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Examination of the placenta can yield information that may be important in the immediate and later
management of mother and infant. This information may also be essential for protecting the
attending physician in the event of an adverse maternal or fetal outcome.
Although some experts argue that all placentas should be examined by a pathologist,1 most hospitals
do not mandate this examination. Instead, the delivering physician is usually responsible for
determining when pathologic interpretation is necessary. In some urgent situations, decisions must
be made before pathologic interpretation is available or has been completed. Therefore, it is essential
that the delivering physician perform a thorough, accurate examination of the placenta.
The examination of normal placentas and most abnormal placentas can be accomplished within one
minute. Universal examination of the placenta in the delivery room, with documentation of findings
and submission of tissue for pathologic evaluation based on abnormal appearance or certain clinical
indications, is standard medical practice.3(pp701–3)
The maternal surface of the placenta should be dark maroon in color and should be divided into
lobules or cotyledons. The structure should appear complete, with no missing cotyledons. The fetal
surface of the placenta should be shiny, gray and translucent enough that the color of the underlying
maroon villous tissue may be seen.
At term, the typical umbilical cord is 55 to 60 cm in length,3 with a diameter of 2.0 to 2.5 cm. The
structure should have abundant Wharton's jelly, and no true knots or thromboses should be present.
The total cord length should be estimated in the delivery room, since the delivering physician has
access to both the placental and fetal ends.
The normal cord contains two arteries and one vein. During the placental examination, the delivering
physician should count the vessels in either the middle third of the cord or the fetal third of the cord,
because the arteries are sometimes fused near the placenta and are therefore difficult to differentiate.
Fetal membranes are usually gray, wrinkled, shiny and translucent. The membranes and the placenta
have a distinctive metallic odor that is difficult to describe but is easily recognized with experience.
Normally, the placenta and the fetal membranes are not malodorous.
The placental abnormalities that may be detected in the delivery room are discussed in the following
sections. Photographs of a number of these abnormalities are presented (Figures 1 through 6). The
examination of the placenta and the significance of clinical findings are summarized in Table 1.3–11
FIGURE 1.
Succenturiate lobe.
FIGURE 2.
Bilobed placenta.
TABLE 1
Diameter: about 22
cm
Increased incidence of
postpartum infection and
hemorrhage
Factors to assess Condition Appearance Clinical significance
Placental infarcts
Factors to assess Condition Appearance Clinical significance
Pregnancy-induced hypertension
Fresh infarcts
Pregnancy-induced hypertension
Dark areas
Systemic lupus erythematosus
Clot, especially an
adherent clot toward
the center of the
Associated with abruption
placenta, with
Placental bleeding distortion of
(e.g., abruption) placental shape
Resembles a fresh
Choriocarcinoma Very rare with a normal gestation
infarct
Grape-like cluster of
Hydatidiform mole Very rare with a normal gestation
edematous villi
Factors to assess Condition Appearance Clinical significance
Anemia in newborn
Fetal hydrops
Fetal anemia Pale fetal surface
Hemorrhage requiring
transfusion
Prematurity
Prenatal bleeding
Thick ring of
Circumvallate
membranes (see Abruption
placenta
Figure 3)
Multiparity
Deceased twin
Fetus papyraceus One or several
and fetus nodules or May be associated with
compressus thickenings otherwise unexplained fetal
demise
Down syndrome
Werdnig-Hoffmann disease
Fetal malformations
Abruption
Uterine inversion
Thromboses
Prematurity
Cesarean section
Maternal preeclampsia
Factors to assess Condition Appearance Clinical significance
Eclampsia
Patent urachus
Omphalocele
Distinctive
segmental
resemblance to a
barber's pole Syphilis and other acute,
Necrotizing funisitis
subacute and chronic infections
Possible swelling,
necrosis, thrombosis
and calcifications
Smoking
Fetal malformations
Meconium staining
Infection (myeloperoxidase in
leukocytes)
Abnormalities of
the membranes Possible infection
Placental Completeness
Evaluating placental completeness is of critical, immediate importance in the delivery room. Retained
placental tissue is associated with postpartum hemorrhage and infection.
The maternal surface of the placenta should be inspected to be certain that all cotyledons are
present. Then the fetal membranes should be inspected past the edges of the placenta. Large vessels
beyond these edges indicate the possibility that an entire placental lobe (e.g., succenturiate or
accessory lobe) may have been retained (Figure 1).
All or part of the placenta is retained in placenta accreta, placenta increta and placenta percreta. In
these conditions, the placental tissues grow into the myometrium to lesser or greater depths. Manual
exploration and the removal of retained placental tissue are necessary in these cases.
Placental Size
Placentas less than 2.5 cm thick are associated with intrauterine growth retardation of the fetus.4
Placentas more than 4 cm thick have an association with maternal diabetes mellitus, fetal hydrops (of
both immune and nonimmune etiology) and intrauterine fetal infections.5(pp423–36,476,542–613)
An extremely thin placenta may represent placenta membranacea. In this condition, the entire uterine
cavity is lined with thin placenta. Placenta membranacea is associated with a very poor fetal
outcome.
Placental Shape
Extra placental lobes are important, primarily because they may lead to retained placental tissue
(Figure 2).
Blood may be adherent to the maternal surface of the placenta, particularly at or near the margin. If
the blood is rather firmly attached, and especially if it distorts the placenta, it may represent an
abruption. The dimensions and volume of the placenta should be estimated.
The placenta should be palpated, and the fetal and maternal surfaces should be carefully examined.
Maternal Surface. In a term infant without anemia, the maternal surface of the placenta should be
dark maroon. In a premature infant, the placenta is lighter in color. Pallor of the maternal surface
indicates the presence of fetal anemia, which may be a sign of hemorrhage. With prompt recognition
of fetal hemorrhage (such as occurs in vasa previa), lifesaving transfusion can be performed.
Clots on the maternal surface, particularly adherent centrally located clots, may represent placental
abruption. It should be emphasized, however, that abruption is a clinical diagnosis.
Fetal Surface. A thick ring of membranes on the fetal surface of the placenta may represent a
circumvallate placenta (Figure 3), which is associated with prematurity, prenatal bleeding, abruption,
multiparity and early fluid loss.5(pp386–91) A similar but thinner ring of membrane tissue represents a
circummarginate placenta (Figure 4). A circummarginate placenta is probably of no clinical
significance, although one study found an association between this structural anomaly and an
increase in fetal malformations.5(pp386–91)
FIGURE 3.
Circumvallate placenta.
FIGURE 4.
Circummarginate placenta.
Numerous small, firm, white, gray or yellow nodules on the fetal surface may represent either amnion
nodosum (Figure 5) or squamous metaplasia. Amnion nodosum is associated with oligohydramnios,
renal agenesis and poor fetal outcome. Squamous metaplasia is common and is probably of no fetal
significance.
FIGURE 5.
Amnion nodosum.
A nodule or thickening on the fetal surface may represent a vanished twin or a fetus papyraceus. A
deceased twin sometimes coexists with a normal fetus, but it may also be associated with demise of
the second twin, and this second death may be of uncertain cause.5(pp684–70)
Delicate or more robust bands of amnionic tissue may strangle and amputate fetal parts, including
digits, entire limbs, head, neck or trunk. In such cases, amnion may be missing from the placenta but
present on the cord.5(pp162–8) When fetal parts are missing or amputated, careful pathologic
examination of the placenta is warranted.
Placental Parenchyma
A diffusely soft placenta may represent infection, particularly if the structure is also thickened. Firm
areas in the placenta may represent fibrin deposition or infarction. Fresh infarcts are red, while older
infarcts are gray. Fibrin deposits are gray and, if extensive, may be associated with intrauterine growth
retardation and other poor fetal outcomes. If infarcts or fibrin occupy less than 5 percent of the
placental mass, they are usually unimportant.
Focal fleshy, dark-red areas may represent chorioangiomas.5(pp423–36) These benign hemangiomas
occur in 1 percent of placentas. While small chorioangiomas are usually of no clinical significance,
large chorioangiomas are associated with fetal anemia, thrombocytopenia, hydrops, hydramnios,
intrauterine growth retardation, prematurity and stillbirth.5(pp841–6)
Gestational trophoblastic neoplasia, including benign hydatidiform moles, invasive moles and
choriocarcinoma, only rarely coexist with viable gestations. Moles appear as grape-like clusters of
edematous villi, while choriocarcinoma may look much like an infarct.6
Apparent hemorrhage deep to the fetal membranes or a dark-colored cyst may represent Breus' mole,
which is associated with Turner's syndrome (45, X) and with fetal demise.5(pp293–6)
Any suspicious specimen must be examined by a pathologist, with follow-up as indicated by the
disease process.
Umbilical Cord
While opinions of authorities differ with regard to the limits of normal for cord length, 40 to 70 cm
would appear to be a reasonable range.3,5(pp183–5),7 The typical umbilical cord is long enough (55 to 60
cm) to allow the infant to begin nursing before placental delivery. This provides a release of oxytocin
to facilitate uterine contractions and both the shearing and delivery of the placenta.3
In part, cord length is genetically determined. However, the length of the umbilical cord is also
increased by the tension the fetus places on the cord. Hence, a short cord is associated with a less
active fetus, fetal malformations, myopathic and neuropathic diseases, Down syndrome and
oligohydramnios.
Short cords may result in cord rupture, hemorrhage and stricture. Cords of insufficient length may
also result in breech and other fetal malpresentations, a prolonged second stage of labor, abruption
and uterine inversion.3
The umbilical cord may become excessively long because of fetal hyperkinesis. Long cords are
associated with entanglements, torsion, knots and thromboses.
Abnormalities of cord length are clearly associated with an array of longstanding intrauterine factors
and consequences, some of which may become apparent only much later in a child's life. Hence, cord
length should be documented for every delivery.
Throughout its length, the typical umbilical cord has a fairly uniform diameter (2.0 to 2.5 cm). Narrow
areas may represent a focal deficiency of Wharton's jelly and are associated with torsion and fetal
death.3
Diffuse edema of the cord is associated with hemolytic disease, prematurity, cesarean section,
maternal preeclampsia, eclampsia and diabetes mellitus. Cord edema may also be associated with
either transient tachypnea of the newborn or idiopathic respiratory distress syndrome. Focally
edematous cords are associated with trisomy 18 syndrome, patent urachus and omphalocele.
Necrotizing funisitis is a severe inflammation of the cord that sometimes has a distinctive segmental
resemblance to a barber's pole.8 This inflammatory condition may represent syphilis or some other
acute, subacute or chronic infection. Swelling, necrosis, thrombosis and calcifications may be
present.5(pp278–80)
Cord Insertion
The umbilical cord typically inserts into the placenta near its center. About 90 percent of cord
insertions are central or eccentric. About 7 percent of umbilical insertions occur at the placental
margin. Marginal insertions are generally benign.
In about 1 percent of singleton fetuses, cord insertion is velamentous (Figure 6). This type of cord
insertion is associated with an increased risk of fetal hemorrhage from the unprotected vessels, as
well as vascular compression and thrombosis. Velamentous cord insertion is also associated with
advanced maternal age, diabetes mellitus, smoking, a single umbilical artery and fetal malformations.
FIGURE 6.
Webs of amnion at the base of the cord may compromise circulation to the fetus.
Cord Knots
A true cord knot occurs when the fetus passes through a loop of umbilical cord, usually early in
pregnancy. In most cases, a knot does not cause fetal compromise. However, if sufficient tension is
placed on the cord before or during labor and delivery, blood flow may be cut off, and signs of fetal
asphyxia may occur.
Cord Vessels
The umbilical cord typically contains two arteries and a single vein. If only one artery and one vein are
grossly visible, the fetal anomaly rate is nearly 50 percent.11 These anomalies may affect the
9
cardiovascular, genitourinary or gastrointestinal system, and other systems as well.5(pp183–5),
Thromboses
Thrombosis of cord vessels is often overlooked by both delivering physicians and pathologists. This is
an important cause of fetal injury.10
Fetal membranes should be thin, gray and glistening. Thick, dull, discolored or foul-smelling
membranes indicate the possibility of infection. The nature of the odor may provide a clue to the
infecting organism: a fecal odor may indicate Fusobacterium or Bacteroides, while a sweet odor may
indicate Clostridium or Listeria.5(pp542)
Green-colored fetal membranes are frequently the result of meconium staining. However, a green
color may be imparted by changing blood pigments from an earlier bleeding event or by the
myeloperoxidase in leukocytes in the case of infection.
Thick green slime that easily rinses off the membranes is meconium. Any other pigmentation requires
histologic determination.
When any abnormality of potential clinical significance is identified, the placenta should be sent for
pathologic examination. Cultures or additional special studies should be obtained before the placenta
is sent to pathology.
Indications for pathologic examination include a poor pregnancy outcome (prematurity, intrauterine
growth retardation, perinatal death and asphyxia), systemic maternal disorders, third-trimester
bleeding and evidence of fetal or maternal infection.2(pp701–3)
In patients with multiple gestations, the placenta must be examined for zygosity, vascular
anastomoses and numerous common abnormalities. The individual cords should be labeled for the
pathologist (i.e., twin A and twin B).
Controversy exists as to whether the placental specimen should be fixed in formalin or refrigerated.
Therefore, the guidelines of the delivering physician's institution should be followed. If the specimen is
to be fixed, copious amounts of formalin (at least 10 times as much formalin as placental tissue)
should be used. Refrigerating the specimen in a container the size of a large ice cream carton
preserves the placenta very well for a few days and allows it to be available if the infant shows some
abnormal clinical findings during the first few days of life.
The pathologist should be notified of the clinical situation, and questions should be answered. Interest
in placental pathology has increased in recent years, and the pathologist can contribute to the
diagnosis and treatment of the mother and infant.2(pp660–721)
Ultrasonography can be used to identify many of the abnormalities described in this article. Indeed,
ultrasonography and the possibility of surgical intervention have been partly responsible for the
resurgence of interest in placental pathology. Discussions of ultrasound examination and fetal
surgery, as well as the development of the placenta, are beyond the intended scope of this article.
However, an excellent review article on placental ultrasonography is available.4
Final Comment
Pathology fees for placental examination vary but are similar to those for a surgical specimen. The
question of whether pathologic examination of the placenta will change outcome must be
considered.
Documentation of the delivery room examination of the placenta, plus the pathologic examination
when indicated clinically or by hospital policy, will preserve valuable information.12 A suggested form
for documenting the clinical findings and the indications for pathologic evaluation is presented in
Figure 7. Since some indications for placental examination are not apparent at the time of delivery, it
may be wise to save the placenta (labeled and refrigerated or preserved in formalin) until the neonatal
outcome is determined.
FIGURE 7.
Suggested form for documenting the clinical findings of the placental examination, as well as the indications for
pathologic examination.
It has been suggested that all placentas should be sent for complete pathologic examination,7 but
this approach may represent an overuse of resources. In any event, if placentas are sent to pathology
for the indications that have been discussed in this article, few necessary examinations are likely to be
missed.1 At minimum, the hospital's requirements for the handling of placentas should be followed.
Author Information
JOSEPH F. YETTER III, col, mc, usa, is a faculty development fellow in the Department of Family
Practice at Madigan Army Medical Center, Fort Lewis, Wash. Dr. Yetter graduated from Indiana
University School of Medicine, Indianapolis. He completed an internship in surgery, a residency in
pathology and a residency in family practice at Madigan Army Medical Center.
The author gratefully acknowledges the contributions and suggestions made by the physicians who
reviewed the manuscript: Kurt Benirschke, M.D.; Paul Evans, D.O., COL, MC; Mark J. Stephan, M.D.;
William F. Miser, M.D., LTC, MC; Jeff Clark, M.D., LTC, MC; Anne B. Shrout, M.D., MAJ, MC; Bruce A. Britton,
M.D., MAJ, MC, and Mary Biglow, D.O., CPT, MC.
Address correspondence to Joseph F. Yetter III, M.D., 79 Hewitt Dr., Steilacoom, WA 98388. Reprints are
not available from the author.
Reference(s)
1. Salafia CM, Vintzileos AM. Why all placentas should be examined by a pathologist in 1990. Am J
Obstet Gynecol. 1990;163(4 Pt 1):1282-93.
2. College of American Pathologists. Conference XIX on the Examination of the Placenta: report of the
Working Group on Indications for Placental Examination. Arch Pathol Lab Med. 1991;115:660-721.
3. Heifetz SA. The umbilical cord: obstetrically important lesions. Clin Obstet Gynecol. 1996;39:571-87.
4. Kuhlmann RS, Warsof S. Ultrasound of the placenta. Clin Obstet Gynecol. 1996;39:519-34.
5. Benirschke K, Kaufmann P. Pathology of the human placenta. 2d ed. New York: Springer-Verlag,
1990.
6. Driscoll SG. Choriocarcinoma: “incidental finding” within a term placenta. Obstet Gynecol.
1963;21:96-101.
7. Kaplan CG. Postpartum examination of the placenta. Clin Obstet Gynecol. 1996;39:535-48.
8. Fojaco RM, Hensley GT, Moskowitz L. Congenital syphilis and necrotizing funisitis. JAMA.
1989;261:1788-90.
9. Macpherson T. Fact and fancy. What can we really tell from the placenta?. Arch Pathol Lab Med.
1991;115:672-81 1991;115:1211]
10. Rayne SC, Kraus FT. Placental thrombi and other vascular lesions. Classification, morphology, and
clinical correlations. Pathol Res Pract. 1993;189:2-17.
11. Leung AK, Robson WL. Single umbilical artery. A report of 159 cases. Am J Dis Child.
1989;143:108-11.
12. Kaplan CG. Forensic aspects of the placenta. Perspect Pediatr Pathol. 1995;19:20-42.
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