The first part of placental evaluation is gross inspection of the placenta. Abnormal shapes may reflect a variety of genetic or mechanical issues. A circumvallate placenta (Fig. 12.1a) is thought to be secondary to chronic marginal abruption lifting up the peripheral membranes, with folding over of the membranes upon themselves. The fold in the membranes inserts internal to the edge of the placental disk. Circumvallation may be partial or circumferential. There is some association with preterm labor and abruption according to some authors [1]; however, the clinical significance is unclear [2]. Circummarginate placentas show a similar ridge of fibrin internal to the placental edge (Fig. 12.1b) on the fetal surface, but the placental membranes have not folded upon themselves. These lesions are not thought to be significant clinically in most cases.

Bilobed placentas consist of two lobes of fairly equal size (Fig. 12.2). Intervening vessels may be vulnerable to trauma. In succenturiate lobe, one lobe is smaller. The danger here is thinking the placenta is complete at delivery, with risk of postpartum hemorrhage from unsuspected retained placental tissue.

Gross examination of the membranes may provide a clue to underlying pathology. Meconium staining, if recent and heavy, is a pea soup green color. Histologically, meconium may denude the amniotic epithelium entirely or may show as pigmented macrophages in the membranes (Fig. 12.3a). The timing of meconium spread from amnion to chorion to decidua is not reliable. The presence of meconium in and of itself does not have major clinical significance and is very common. However, meconium may cause vasospasm, which can cause fetal hypoxic stress (not discernable on histopathology), and if the placenta is exposed to prolonged meconium, myonecrosis of the vessels of the cord and chorionic plate may occur (Fig. 12.3b), significantly associated with fetal compromise.

Acute chorioamnionitis, if severe, may turn yellow, or membranes may opacify the membranes. Opaque membranes may also simply indicate a larger amount of adherent decidua to the membranes. For the histology of acute chorioamnionitis, see below section on infectious lesions.

Amnion nodosum may be seen as multiple small white nodules on the placental membranes and fetal surface. Amnion nodosum is comprised of clusters of fetal squamous cells and lanugo hairs that become adherent to the amnion, sometimes with amnion epithelium overgrowing, in cases of severe oligohydramnios (Fig. 12.4).

Many of the abnormalities of the umbilical cord are gross rather than microscopic diagnoses. Abnormal insertions, including velamentous insertion into the membranes, and battledore, which is marginal insertion into the disk, should be noted. Velamentous insertions are important because the exposed vessels are subject to trauma, which can compromise the fetus, as well as rupture, particularly if there is vasa previa. This can lead to fetal exsanguination. There may be increased twisting of the cord, with torsion along the length, or with stricture focally (Fig. 12.5). Hematomas of the cord are often iatrogenic, occurring during traction during the third stage of labor. However, if spontaneous, they may compress the fetal vessels and cause compromise (Fig. 12.6). Single umbilical artery can be recognized both grossly and microscopically. It is the most common placental anomaly. It is sometimes associated with abnormalities in the fetus, particularly genitourinary. True knots are common and are only significant if there is obstruction. This can be concluded from congestion of the cord on one side, or thrombi. False knots are varicosities due to the vessels being longer than the cord and are of no clinical significance.