Williams Obstetrics, 24th Edition

CHAPTER 6. Placental Abnormalities

HISTOPATHOLOGICAL EXAMINATION

NORMAL PLACENTA

ABNORMALITIES OF THE PLACENTA

SHAPE AND SIZE

EXTRACHORIAL PLACENTATION

CIRCULATORY DISTURBANCES

PLACENTAL TUMORS

ABNORMALITIES OF THE MEMBRANES

ABNORMALITIES OF THE UMBILICAL CORD

Obstetrical practice has always emphasized that gross examination of the placenta is integral following delivery. In some cases, findings prompt further action by the obstetrician or pediatrician. In addition, great strides have been made concerning the histopathological examination of placental tissue to provide clinically useful information. Pioneering efforts in this field include those of Benirschke, Driscoll, Fox, Naeye, Salafia, and Faye-Petersen.

HISTOPATHOLOGICAL EXAMINATION

We agree with most authorities that routine placental examination by a pathologist is not indicated, although there is still debate as to which placentas should be submitted. For example, the College of American Pathologists recommends routine examination for an extensive list of indications (Langston, 1997). However, data may be insufficient to support all of these. Certainly, the placenta and cord should be examined in the delivery room. As some correlation of specific placental findings with both short- and long-term neonatal outcomes is possible, the decision to request pathological examination should be based on clinical and placental findings (Redline, 2008; Roberts, 2008). Shown in Table 6-1 are indications used at Parkland Hospital to submit a placenta to the Pathology Department.

TABLE 6-1. Some Indications for Placental Pathological Examinationa

Maternal Indications

Abruption

Antepartum infection with fetal risks

Anti-CDE alloimmunization

Cesarean hysterectomy

Oligohydramnios or hydramnios

Peripartum fever or infection

Preterm delivery

Postterm delivery

Severe trauma

Suspected placental injury

Systemic disorders with known effects

Thick or viscid meconium

Unexplained late pregnancy bleeding

Unexplained or recurrent pregnancy complications

Fetal and Neonatal Indications

Admission to an acute care nursery

Birth weight ≤ 10th or ≥ 95th percentile

Fetal anemia

Fetal or neonatal compromise

Neonatal seizures

Hydrops fetalis

Infection or sepsis

Major anomalies or abnormal karyotype

Multifetal gestation

Stillbirth or neonatal death

Vanishing twin beyond the first trimester

Placental Indications

Gross lesions

Marginal or velamentous cord insertion

Markedly abnormal placental shape or size

Markedly adhered placenta

Term cord < 32 cm or > 100 cm

Umbilical cord lesions

aIndications are organized alphabetically.

NORMAL PLACENTA

Placental abnormalities are better understood with knowledge of placental implantation, development, and anatomy presented in Chapter 5 (p. 88). At term, the “typical” placenta weighs 470 g, is round to oval with a 22-cm diameter, and has a central thickness of 2.5 cm (Benirschke, 2012). It is composed of a placental disc, extraplacental membranes, and three-vessel umbilical cord. The maternal surface is the basal plate, which is divided by clefts into portions—termed cotyledons. These clefts mark the site of internal septa, which extend into the intervillous space. The fetal surface is the chorionic plate, into which the umbilical cord inserts, typically in the center. Large fetal vessels that originate from the cord vessels then spread and branch across the chorionic plate before entering stem villi of the placenta parenchyma. In tracing these, fetal arteries almost invariably cross over veins. The chorionic plate and its vessels are covered by thin amnion, which can be easily peeled away from a postdelivery specimen.

Sonographically, the normal placenta is homogenous and 2 to 4 cm thick, lies against the myometrium, and indents into the amnionic sac. The retroplacental space is a hypoechoic area that separates the myometrium from the placenta’s basal plate and measures less than 1 to 2 cm. During prenatal sonographic examinations, placental location and relationship to the internal cervical os are recorded. The umbilical cord is also imaged, its fetal and placental insertion sites examined, and its vessels counted.

Many placental lesions can be identified grossly or sonographically, but many abnormalities require histopathological examination for clarification. A detailed description of these is beyond the scope of this chapter, and interested readers are referred to textbooks by Benirschke (2012), Fox (2007), Faye-Petersen (2006), and their colleagues.

ABNORMALITIES OF THE PLACENTA

image Shape and Size

In contrast to the normal architecture described earlier, placentas may infrequently form as separate, nearly equally sized discs. This is a bilobate placenta, but is also known as bipartite placenta or placenta duplex. In these, the cord inserts between the two placental lobes—either into a connecting chorionic bridge or into intervening membranes.

A placenta containing three or more equally sized lobes is rare and termed multilobate. However, more frequently, one or more small accessory lobes—succenturiate lobes—may develop in the membranes at a distance from the main placenta (Fig. 6-1). These lobes have vessels that course through the membranes. If these vessels overlie the cervix to create a vasa previa, they can cause dangerous fetal hemorrhage if torn (p. 123). An accessory lobe may also be retained in the uterus after delivery and cause postpartum uterine atony and hemorrhage.

image

FIGURE 6-1 Succenturiate lobe. A. Vessels extend from the main placental disk to supply the small round succenturiate lobe located beneath it. (Photograph contributed by Dr. Jaya George.) B. Sonographic imaging with color Doppler shows the main placental disk implanted posteriorly (asterisk). The succenturiate lobe is located on the anterior uterine wall across the amnionic cavity. Vessels are identified as the long red and blue crossing tubular structures that travel within the membranes to connect these two portions of placenta.

Rarely, the portion of fetal membranes covered by functioning villi varies from the norm. With placenta membranacea, all or nearly all of the membranes are covered with villi. This placentation may occasionally give rise to serious hemorrhage because of associated placenta previa or accreta (Greenberg, 1991). A ring-shaped placenta may be a variant of placenta membranacea. The placenta is annular, and a partial or complete ring of placental tissue is present. These abnormalities appear to be associated with a greater likelihood of antepartum and postpartum bleeding and fetal-growth restriction (Faye-Petersen, 2006). With placenta fenestrata, the central portion of a placental disc is missing. In some instances there is an actual hole in the placenta, but more often, the defect involves only villous tissue, and the chorionic plate remains intact. Clinically, it may erroneously prompt a search for a retained placental cotyledon.

During pregnancy, the normal placenta increases its thickness at a rate of approximately 1 mm per week. Although not measured as a component of routine sonographic evaluation, this thickness typically does not exceed 40 mm (Hoddick, 1985). Placentomegaly defines those thicker than 40 mm and commonly results from striking villous enlargement. This may be secondary to maternal diabetes or severe maternal anemia, or to fetal hydrops or infection caused by syphilis, toxoplasmosis, or cytomegalovirus. Less commonly, villi are enlarged and edematous and fetal parts are present, such as in cases of partial mole or a complete mole that coexists with a normal twin (Chap. 20p. 398). Cystic vesicles are also seen with placental mesenchymal dysplasia. Vesicles in this rare condition correspond to enlarged stem villi, but unlike molar pregnancy, there is not excessive trophoblast proliferation (Woo, 2011). And in some cases, rather than villous enlargement, placentomegaly may result from collections of blood or fibrin. Examples of this that are subsequently discussed on page 119 include massive perivillous fibrin deposition, intervillous or subchorionic thromboses, and large retroplacental hematomas.

image Extrachorial Placentation

The chorionic plate normally extends to the periphery of the placenta and has a diameter similar to that of the basal plate. With extrachorial placentation, however, the chorionic plate fails to extend to this periphery and leads to a chorionic plate that is smaller than the basal plate (Fig. 6-2). In a circummarginate placenta, fibrin and old hemorrhage lie between the placenta and the overlying amniochorion. In contrast, with a circumvallate placenta the peripheral chorion is a thickened, opaque, gray-white circular ridge composed of a double fold of chorion and amnion. Sonographically, the double fold can be seen as a thick, linear band of echoes extending from one placental edge to the other. On cross section, it appears as a “shelf.” This is important clinically because its location may help to differentiate this shelf from amnionic bands and amnionic sheets, which are described subsequently.

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FIGURE 6-2 A. In this illustration, circummarginate (left) and circumvallate (right) varieties of extrachorial placentation are shown. A circummarginate placenta is covered by a single layer of amniochorion. B. This transabdominal gray-scale sonographic image shows a circumvallate placenta. The double fold of amnion and chorion creates a broad, opaque white ring and ridge on the fetal surface.

Clinically, most pregnancies with an extrachorial placenta have normal outcomes. In observational studies in which the diagnosis was made by placental examination, circumvallate placenta was associated with increased risk for antepartum bleeding and preterm birth (Lademacher, 1981; Suzuki, 2008a). In a prospective sonographic investigation, however, Shen and colleagues (2007a) found a circumvallate placenta—described as a placental “shelf”—in more than 10 percent of early second-trimester pregnancies. Importantly, they reported that these were transient and benign.

image Placenta Accreta, Increta, and Percreta

These clinically important placental abnormalities develop when trophoblast invades the myometrium to varying depths to cause abnormal adherence. They are much more likely when there is placenta previa or when the placenta implants over a prior uterine incision or perforation. As discussed further in Chapter 41 (p. 804), torrential hemorrhage is a frequent complication.

image Circulatory Disturbances

These are clinically important syndromes, and in most cases, the placenta is a target organ of maternal disease. Functionally, placental perfusion disorders can be grouped into: (1) those in which there is disrupted maternal blood flow to or within the intervillous space and (2) those with disturbed fetal blood flow through the villi. These lesions are frequently identified in the normal, mature placenta. Although they can limit maximal placental blood flow, placental functional reserve prevents harm in most cases. Indeed, some estimate that up to 30 percent of placental villi can be lost without untoward fetal effects (Fox, 2007). If extensive, however, these lesions can profoundly limit fetal growth.

Placental lesions that cause abnormal perfusion are frequently seen grossly or sonographically, whereas smaller lesions are seen only by microscopic examination. Sonographically, many of these lesions, such as subchorionic fibrin deposition, perivillous fibrin deposition, and intervillous thrombosis, may be appear as focal sonolucencies within the placenta. Importantly, in the absence of maternal or fetal complications, isolated placental sonolucencies are considered incidental findings.

Maternal Blood Flow Disruption

Subchorionic Fibrin Deposition. These are caused by slowing of maternal blood flow within the intervillous space with subsequent fibrin deposition. Blood stasis specifically occurs in the subchorionic area, and lesions that develop are commonly seen as white or yellow firm plaques on the fetal surface.

Perivillous Fibrin Deposition. Maternal blood flow stasis around an individual villus results in fibrin deposition and can lead to diminished villous oxygenation and syncytiotrophoblastic necrosis (Fig. 6-3). Within limits, these grossly visible small yellow-white placental nodules are considered to be normal placental aging.

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FIGURE 6-3 Potential sites of maternal- and fetal-related placental circulatory disturbances. (Adapted from Faye-Petersen, 2006.)

Maternal Floor Infarction. This extreme variant of perivillous fibrinoid deposition is a dense fibrinoid layer within the placental basal plate and is erroneously termed an infarction. The lesion has a thick, white, firm, corrugated surface that impedes normal maternal blood flow into the intervillous space. These lesions are associated with miscarriage, fetal-growth restriction, preterm delivery, and stillbirths (Andres, 1990; Mandsager, 1994). These adverse outcomes occasionally recur in subsequent pregnancies. Their etiopathogenesis is not well defined, but some cases are associated with lupus anticoagulant (Sebire, 2002, 2003). Although unsettled, other cases may be associated with maternal thrombophilias (Gogia, 2008; Katz, 2002). These lesions are not reliably imaged with prenatal sonography, but they may create a thicker basal plate.

Intervillous Thrombus. This is a collection of coagulated maternal blood normally found in the intervillous space mixed with fetal blood from a break in a villus. Grossly, these round or oval collections vary in size up to several centimeters. They appear red if recent or white-yellow if older, and they develop at any placental depth. Intervillous thrombi are common and typically not associated with adverse fetal sequelae. Because there is potential for a communication between maternal and fetal circulations, they can cause elevated maternal serum alpha-fetoprotein levels (Salafia, 1988).

Infarction. Chorionic villi themselves receive oxygen solely from maternal circulation supplied to the intervillous space. Any uteroplacental disease that diminishes or obstructs this supply can result in infarction of individual villus. These are common lesions in mature placentas and are benign in limited numbers. If they are numerous, however, placental insufficiency can develop. When they are thick, centrally located, and randomly distributed, they may be associated with preeclampsia or lupus anticoagulant.

Hematoma. The maternal-placental-fetal unit can develop a number of hematoma types as depicted in Figure 6-3. These include: (1) retroplacental hematoma—between the placenta and its adjacent decidua; (2) marginal hematoma—between the chorion and decidua at the placental periphery—known clinically as subchorionic hemorrhage; (3) subchorial thrombosis—also known as Breus mole—along the roof of the intervillous space and beneath the chorionic plate; and (4) subamnionic hematoma—these are of fetal vessel origin and found beneath the amnion but above the chorionic plate.

Sonographically, these hematomas may resemble a crescent-shaped fluid collection that is hyperechoic to isoechoic in the first week after hemorrhage, hypoechoic at 1 to 2 weeks, and finally, anechoic after 2 weeks. Most subchorionic hematomas visible sonographically are fairly small and of no clinical consequence. Extensive retroplacental, marginal, and subchorial collections have been associated with higher rates of miscarriage, placental abruption, fetal-growth restriction, preterm delivery, and adherent placenta (Ball, 1996; Madu, 2006; Nagy, 2003). In essence, placental abruption is a large clinically significant retroplacental hematoma (Chap. 41p. 793)

Fetal Blood Flow Disruption

Placental lesions that arise from fetal circulatory disturbances are also depicted in Figure 6-3.

Fetal Thrombotic Vasculopathy. Deoxygenated fetal blood flows from the two umbilical arteries into arteries within the chorionic plate that divide and send branches out across the placental surface. These eventually supply individual stem villi, and their thrombosis will obstruct fetal blood flow. Distal to the obstruction, affected portions of the villus become infarcted and nonfunctional. Thrombi in limited numbers are normally found in mature placentas, but these may be clinically significant if many villi become infarcted.

Subamnionic Hematoma. As indicated earlier, these hematomas lie between the placenta and amnion. They most often are acute events during third-stage labor when cord traction ruptures a vessel near the cord insertion. Chronic lesions may cause fetomaternal hemorrhage or fetal-growth restriction (Deans, 1998). They also may be confused with other placental masses such as chorioangioma, which is discussed subsequently (Sepulveda, 2000; Van Den Bosch, 2000; Volpe, 2008). In most cases, Doppler interrogation will show absence of internal blood flow that permits differentiation of hematomas from other placental masses.

image Placental Calcification

Calcium salts may be deposited throughout the placenta, but are most common on the basal plate. Calcification accrues with advancing gestation and is associated with nulliparity, smoking, higher socioeconomic status, and increasing maternal serum calcium levels (Fox, 2007). Calcifications can easily be seen sonographically, and Grannum and coworkers (1979) created a grading scale from 0 to 3 that reflected increasing calcification with increasing numerical grade. However, such grading criteria have not been found useful to predict neonatal outcome (Hill, 1983; McKenna, 2005; Montan, 1986; Sau, 2004).

image Placental Tumors

Gestational Trophoblastic Disease

These pregnancy-related trophoblastic proliferative abnormalities are discussed in Chapter 20 (p. 396).

Chorioangioma

These benign tumors have components similar to blood vessels and stroma of the chorionic villus. Also called chorangioma, these placental tumors have an incidence of approximately 1 percent (Guschmann, 2003). In some cases, maternal serum alpha-fetoprotein (MSAFP) levels may be elevated with these tumors, an important diagnostic finding as discussed in Chapter 14 (p. 285). Their characteristic sonographic appearance has a well-circumscribed, rounded, predominantly hypoechoic lesion near the chorionic surface and protruding into the amnionic cavity. As shown in Figure 6-4, documenting increased blood flow by color Doppler helps to distinguish these lesions from other placental masses such as hematoma, partial hydatidiform mole, teratoma, metastases, and leiomyoma (Prapas, 2000).

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FIGURE 6-4 Placental chorioangioma. A. Color Doppler imaging displays blood flow through a large chorioangioma with its border outlined by white arrows. B. Grossly, the chorioangioma is a round, well-circumcised mass protruding from the fetal surface.

Small chorioangiomas are usually asymptomatic. Large tumors, typically those measuring > 5 cm, may be associated with significant arteriovenous shunting within the placenta that can cause fetal anemia and hydrops. Hemorrhage, preterm delivery, amnionic fluid abnormalities, and fetal-growth restriction may also complicate large tumors (Sepulveda, 2003a; Zalel, 2002). Because of this, some have treated large tumors by interdicting excessive blood flow using vessel occlusion or ablation (Lau, 2003; Nicolini, 1999; Quintero, 1996; Sepulveda, 2009).

Tumors Metastatic to the Placenta

Malignant tumors rarely metastasize to the placenta. Of those that do, melanomas, leukemias and lymphomas, and breast cancer are the most common (Al-Adnani, 2007a). Tumor cells usually are confined within the intervillous space. As a result, metastasis to the fetus is uncommon but is most often seen with melanoma (Alexander, 2003; Altman, 2003). These are discussed further in Chapter 63 (p. 1233).

ABNORMALITIES OF THE MEMBRANES

There are a few abnormalities of the fetal membranes that may be associated with adverse outcomes.

image Meconium Staining

Fetal passage of meconium before or during labor is common with cited incidences that range from 12 to 20 percent (Ghidini, 2001; Oyelese, 2006; Tran, 2004). Importantly, staining of the amnion can be obvious within 1 to 3 hours, but its passage cannot be timed or dated accurately (Benirschke, 2012). This subject and its clinical implications are discussed in detail in Chapter 33 (p. 637).

image Chorioamnionitis

Normal genital-tract flora can colonize and infect the membranes, umbilical cord, and eventually the fetus. Bacteria most commonly ascend after prolonged membrane rupture and during labor to cause infection. Organisms initially infect the chorion and adjacent decidua in the area overlying the internal os. Subsequently, progression leads to full-thickness involvement of the membranes—chorioamnionitis. Organisms may then spread along the chorioamnionic surface to colonize and replicate in amnionic fluid. Subsequently, inflammation of the chorionic plate and of the umbilical cord—funisitis—may follow (Al-Adnani, 2007b; Goldenberg, 2000; Redline, 2006).

Fetal infection may result from hematogenous spread if the mother has bacteremia, but more likely is from aspiration, swallowing, or other direct contact with infected amnionic fluid. Most commonly, there is microscopic or occult chorioamnionitis, which is caused by a wide variety of microorganisms. This is frequently cited as a possible explanation for many otherwise unexplained cases of ruptured membranes, preterm labor, or both as discussed in Chapter 42 (p. 838). In some cases, gross infection is characterized by membrane clouding and is sometimes accompanied by a foul odor that depends on bacterial species.

image Other Membrane Abnormalities

The condition of amnion nodosum is characterized by numerous small, light-tan nodules on the amnion overlying the chorionic plate. These may be scraped off the fetal surface and contain deposits of fetal squames and fibrin that reflect prolonged and severe oligohydramnios (Adeniran, 2007).

There are at least two band-like structures that can be formed by the fetal membranes. Amnionic band sequence is an anatomic fetal disruption sequence caused by bands of amnion that entrap fetal structures and impair their growth and development. The most widely held theory concerning their etiology is that early rupture of the amnion results in adherence of part of the fetus to the underlying “sticky” chorion (Torpin, 1965). Amnionic bands commonly involve the extremities to cause limb-reduction defects and more subtle deformations. They may also affect other fetal structures such as the cranium, causing encephalocele.

In contrast, an amnionic sheet is formed by normal amniochorion draped over a preexisting uterine synechia. Generally these sheets pose little fetal risk, although slightly higher rates of preterm membrane rupture and placental abruption were recently described (Tuuli, 2012).

ABNORMALITIES OF THE UMBILICAL CORD

image Length

Most umbilical cords are 40 to 70 cm long, and very few measure < 32 cm or > 100 cm. Cord length is influenced positively by both amnionic fluid volume and fetal mobility. Short cords may be associated with fetal-growth restriction, congenital malformations, intrapartum distress, and a twofold risk of death (Berg, 1995; Krakowiak, 2004). Excessively long cords are more likely to be linked with cord entanglement or prolapse and with fetal anomalies, acidemia, and demise.

Because antenatal determination of cord length is technically limited, cord diameter has been used as a predictive marker for fetal outcomes. Some have linked lean cords with poor fetal growth and large-diameter cords with macrosomia. However, the clinical utility of this parameter is still unclear (Barbieri, 2008; Cromi, 2007; Raio 1999, 2003).

image Coiling

Although cord coiling characteristics have been reported, these are not currently part of standard sonography (Predanic, 2005a). Usually the umbilical vessels spiral through the cord in a sinistral, that is, left-twisting direction (Lacro, 1987). The number of complete coils per centimeter of cord length has been termed the umbilical coiling index (Strong, 1994). A normal antepartum index derived sonographically is 0.4, and this contrasts with a normal value of 0.2 derived postpartum by actual measurement (Sebire, 2007). Clinically, hypocoiling has been linked with fetal demise, whereas hypercoiling has been associated with fetal-growth restriction and intrapartum fetal acidosis. Both have been reported in the setting of trisomic fetuses and with single umbilical artery (de Laat, 2006, 2007; Predanic, 2005b).

image Vessel Number

Occasionally, the usual arrangement of two thick-walled arteries and one thin, larger umbilical vein is altered. The most common aberration is that of a single umbilical artery, with a cited incidence of 0.63 percent in liveborn neonates, 1.92 percent with perinatal deaths, and 3 percent in twins (Heifetz, 1984).

The cord vessel number is a component of the standard prenatal ultrasound examination (Fig. 6-5). Identification of a single umbilical artery frequently prompts consideration for targeted sonography and possibly fetal echocardiography. As an isolated finding in an otherwise low-risk pregnancy with no apparent fetal anomalies, it does not significantly increase the fetal aneuploidy risk. But fetuses with major malformations frequently have a single umbilical artery. And when seen in an anomalous fetus, the aneuploidy risk is greatly increased, and amniocentesis is recommended (Dagklis, 2010; Lubusky, 2007). The most frequent anomalies described are cardiovascular and genitourinary. A single artery has also been associated with fetal-growth restriction in some but not all studies (Chetty-John, 2010; Hua, 2010; Murphy-Kaulbeck, 2010; Predanic, 2005c).

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FIGURE 6-5 Two umbilical arteries are typically documented sonographically in the second trimester. They encircle the fetal bladder (asterisk) as extensions of the superior vesical arteries. In this color Doppler sonographic image, a single umbilical artery, shown in red, runs along the bladder wall before joining the umbilical vein (blue) in the cord. Below this, the two vessels of the cord, seen as a larger red and smaller blue circle, are also seen floating in a cross section of a cord segment.

A rare anomaly is that of a fused umbilical artery with a shared lumen. It arises from failure of the two arteries to split during embryological development. The common lumen may extend through the entire cord, but if partial, is typically found near the placental insertion site (Yamada, 2005). In one report, these were associated with a higher incidence of marginal or velamentous cord insertion, but not congenital fetal anomalies (Fujikura, 2003).

image Remnants and Cysts

A number of structures are housed in the umbilical cord during fetal development, and their remnants may be seen when the mature cord is viewed transversely. Recall that embryos in early development initially have two umbilical veins, and thus an umbilical vein remnant may be seen on careful inspection. Indeed, Jauniaux and colleagues (1989) sectioned 1000 cords, and in one fourth of the specimens, they found remnants of vitelline duct, allantoic duct, and embryonic vessels. These were not associated with congenital malformations or perinatal complications.

Cysts occasionally are found along the course of the cord. They are designated according to their origin. True cysts are epithelium-lined remnants of the allantoic or vitelline ducts and tend to be located closer to the fetal insertion site. In contrast, the more common pseudocysts form from local degeneration of Wharton jelly and occur anywhere along the cord. Both have a similar sonographic appearance. Single umbilical cord cysts identified in the first trimester tend to resolve completely, however, multiple cysts may portend miscarriage or aneuploidy (Ghezzi, 2003; Gilboa, 2011). Cysts persisting beyond this time are associated with a risk for structural defects and chromosomal anomalies (Bonilla, 2010; Zangen, 2010).

image Insertion

The cord normally inserts centrally into the placental disc, but eccentric, marginal, or velamentous insertions are variants. The latter two are clinically important in that the cord or its vessels may be torn during labor and delivery. Of these, marginal insertion is a common variant—sometimes referred to as a battledore placenta—in which the cord anchors at the placental margin. These are more frequent with multifetal pregnancy, especially those conceived using assisted reproductive technology, and they may be associated with weight discordance (Delbaere, 2007; Kent, 2011). This common insertion variant rarely causes problems, but it occasionally results in the cord being pulled off during delivery of the placenta (Liu, 2002).

A velamentous insertion is a variant of considerable clinical importance. The umbilical vessels characteristically spread within the membranes at a distance from the placental margin, which they reach surrounded only by a fold of amnion (Fig. 6-6) As a result, vessels are vulnerable to compression, which may lead to fetal hypoperfusion and acidemia. The incidence of velamentous insertion is approximately 1 percent, but it is more commonly seen with placenta previa and multifetal gestations (Feldman, 2002; Fox, 2007; Papinniemi, 2007). When seen during prenatal sonography, cord vessels with velamentous insertion are seen traveling along the uterine wall before entering the placental disc.

image

FIGURE 6-6 Velamentous cord insertion. A. The umbilical cord inserts into the membranes. From here, the cord vessels branch and are supported only by membrane until they reach the placental disk. B.When viewed sonographically and using color Doppler, the cord vessels appear to lie against the myometrium as they travel to insert marginally into the placental disk, which lies at the top of this image.

Last, with the very uncommon furcate insertion, the topographic site of cord connection onto the placental disc is central, but umbilical vessels lose their protective Wharton jelly shortly before they insert. As a result, they are covered only by an amnion sheath and prone to compression, twisting, and thrombosis.

Vasa Previa

This is a particularly dangerous variation of velamentous insertion in which the vessels within the membranes overlie the cervical os. The vessels can be interposed between the cervix and the presenting fetal part. Hence, they are vulnerable to compression and also to laceration or avulsion with rapid fetal exsanguination. Vasa previa is uncommon, and Lee and coworkers (2000) identified it in 1 in 5200 pregnancies. Risk factors include bilobate or succenturiate placentas and second-trimester placenta previa, with or without later migration (Baulies, 2007; Suzuki, 2008b). It is also increased in pregnancies conceived by in vitro fertilization (Schachter, 2003).

Because antepartum diagnosis has improved perinatal survival compared with intrapartum diagnosis, vasa previa would ideally be identified early (Oyelese, 2004). Unfortunately, this is not always possible. Clinically, an examiner is occasionally able to palpate or directly see a tubular fetal vessel in the membranes overlying the presenting part. With transvaginal sonography, cord vessels may be seen inserting into the membranes—rather than directly into the placenta—with vessels running above the cervical internal os (Fig. 6-7). Routine color Doppler interrogation of the placental cord insertion site, particularly in cases of placenta previa or low-lying placenta, may aid its detection.

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FIGURE 6-7 Vasa previa. Using color Doppler, an umbilical vessel (red circle) is seen overlying the internal os. At the bottom, the Doppler waveform seen with this vasa previa has the typical appearance of an umbilical artery, with a pulse rate of 141 beats per minute.

Once vasa previa is identified, early scheduled cesarean delivery is planned. Bed rest apparently has no added advantage. Robinson and Grobman (2011) performed a decision analysis and recommend elective cesarean delivery at 34 to 35 weeks to balance the risks of perinatal exsanguination versus preterm birth morbidity. At delivery, the infant is expeditiously delivered after the hysterotomy incision in case a vessel is lacerated during uterine entry.

Whenever there is otherwise unexplained hemorrhage either antepartum or intrapartum, vasa previa with a lacerated fetal vessel should be considered. In many cases, bleeding is rapidly fatal, and infant salvage is not possible. With less hemorrhage, however, it may be possible to distinguish fetal versus maternal bleeding. Various tests may be used, and each relies on the characteristically increased resistance of fetal hemoglobin to denaturation by alkaline or acid reagents (Lindqvist, 2007; Oyelese, 1999).

image Knots, Strictures, and Loops

Various mechanical and vascular abnormalities can impede cord vessel blood flow either toward or away from the fetus, and these sometimes cause fetal harm. True knots are caused by fetal movement and are seen in approximately 1 percent of births. They are especially common and dangerous in monoamnionic twins as described in Chapter 45 (p. 901). When true knots are associated with singleton fetuses, the stillbirth risk is increased four- to tenfold (Airas, 2002; SØrnes, 2000). Abnormal fetal heart rate tracings are more often encountered during labor. However, cesarean delivery rates are not increased, and cord blood acid-base values are usually normal (Airas, 2002; Maher, 1996). False knots are of no clinical significance and appear as knobs protruding from the cord surface. These are focal redundancies of a vessel or Wharton jelly.

A cord stricture is a focal narrowing of its diameter that usually develops near the fetal cord insertion (Peng, 2006). Characteristic pathological features of strictures are absence of Wharton jelly and stenosis or obliteration of cord vessels at the narrow segment (Sun, 1995). In most instances, the fetus is stillborn (French, 2005). Even less common is a cord stricture caused by an amnionic band.

Cord loops are frequently encountered and are caused by coiling around various fetal parts during movement. As expected, they are more common with longer cords. A cord around the neck—a nuchal cord—is extremely common. One loop is reported in 20 to 34 percent of deliveries; two loops in 2.5 to 5 percent; and three loops in 0.2 to 0.5 percent (Kan, 1957; SØrnes, 1995; Spellacy, 1966). During labor these loops can result in fetal heart rate decelerations that persist during a contraction. Up to 20 percent of fetuses with a nuchal cord have moderate to severe variable heart rate decelerations, and these are associated with a lower umbilical artery pH (Hankins, 1987). Despite their frequency, nuchal cords are relatively uncommon causes of adverse perinatal outcome (Mastrobattista, 2005; Sheiner, 2006).

A funic presentation describes when the umbilical cord is the presenting part in labor. These are uncommon and most often are associated with fetal malpresentation. A funic presentation in some cases is identified with placental sonography and color flow Doppler (Ezra, 2003). Fetal heart rate abnormalities and overt or occult cord prolapse may complicate labor and lead to cesarean delivery.

image Vascular

Cord hematomas are uncommon and have been associated with abnormal cord length, umbilical vessel aneurysm, trauma, entanglement, umbilical vessel venipuncture, and funisitis (Gualandri, 2008). They can follow varix rupture, which is usually of the umbilical vein. They are recognized sonographically as hypoechoic masses that lack blood flow.

Umbilical cord vessel thromboses are in utero events. Approximately 70 percent are venous, 20 percent are venous and arterial, and 10 percent are arterial thromboses (Heifetz, 1988). Compared with venous thromboses, those in the artery have higher perinatal morbidity and mortality rates and are associated with fetal-growth restriction, fetal acidosis, and stillbirths (Sato, 2006).

Another rare anomaly is an umbilical vein varix, which is a marked focal dilatation that can be within either the intraamnionic or fetal intraabdominal portion of the umbilical vein. The latter anomalies are associated with increased rates of fetal structural anomalies and aneuploidy (Byers, 2009; Mankuta, 2011). Complications may include rupture or thrombosis, compression of the umbilical artery, and fetal cardiac failure due to increased preload (Mulch, 2006). They may be visualized during sonography as a cystic dilatation of the umbilical vein. Continuity of the varix with a normal-caliber portion of the umbilical vein is confirmed using color-flow Doppler.

The rare umbilical artery aneurysm is caused by congenital thinning of the vessel wall with diminished support from Wharton jelly. Indeed, most form at or near the cord’s placental insertion, where support is absent. These are associated with single umbilical artery, trisomy 18, amnionic fluid volume abnormalities, fetal-growth restriction, and stillbirth (Hill, 2010; Weber, 2007). At least theoretically, these aneurysms could cause fetal compromise and death by compression of the umbilical vein. These aneurysms may appear sonographically as a cyst with a hyperechoic rim. Within the aneurysm, color flow and spectral Doppler interrogation demonstrate either low-velocity or turbulent nonpulsatile flow (Olog, 2011; Sepulveda, 2003b; Shen, 2007b).

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