Evaluation of the Placenta

Pitfalls

Two caveats regarding placental karyotypes should be noted: (1) a karyotype revealing a 46,XX genotype may reflect contamination by maternal tissues; and (2) rarely, the placental karyotype may differ from that of the fetus (e.g., confined placental mosaicism).

Photography of any suspicious gross placental abnormality is always recommended for documentation and correlation with histology.

Shape

Variations in placental shape can occur related to an unusual uterine shape, nonuniform uteroplacental perfusion, or incomplete regression of membranous villi. These shape variations include bilobation—two roughly equal placental hemidiscs ( Fig. 31.3 ), either marginally fused or entirely separated but connected by membranous fetal vessels—trilobation, accessory or succenturiate lobation (smaller islands of placental tissue connected by membranous vessels; Fig. 31.4 ), and, rarely, placenta membranacea (a spherical placenta because of near-total persistence of membranous villi). Although the Collaborative Perinatal Study has suggested that some of these abnormal placental shapes may be associated with adverse outcomes (see Table 31.1 ), little literature exists in this area, and most general placental texts have minimized the significance of these aberrant placental shapes. Of note, however, oddly shaped placentas are often associated with unprotected membranous fetal vessels, and these vessels should be carefully examined for thromboses or evidence of rupture. When membranous vessels are identified adjacent to the site of membrane rupture in a spontaneously delivered placenta, this finding should prompt consideration of vasa previa, defined as membranous fetal vessels traversing the internal cervical os in vivo.

Weight

Placentas should be weighed after removal of the umbilical cord, membranes, and any attached maternal blood clot. Abnormally small placentas are usually associated with maternal vascular malperfusion and fetal growth restriction secondary to maternal disorders associated with vascular disease. Other conditions that may be causally related to growth-restricted placentas are listed in Box 31.2 . Excessively heavy placentas may signify maternal diabetes, placental hydrops in the setting of fetal hydrops, or congenital syphilis, among other conditions. Placental weights above the 90th or below the 10th percentile for gestational age should be noted in the pathology report because an abnormal placental weight may be associated with other clinical and pathologic findings of potential maternal, fetal, or neonatal significance.

Color

The membranes and fetal surface of the placenta are normally colorless, glistening, and transparent. In a normal placenta, chorionic vessels can be readily visualized radiating centrifugally from the umbilical cord insertion ( Fig. 31.5 ). A dull, off-white to tan to green opaque appearance can signal acute chorioamnionitis due to membrane infiltration by acute inflammatory cells, in which case the underlying chorionic vasculature is obscured ( Fig. 31.6 ). This appearance is more common in preterm placentas, particularly with prolonged preterm rupture of the membranes. In addition to the dull or opaque appearance, the placenta in chorioamnionitis may emit a foul odor. Benirschke and Kaufmann have described a characteristic fetid smell with Escherichia coli infection and a sweet smell with listerial infection. Brown discoloration of the membranes and chorionic plate may be due to hemosiderin deposition secondary to chronic abruptio placentae or may reflect old meconium.

With chronic abruption, the brown discoloration develops because marginal retroplacental, subchorionic, and/or retromembranous blood enters the amniotic fluid (so-called port wine fluid), seeps through the extraplacental and/or chorionic membranes, and is picked up by chorion macrophages (discussed later). A diffluent (slimy) texture with green discoloration suggests meconium staining, a finding most common in term or post-term placentas. Green meconium staining begins at 1 to 2 hours and is maximal by 3 to 6 hours after meconium exposure ( Fig. 31.7 ). Prolonged meconium exposure of many hours' to days' duration leads to the aforementioned green-brown to brown discoloration and can result in tissue necrosis, with linear fissures and ulceration of the umbilical cord and microscopic myonecrosis of umbilical and/or chorionic vessels. It has been estimated to take a minimum of 12 to 16 hours for this myonecrosis to develop. When prolonged or thick meconium discharge is suspected, extra sampling of the umbilical cord and chorionic plate is indicated to look for such meconium-induced vascular necrosis (discussed later).

Pitfalls

These are general principles of coloration and cause. Not all chorioamnionitis produce membrane opacity or discoloration and, as noted above, brown discoloration can indicate old meconium, and green discoloration can be seen with chorioamnionitis. Microscopic correlation is necessary.

Umbilical Cord

The umbilical cord should be severed at the insertion to the placental disc, and the following should be recorded.

Insertion

Marginal or battledore insertion ( Fig. 31.8A ) describes cord insertion within 1 cm of the placental disc edge; it is seen in approximately 5% of placentas. Membranous or velamentous insertion (see Fig. 31.8B ) refers to cord insertion onto the extraplacental membranes; it is seen in approximately 1% of placentas. Furcate insertion, which is least common, occurs when umbilical vessels branch before reaching the chorionic plate. Normal umbilical cords are central, paracentral, or eccentric; their relative sites of insertion are self-explanatory.

Twist

Hypocoiled umbilical cords (untwisted vessels, <1 coil/10 cm) in later gestation suggests prolonged fetal hypoactivity (e.g., muscular disorder, fetal entrapment; Fig. 31.9 ). Hypercoiled umbilical cords (>3 coils/10 cm) are associated with increased intrauterine activity. Due to excessive torqueing and localized kinking, hypercoiled cords are a predisposing condition for fetal vascular flow restriction, particularly with segmented and linked hypercoiling. Normally coiled umbilical cords (1 to 3 coils/10 cm, right or left twisted) fall between abnormal coiling indices.

Color

Glistening white or tan-white is normal. Innumerable pinpoint white spots (typically <1 mm in diameter) representing superficial microabscesses suggest fungal (almost always candidal) amniotic fluid infection ( Fig. 31.10A ), yellow-green suggests meconium exposure (for at least many hours before birth), and a diffuse brown-red discoloration due to hemolysis (see Fig. 31.10B ) suggests fetal retention of at least several hours after fetal death or, rarely, can be due to prolonged meconium discharge.

Pitfall

Red-brown discoloration may incorrectly be referred to as thrombosis by health care providers at stillbirth delivery. Correlation with clinical observations indicating an increased risk of fetal flow restriction, as well as downstream (placental disc) correlates of fetal malperfusion, can usually resolve the ambiguity.

Vessel Patency

This includes the exclusion of thrombi ( Fig. 31.11A and B ).

Placental Membranes

The membranes should be examined with the following in mind.

Distribution

This includes circummarginate and circumvallate insertions ( Fig. 31.12A and B ). Circumvallate membrane insertion, particularly when circumferential, is associated with chronic abruption.

Thrombi

Thrombosis of chorionic vessels can affect arteries or veins; a distended vessel that is firm in the unfixed state suggests fresh thrombosis; a collapsed, tan-white or yellow, fibrosed or calcified vessel suggests remote thrombosis.

Cysts

Cysts of the placental surface include single or sometimes multiple thin-walled amniotic cysts or thicker-walled chorionic cysts; both are almost always incidental findings ( Fig. 31.13 ).

Small Nodules

Tiny off-white nodular lesions on the chorionic surface may represent amnion nodosum (nodules of fetal vernix adherent to the amniotic surface because of severe prolonged oligohydramnios) ( Fig. 31.14 ) or (2) incidental squamous metaplasia (small plaques, usually localized to the region of cord insertion). Amnion nodosum can be grossly differentiated from squamous metaplasia in that nodules of amnion nodosum can be rubbed off the placental surface, whereas squamous metaplasia cannot.

Large Nodules

These include the following.

Chorangiomas

These are placental capillary hemangiomas. On cross section, chorangiomas are well circumscribed and round, with a smooth, glistening, tan/red, myxoid consistency ( Fig. 31.15A ). Chorangiomas can have a uniformly dark red appearance, grossly resembling blood clot if engorged, or can be tan if bloodless. Because chorangiomas originate from the chorionic plate or stem villi, they are usually located subjacent to the chorionic surface; in contrast, infarcts are usually basally oriented. Both lesions, however, may be centrally located.

Absent Subchorionic Fibrin

Very premature placentas have little subchorionic fibrin, which accumulates as gestational age increases. Naeye has hypothesized that subchorionic fibrin accumulates from placental trauma resulting from normal fetal movement and further suggested that the absence of subchorionic fibrin at term may indicate a long-standing decrease in fetal mobility, possibly reflecting a long-standing fetal neurologic impairment. In practice, evaluation of subchorionic fibrin is rarely of clinical significance.

Fragmentation

When the placenta separates from the decidua after birth, “lacerations” of the maternal surface may develop, usually located between cotyledons. Such localized fragmentation may suggest that the placenta is incomplete. This issue can usually be resolved by gently molding the placenta back into its original shape; if placental tissue is truly missing, obvious gaps in the maternal surface will appear.

True fragmentation of the placenta is often evident following manual removal of the placenta ( Fig. 31.17 ). This raises the possibility that additional placental tissue may be retained, either because of incomplete placental removal or because of placenta creta. A diagnosis of placenta creta is supported by histologic assessment of myometrial fibers adherent to the basal plate, a result of deficient or absent intervening decidua (see Figs. 36.9 through 36.13 in Chapter 36; see Chapter 33 for details).

Retroplacental Blood Clot

In many placentas, adherent fresh blood clot is present on the maternal surface; when this fresh clot is readily removed, the adjacent maternal surface is unremarkable ( Fig. 31.18 ). With abruptio placentae, an adherent, sometimes grossly laminated blood clot is found ( Fig. 31.19A ). Sometimes the clot destructively dissects into the placental disc, resulting in space-occupying intervillous hemorrhage. Blood clots of a remote abruptio placenta become laminated, consolidated, and eventually turn brown. The placenta adjacent to the adherent blood clot may be dark red due to (1) villous hemorrhage, an early hemorrhagic infarction, (2) compressed and concave due to both collapse of the intervillous space and to the space-occupying effect of the hematoma (see Fig. 31.19B ), or (3) firm and pale, indicating an infarct of at least several days' duration ( Fig. 31.20 ).

Pitfall

Placental abruption occurring shortly before delivery may not have time to manifest pathologic changes; this is an important conceptual point that supports a strong clinical impression of acute abruptio.

Thickness

A diffusely thin placenta suggests marked prematurity or poor placental growth because of chronic maternal vascular malperfusion. Localized placental thinning may result from a remote infarct, a retroplacental leiomyoma or hematoma, or incomplete removal of the placenta. Increased thickness is associated with placentomegaly from hydrops fetalis, maternal diabetes, or congenital syphilis, among other conditions.

Color

A diffuse, dark red color usually indicates congestion of fetal capillaries, a nonspecific finding. Less commonly, it may indicate diffuse fetal capillary proliferation (chorangiosis), an abnormality associated with maternal diabetes. A localized dark red area usually indicates an early infarct or a region of intravillous hemorrhage; the latter is commonly the result of abruptio placentae or placental trauma following manual extraction. A diffuse pallor may indicate remote fetal death (>1–2 weeks before birth), with diffuse villous fibrosis ( Fig. 31.22 ), edema from hydrops fetalis, or marked fetal anemia from any cause. Stillbirth from fetal exsanguination related to massive fetal-maternal hemorrhage may be suggested by placental and fetal pallor and can be documented and quantified by a maternal Kleihauer-Betke test. In a minority of cases, the location of the fetal-maternal hemorrhage will be seen as a fresh intervillous thrombus ( Fig. 31.23 ). Localized pallor usually indicates intervillous fibrin, infarction, or, rarely, regional avascular villi resulting from remote fetal thrombosis.

Masses

Infarcts

These are best recognized by their firm consistency, which is related to their villous composition. Infarcts are commonly wedge-shaped and located close to the maternal surface, reflecting their pathogenesis in the cessation of blood flow from servicing spiral arterioles. Although one or a few small basal or peripheral infarcts are not uncommon at term, central and full-thickness infarcts are always pathologic, as are placentas with multiple infarcts, especially of varying ages. Recent infarcts are dark red; older infarcts gradually change from brown-red to tan and finally to a yellow-white color. The entire sequence takes days to weeks to evolve ( Fig. 31.24 ). It is important to record the maximum size of infarcts as well as the approximate total percentage of placental parenchyma involved by infarction. Representative infarcts should always be sampled histologically to confirm the gross impression because, for example, primary placental choriocarcinoma is often described as grossly resembling placental infarction.

Fibrin Deposition

Localized

Small, tan-white, firm irregularly shaped nodules of fibrin (up to 1–2 cm in size) are relatively common incidental findings in later gestational placentas. They are present beneath the chorionic plate ( Fig. 31.25 ), at the placental margin, and scattered throughout the placental parenchyma.

Extensive

Although excessive fibrin deposition can represent a truly pathologic process associated with fetal growth restriction, stillbirth, and recurrence in future pregnancies, the categorization of placental fibrin as excessive, extensive, or pathologic is subjective. Two general patterns of extensive fibrin deposition have been described.

Maternal Floor Infarction

This is a misnomer because infarction is not present. It is a grossly visible fibrin plaque extending as a rind along the maternal surface; histologically, it consists of extensive fibrin deposits within the decidua and adjacent basal intervillous space.

Gitter Infarct

A gitter infarct, or network of fibrin, now more commonly termed massive perivillous fibrin , consists of diffuse, placental parenchymal infiltration by fibrin. It forms a dense, netlike patchwork of intervillous and perivillous fibrin, occupying a significant percentage of the intervillous space ( Fig. 31.26 ).

In our experience, not only are these two diagnoses subjective, but they can overlap, probably because they are of related pathogenesis. In addition, in many cases, we have found lesions with a histologic admixture of patterns, including perivillous fibrin deposition, proliferation of extravillous cytotrophoblast, ischemic infarction, chronic villitis, and avascular villi. Although one can often ascribe a primary process, such as perivillous fibrin, to secondary changes, such as those enumerated earlier, sometimes there is no single, satisfactory diagnostic term that fits the picture and for which no single pathogenetic process (e.g., ischemic, immunologic, thrombotic) can be invoked.

Inspection of the Umbilical Cords

Obstetricians usually mark umbilical cords regarding birth order. One clip typically denotes the first delivered sibling, and an additional clip for each subsequent delivery identifies umbilical cords of the siblings that follow. Parenthetically, when chorioamnionitis is found, in the absence of birth order designation, it usually affects the placenta closest to the endocervical os exclusively or most severely, reflecting that chorioamnionitis represents an ascending infection that reaches the presenting sac before the nonpresenting sac.

Umbilical cord anomalies, particularly of cord insertion, are common in twins and more common than in singletons due to placental disc growths in opposing directions (discussed later). Their approximate prevalence is shown in Table 31.2 .

Discs Separate or Fused

Separate placental discs indicate dichorionic placentas; these placentas can be assessed as two singleton placentas. There is no need for considering disorders of shared fetal circulations, such as those associated with twin-twin transfusion or twin-reversed arterial perfusion.

Fused discs can be monochorionic or dichorionic. This issue can be resolved by carefully examining the dividing membranes, which are transparent, like cellophane, in monochorionic placentas due to their composition of two amnions only ( Fig. 31.27 ), or they may be thicker and semitranslucent in dichorionic placentas due to two fused chorionic layers between the amnions ( Fig. 31.28 ).