maintain theuteroplacental interface. Pathological Activation of CoagulationIn pathological states, an abnormal cycle of coagulation and fibrinolysismay be initiated. Coagulation may be activated via theextrinsic pathway by thromboplastin from tissue destructionand perhaps via the intrinsic pathway by collagen and othertissue components when there is loss of endothelial integrity(Fig. 35-28). Tissue factor is released and complexes with factorVII. This in turn activates tenase (factor IX) and prothrombinase(factor X) complexes. As a result, fibrin is deposited in small vessels of virtually every organ system. However, this seldomcauses organ failure. Small vessels are protected because offibrinolysis. Coagulation releases fibrin monomers. Thesemonomers combine with tissue plasminogen activator and plasminogen,which releases plasmin as shown in Figure 35-28. Inturn, plasmin lyses fibrinogen, fibrin monomer, and fibrin polymersto form a series of fibrinogen-fibrin derivatives. Measuredby immunoassay, these are known as fibrin degradation productsor fibrin split products that include D-dimers. With this pathologicalcycle of consumption and fibrinolysis, there is depletionof platelets and coagulation factors in variable quantities. As aconsequence, bleeding results.Common inciting factors for consumptive coagulation inobstetrics include thromboplastin from placental abruption aswell as endotoxin and exotoxins. Another mechanism is directactivation of factor X by proteases, for example, as present inmucin or as produced by neoplasms. Amnionic fluid containsabundant mucin from fetal squames, and this likely causes therapid defibrination found with amnionic fluid embolism. Zhouand associates (2009) have presented evidence that in additionto tissue factor, phosphatidylserine expressed by the amnioniccell membrane is an inciting factor.Consumptive coagulopathy is almost always seen as a complicationof an identifiable, underlying pathological process againstwhich treatment must be directed to reverse defibrination. Thus,identification and prompt elimination of the coagulopathysource is the first priority.SignificanceIn addition to bleeding and circulatory obstruction, which maycause ischemia from hypoperfusion, consumptive coagulopathymay be associated with microangiopathic hemolysis. This iscaused by mechanical disruption of the erythrocyte membranewithin small vessels in which fibrin has been deposited. Varyingdegrees of hemolysis with anemia, hemoglobinemia, hemoglobinuria,and erythrocyte morphological changes are produced.According to Pritchard and colleagues (1976), this likely causesor contributes to the hemolysis encountered with the so-calledHELLP syndromehemolysis, elevated liver enzymes, low platelets(see Chap. 34, p. 720).In obstetrical syndromes involving consumptive coagulopathy,the importance of vigorous restoration and maintenance ofthe circulation to treat hypovolemia and persistent intravascularcoagulation cannot be overemphasized. With adequate perfusionof vital organs, activated coagulation factors and circulatingfibrin and fibrin degradation products are promptly removedby the reticuloendothelial system. At the same time,hepatic and endothelial synthesis of procoagulants is promoted.The likelihood of life-threatening hemorrhage in obstetricalsituations complicated by defective coagulation depends notonly on the extent of the coagulation defects butof great importanceon whether the vasculature is intact or disrupted.With gross derangement of blood coagulation, there may be fatalhemorrhage when vascular integrity is disrupted, yet nohemorrhage as long as all blood vessels remain intact. Clinical and Laboratory Evidence ofDefective HemostasisBioassay is an excellent method to clinically detect or suspect significantcoagulopathy. Excessive bleeding at sites of modest traumacharacterizes defective hemostasis. Persistent bleeding fromvenipuncture sites, nicks from shaving the perineum or abdomen,trauma from insertion of a catheter, and spontaneous bleedingfrom the gums or nose are signs of possible coagulation defects.Purpuric areas at pressure sites such as blood pressure cuffs may indicateincoagulable blood, or more commonly, clinically significantthrombocytopenia. A surgical procedure provides the ultimatebioassay for coagulation. Continuous generalized oozingfrom the skin, subcutaneous and fascial tissues, the retroperitonealspace, or episiotomy site should at least suggest coagulopathy.HypofibrinogenemiaIn late pregnancy, plasma fibrinogen levels typically are 300 to600 mg/dL. With consumptive coagulopathy, these high levelsmay sometimes serve to protect against clinically significant hypofibrinogenemia.To promote clinical coagulation, fibrinogenlevels must be approximately 150 mg/dL. If serious hypofibrinogenemiais present, the clot formed from whole blood in a glasstube may initially be soft but not necessarily remarkably reducedin volume. Then, over the next half hour or so, as plateletinducedclot retraction develops, it becomes quite small, so thatmany of the erythrocytes are extruded, and the volume of liquidclearly exceeds that of clot.Fibrin and Fibrinogen DerivativesSerum fibrin degradation products may be detected by a numberof sensitive test systems. Monoclonal antibodies to detect D-dimersare commonly used. With clinically significant consumption coagulopathy,these measurements are always abnormally high.ThrombocytopeniaSerious thrombocytopenia is likely if petechiae are abundant, ifclotted blood fails to retract over a period of an hour or so, or ifplatelets are rare in a stained blood smear. Confirmation is providedby platelet count. With severe preeclampsia and eclampsia, theremay also be qualitative platelet dysfunction (see Chap. 34, p. 717).Prothrombin and Partial Thromboplastin TimesProlongation of these standard coagulation tests may result fromappreciable reductions in those coagulants essential for generatingthrombin, from fibrinogen concentrations below a criticallevelapproximately 100 mg/dL, or from appreciable amountsof circulating fibrinogen-fibrin degradation products. Prolongationof the prothrombin time and partial thromboplastin timeneed not be the consequence of consumptive coagulopathy. Coagulation- and Fibrinolysis-DirectedAgentsHeparinThe infusion of heparin to try to block disseminated intravascularcoagulation associated with placental abruption or other situationsin which the integrity of the vascular system is compromised is mentionedonly to condemn its use.Epsilon-Aminocaproic AcidThis agent has been administered in an attempt to control fibrinolysisby inhibiting the conversion of plasminogen to plasmin.Epsilon-aminocaproic acid inhibits the proteolytic actionof plasmin on fibrinogen, fibrin monomer, and fibrin polymer(clot). Failure to clear fibrin polymer from the microcirculationcould result in organ ischemia and infarction, such as renal corticalnecrosis. Its use in most types of obstetrical coagulopathyhas not been efficacious and is not recommended. Placental AbruptionThis is the most common cause of severe consumptive coagulopathyin obstetrics and is discussed on page 761. Fetal Death and Delayed DeliveryIn the past, in most women with fetal death, spontaneous laboreventually ensued, most often within 2 weeks. Studies indicatedthat gross disruption of the maternal coagulation mechanismrarely developed within 1 month after fetal death (Pritchard,1959, 1973). If the fetus was retained longer, however, approximately25 percent of the women developed a coagulopathy.Today, because of certainty with which fetal death can beconfirmed with sonography and because highly effective methodsare available to induce labor, coagulopathy from a retaineddead fetus is unusual.CoagulopathyThe fibrinogen concentration typically falls over 6 weeks ormore to levels that are normal for the nonpregnant stateand in some cases, it falls to critical concentrations of 100mg/dL or less. Simultaneously, fibrin degradation productlevels become elevated in serum (Pritchard, 1973). Thesechanges are presumably mediated by thromboplastin fromthe dead products of conception (Jimenez and Pritchard,1968; Lerner and associates, 1967). The platelet count tendsto decrease in these instances, but severe thrombocytopeniais uncommon even if the fibrinogen level is quite low. Althoughcoagulation defects may correct spontaneously beforeevacuation, this is unusual and happens slowly (Pritchard,1959).HeparinCorrection of coagulation defects in this circumstance has beenaccomplished using low doses of heparin5000 U, two tothree times dailyunder carefully controlled conditions inwomen with an intact circulation (Pacheco and colleagues,2004). Heparin appropriately administered can block furtherpathological consumption of fibrinogen and other clotting factors,thereby slowing or temporarily reversing the cycle of consumptionand fibrinolysis. Such correction should be undertakenonly if the patient is not actively bleeding and withsimultaneous steps to effect delivery. Fetal Death in Multifetal PregnancyIt is uncommon that an obvious coagulation derangement developsin a multifetal pregnancy complicated by the death of atleast one fetus and survival of another (Landy and Weingold,1989). Petersen and Nyholm (1999) followed 22 women with amultifetal pregnancy with one fetal death after the first trimesterand did not detect a coagulopathy in any of these cases.Chescheir and Seeds (1988) reported a woman in whom,following the death of one twin fetus, there was a progressivebut transient fall in the plasma fibrinogen concentration andrise in the level of fibrin degradation products. Most cases areseen in monochorionic twins with vascular anastomoses (seeChap. 39, p. 878). We have encountered a few such cases atParkland Hospital, and one is shown in Figure 35-29. Coagulationchanges ceased spontaneously, and the surviving fetus,when delivered near term, was healthy. The placenta of thelong-dead fetus was filled with fibrin. Amnionic Fluid EmbolismThis is a complex disorder classically characterized by the abruptonset