Join us in creating a paradigm shift in how placentas are handled in the delivery room !

Placental triage is the standardized, thorough gross examination of the placenta in the delivery room, to identify abnormal placentas to send to surgical pathology for complete gross and microscopic examination and to save the normal placentas for 7 days, refrigerated, until the condition of the infant and mother are stabilized, with documentation in the medical record of the examination findings. Despite the long description, once well practiced, placental triage only takes a couple of minutes.

No doubt the concept of placental triage has been around for quite a while, practiced to varying degrees with varying consistency across the country, with variable numbers of placentas submitted to pathology for various reasons. To address this inconsistency in placental handling, in 1989 a consensus group of experts in placental pathology, obstetrics, neonatology, perinatology, epidemiology and malpractice law gathered to discuss the numerous issues surrounding placental examination. The group formally recommended that placental examination start with universal placental triage in the delivery room. This and other recommendations for placental handling, were published in the July 1991 issue of the Archives of Pathology and Laboratory Medicine, with the entire issue dedicated to "The Examination of the Placenta: Patient Care and Risk Management."

Regarding placental triage, Dr. Kurt Benirschke summarized the conference recommendations as follows. Obstetricians are encouraged to make an initial detailed and recorded examination of all placentas. Abnormal placentas, those from abnormal deliveries and placentas which meet other parameters as defined by their institution, are submitted to pathology for gross and microscopic examination; the remainder are saved for 7 days, refrigerated, until the condition of the child and mother are stabilized.

Conference participants acknowledged this will not happen all at once. Unmotivated or uniformed examiners will inadequately study the placenta, and understand little in terms of its significant features. The assurance that a genuinely expert study of the placenta is undertaken will come only after motivation and wider dissemination of knowledge of placental pathology.

Placentology is a young field. Admittedly, many gross and microscopic abnormalities are of uncertain clinical significance. This doesn't imply they are unimportant, only that gaps exist in the current knowledge of antenatal and intranatal pathology. But there is consensus, that placental knowledge starts with placental triage.

Placentas may be referred to the pathology laboratory for a variety of reasons: diagnostic, either for child or mother; prognostic, to predict the risk for and outcomes of future pregnancy; investigative; and legal. Although the primary goal of placental triage is to identify placentas which would benefit from examination in pathology, placental triage may also provide immediate, valuable information in the delivery room. For example, it may identify: abnormalities which may explain problems encountered during labor and delivery (e.g. marginally inserted umbilical cord near the point of rupture); potential maternal problems (e.g. fragmented maternal surface suggesting retained placental tissue, increasing the risk for postpartum bleeding and, if not removed, possibly choriocarcinoma); potential fetal problems (e.g. disrupted umbilical cord or fetal surface blood vessels, suggesting fetal hemorrhage); and potential infection (e.g. spots on the umbilical cord suggesting prenatal Candida infection); to name a few.

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TASK 1: Create or review your institution-specific "INDICATIONS FOR PLACENTAL EXAMINATION"

Placental triage starts with the establishment of institution specific "Indications for Placental Examination", as a guide to those attending the birth for selecting placentas to send to surgical pathology. Typically, these indications are classified as "Maternal Indication", "Fetal Indications", and "Placental Indications."

"Maternal Indications" include things like:

  • History of reproductive failure
  • Unusual disorder of mother
  • History of or strong suspicion of maternal drug use
  • Systemic lupus erythematosus
  • Poor obstetric history
  • Diabetes mellitus or gestational glucose intolerance
  • Hypertensive states of pregnancy
  • Repetitive bleeding (other than minor first trimester bleeding)
  • Placenta previa
  • Oligohydramnios
  • Polyhydramnios
  • Premature rupture of membranes
  • Maternal fever
  • Maternal infection
  • Abruptio placentae

"Fetal Indications" include things like:

  • All multiple gestations
  • All intrauterine and neonatal deaths
  • Any evidence of fetal distress during labor and delivery
  • Fetal tachycardia
  • Ominous fetal heart tracings
  • Viscid/thick meconium
  • Suspected infection prenatally or with the neonate
  • All admissions to the NICU
  • Prematurity (recommendations vary: 32 weeks or less, 35 weeks or less, 36 weeks or less)
  • Postmaturity (more than 42 weeks)
  • Unexplained premature births
  • Intrauterine/fetal growth retardation
  • Neonatal respiratory distress or tachypnea
  • Unusual disorder of the fetus/neonate
  • Congenital anomalies
  • Hydrops
  • Erythroblastosis fetalis
  • Severe CNS depression (some say, Apgar score 3 or less at 5 minutes, others say less than 5 at 1 minute and/or 5 at 5 minutes)
  • Neurologic problems including seizures
  • Neonatal diagnostic enigmas (may not know right away, that is why the placenta should be saved for 7 days)
  • Any clinical abnormality that keeps the neonate in the hospital longer than is usual for normal newborns

"Placental Indications" include:

  • any gross abnormality of the placenta, its membranes or its umbilical cord, as identified prenatally or during placental triage

And of course there are "Other Conditions", including:

  • when innovative or unusual therapeutic or diagnostic procedures have been performed during pregnancy, especially if invasive
  • all high risk pregnancies, however they are defined
  • any abnormality pregnancy, during delivery, or in the clinical condition of the neonate or mother
  • any case with suspicion of potential litigation
  • in other words: any placenta with suspicion of an abnormal pregnancy, abnormal delivery, abnormal infant or potential litigation

Placental Triage is the tool used to identify those placentas which meet the placental indications.

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Early placental development

With fertilization of the ovum by a sperm, usually within the fallopian tube, human development begins. Coupling of the ovum, which contributes half the chromosomes, and the sperm, which contributes the other half of the chromosomes, creates a single cell called the zygote, which carries all of the chromosomes. About 30 hours after fertilization, the zygote begins to divide, first into 2 daughter cells called the blastomeres, and then into progressively smaller blastomeres, until at about 3 days after fertilization a 16 blastomere ball called the morula, enters the uterus.


Early placental developement

A day later, fluid from the uterus infiltrates the morula, into the spaces between the cells. As the fluid increases, the still dividing and growing ball of cells, separates into 2 parts: the trophoblast (most of the cells form this outer layer, from the Greek word trophe meaning nutrition, the forerunner of the placenta) and the embryoblast (a smaller central, inner mass of larger cells, forerunner of the embryo and umbilical cord.) The remaining fluid filled spaces coalesce to form a large single space, the blastocyst cavity. With these changes, by 4-5 days, the morula is converted into the blastocyst. The blastocyst lies free in the uterus for about 2 days before implantation.


Placenta at 6-7 days

*syncytiotrophoblast: sin-sish-e (long e) -o-tro-fe (short e) -blast, emphasis on "sish"
**cytotrophoblast: sigh-te (short e) -tro-fe (short e) - blast, emphasis on "sigh"

At 6-7 days, the now 107-256 cell blastocyst is a 0.1x0.3x0.3 mm flattened cyst which orients itself so the embryoblast end attaches to the endometrium lining the uterus, as the implantation pole. The tiny blastocyst sinks deeper and deeper into the up to 1.0 cm thick mid-cycle endometrium, eventually being completely covered by it.

Contact of the blastocyst trophoblast shell with the endometrium (i.e., implantation) stimulates the trophoblast shell to split into 2 layers of cells - an inner layer and an outer layer. As the blastocyst sinks deeper into the endometrium, the outer layer of cells, progressively outward from the implantation pole, is transformed into a single, gigantic multi-nucleated syncytiotrophoblast* by fusion of the individual cells. The inner layer of cells, not in contact with the endometrium, remain unfused as cytotrophoblasts**. The syncytiotrophoblast no longer has the ability to evolve into other cell types, whereas the cytotrophoblasts acts as the placenta's stem cells from which all the other specialized placental cells develop.

Placental development at the implantation pole

At the implantation pole, the syncytiotrophoblast becomes very thick and extends finger-like branches deep into the endometrium. As the blastocyst sinks deeper and deeper into the endometrium, as more and more of the outer trophoblast layer comes in contact with the endometrium, more and more of the trophoblast shell is transformed into syncytiotrophoblast. Eventually, when the blastocyst is entirely covered by endometrium, the entire outer trophoblast shell is transformed into syncytiotrophoblast. Later, when the blastocyst grows bigger, up and out of the endometrium, the syncytiotrophoblast at the anti-implantation pole loses contact with the endometrium and atrophies. That is why the placenta is not present around the entire circumference of the gestational sac at delivery.






As placental development continues, the embryoblast is also evolving. Only the embryoblast development pertinent to the placenta will be reviewed here.

Placenta at about 7 days

Just as the trophoblast divides into 2 layers of cells, so does the embryoblast.

About day 7, a layer of flat cells forms on the outer aspect of the embryoblast, facing the blastocyst cavity, called the embryonic endoderm. Spaces form between the remaining cells of the blastocyst, "pushing" them together to form an inner mass of cells surrounded by the growing cystic spaces, which gradually fill with fluid. At this point, development of the embryo begins in earnest with creation of the bilaminar embryonic disc within the inner mass of cells.

Placental development: amnion, chorion, amniotic cavity

The cytotrophoblast cells underlying the embryo generate a thin layer of cells which expand over the embryonic endoderm, surrounding the embryonic disc within its growing, fluid filled cavity. These cells become the amnion, and hence the amniotic sac, of amnion cells containing the embryo/fetus and amniotic fluid in the amniotic cavity, is created.

The cytotrophoblasts of the anti-implantation pole transform into a layer of chorion cells, which form the chorionic sac encasing the amniotic sac.

Therefore, in early gestation there are 2 distinct sacs, the amniotic sac and the chorionic sac. Between the 7th and 12th weeks of gestation, the fetus has grown enough that the amniotic sac completely fills the chorionic sac, with the amnion pressing tightly against the chorion creating the single gestational sac present at delivery.

Placental development: decidua

During this time, the endometrium is also changing. It is transformed by the hormones of pregnancy into decidua. The decidua produces various hormones, enzymes and proteins during pregnancy, and regulates the transfer of water and electrolytes between the uterus and placenta. It may also have an immunologic function that helps support the pregnancy.

The decidua is named based upon where it is in the uterus. It is the decidua basalis where it is under the placenta. It is the decidua capsularis over the rest of the placenta (recall: in early gestation, the entire sinking blastocyst is gradually completely covered by endometrium; later as the blastocyst grows up and out of the endometrium, residual endometrium clings to the anti-implantation surface as the decidua capsularis.) It is the decidua parietalis everywhere else in the uterus. Between the 15th and 20th weeks of gestation, the gestational sac grows to completely fill the uterus, resulting in the decidua capsularis and decidua parietalis pressing tightly against each other to create the decidua vera for the rest of pregnancy.

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Now, the placenta is forming at the implantation pole and the embryo is developing within the amniotic sac. How do they get together? How does the placental-fetal system hook up to the maternal blood supply?

Development of placental blood flow

During this time, the bottom layer of syncytiotrophoblast is continuing its adventure into the endometrium in search of maternal blood vessels to tap into, first into maternal capillaries and eventually into the spiral arteries (so named because they are somewhat tortuous vessels.) The syncytiotrophoblast actually erodes the maternal blood vessel wall, invades the wall through the eroded area, and allows the wall to heal over it.

The incorporation of the syncytiotrophoblast into the spiral artery wall is a critical part of establishing maternal-placental, utero-placental blood flow. The modification makes the spiral arteries resistant to the vasoconstrictors circulating in the maternal blood, allowing the spiral arteries to remain open and fully dilated, with unimpeded blood flow from the maternal uterus into the placenta. With conditions like pre-eclampsia, this modification is incomplete, flawed, and the spiral arteries remain responsive to the vasoconstrictors with subsequent decreased utero-placental blood flow.

The mass of syncytiotrophoblast prepares for this maternal vascular connection by creating spaces within its mass to accept the maternal blood, thereby establishing blood flow from the maternal uterus into the placenta.

Placental development of fetal villous trees

Placental villous tree

At the same time, the cytotrophoblasts underlying the amniotic sac, tunnel down into the syncytiotrophoblast mass to the same spaces. Once the cytotrophoblast tunnels are created, the embryo sends capillaries across the fetal surface of the developing placenta which then dive into the tunnels until their ends dangle in the placental vascular spaces, thereby establishing blood flow between the embryo/fetus and placenta.

The embryonic, then fetal vascular structures dangling into the placental vascular spaces develop into villous trees, and the vascular spaces coalesce to form the intervillous space (e.g. the space between the villous trees.)

The villous trees are so named because they resemble trees and their basic structure is established early in gestation. A "trunk" dives down into the placenta from the fetal surface vessels, as the stem villus, which divides into large branches, the intermediate villi, with nutrient gathering structures at their ends, the terminal villi. However, during the second and third trimesters, the terminal villi continue to mature in such a way as to increase the quantity and quality of oxygen and nutrient exchange across the terminal villi between the maternal and fetal blood, in response to the demands of the growing fetus.





About 60 villous trees hang into the intervillous space. They float in, are bathed by the maternal blood that has literally been squirted into the intervillous space from the spiral arteries. Oxygen and nutrients are absorbed by the terminal villi from the maternal blood and are transferred across the terminal villi into the fetal blood circulating in the villous trees, which is then carried out of the villous trees, through the placental fetal surface blood vessels to the umbilical cord to the fetus.

And there you have it: maternal to placental to fetal blood flow. Any condition that interferes with the maternal blood flow into the placenta, any condition that interferes with the extraction of oxygen and nutrients by the terminal villi, any condition that interferes with the transfer of oxygen and nutrients across the terminal villi into the fetal blood, or any condition that interferes with the transport of the fetal blood out of the placenta to the fetus, may hamper fetal growth and development. Keep this in mind as you learn about the placenta.

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Normal term placenta, with near marginal cord insertion and normal extraplacental membranes


The placenta at birth includes:

  • the extraplacental membranes of the gestational sac that encase the fetus and amniotic fluid
  • the umbilical cord that allows the transfer of fetal blood between the fetus and placenta
  • and the placental disk, which includes:
    • the fetal surface that faces the fetus
    • the maternal surface that is attached to the uterus
    • the parenchyma in between the fetal and maternal surfaces (intervillous space with villous trees)


Extraplacental membranes layers (formalin fixed)




The extraplacental membranes consist of 3 layers: the amnion, the chorion and the decidua vera. Ror the most part, the membranes should be translucent, smooth and glistening. They may show patchy opacity, depending upon how much residual atrophied placental tissue remains (recall: during early gestation, syncytiotrophoblast develops around the entire circumference of the blastocyst when it is completely covered by endometrium) and how much decidua vera is attached.


Normal term placenta with central cord, membranes trimmed off


The fetal surface should also be smooth and glistening, as it is also covered by amnion and chorion. The fetal surface blood vessels should be distended and supple. It is impossible to differentiate between the arteries and veins on the fetal surface as they are grossly and microscopically similar. However, the arteries (which actually carry deoxygenated fetal blood back to the placenta) cross over the veins (which carry the oxygenated blood from the placenta to the fetus), especially at the base of the umbilical cord. It is important, if there is a fetal surface vascular lesion, to identify the vessel type grossly as it cannot be done microscopically.

Increasing progressively toward term, there are white bumps and patches of subchorionic fibrin on the fetal surface. They are superficial, inconsequential areas of "scarring" on the fetal surface which develop in response to repeated assault by the fetus from above and from the maternal blood flow from underneath.

The fetal surface is blue-purple, as a reflection of the blood flowing through the underlying placental parenchyma.

The umbilical cord consists of white, homogeneous Wharton's jelly, a simple "ground" substance of structural tissue, a few cells and much water, surrounding and protecting the umbilical vessels that traverse the cord between the fetus and placenta.

There are typically 3 umbilical vessels: 1 vein which carries the oxygenated blood from the placenta to the fetus (anatomically a vein because it hooks into the fetal circulation at the level of the liver, on the venous return side of the heart) and 2 arteries which carry the deoxygenated blood from the fetus back to the placenta (anatomically arteries because they are branches of the right and left iliac arteries.)

Umbilical cord twist direction and severity

Most umbilical cords are twisted at birth. Twist direction is easily determined by identifying the upward direction of the twist. Left twists outnumber right twists, 7:1. The twist configuration is thought to confer strength to the cord, to protect the umbilical blood vessels. Think how hard it is to tie a coiled phone cord into a knot, or to wrap it tightly around something.

Cord twist direction is unimportant, and is not related to handedness of mother or child. The severity of the twist, however, is important. Cord twisting is, at least in part, related to fetal activity. Accordingly, expect a very active fetus to have a more twisted umbilical cord - a good sign. On the other hand, expect a more sedate fetus to have a less twisted umbilical cord - a potentially worrisome sign. Then the question becomes, why was the fetus sedate?

Typically, the umbilical cord inserts on the placental disk fetal surface (as in the 2nd placental photo above), usually at or around its center, occasionally eccentrically, and with the protection of Wharton's jelly all the way to the placental surface.

Velamentously inserted umbilical cord


In 7% of placentas, the umbilical cord inserts at the placental margin (as in the 1st placental photo above), hence the designation marginally inserted umbilical cord. This is also referred to as a battledore insertion, resembling a "battledore" (i.e., a badminton racquet.)

In 1% of placentas, the cord "inserts" into the extraplacental membranes, a condition called velamentous insertion of the umbilical cord. This cord insertion is potentially dangerous for the fetus, during gestation and at delivery, because after the "insertion" point, the umbilical cord blood vessels traverse the extraplacental membranes for some distance without the protection of Wharton's jelly. During gestation and labor, pressure by the fetus on those vulnerable vessels could impair fetal blood flow through them.

Placental maternal surface, with digitate lobe (10 o'clock) - formalin fixed placenta

The maternal surface is also called the basal plate, as it is the base of the placenta attached to the maternal uterus. It is composed of 10-40 islands of parenchyma called cotyledons, subdivided by an incomplete system of grooves called septa (the placenta in this picture is formalin fixed, hence the overall gray-brown color.) During gestation, the placenta grows in the confined space of the uterus. When it can no longer grow laterally, the placenta buckles in on itself creating the septa which randomly divide the parenchyma into the cotyledons. At delivery, all of the cotyledons should be present and accounted for. Retained placental tissue puts the mother at risk for postpartum hemorrhage and, if not removed, choriocarcinoma.

Accessory lobes of parenchyma occasionally form along and attach to the placental margin (digitate lobes, pictured above - at the 10 o'clock position) or away from the placenta in the extraplacental membranes (succenturiate lobes, not pictured.)

Placental maternal surface with nodule (presumed infarct)

The maternal surface should be homogeneously dark red and the parenchyma should have a uniform consistency (the placenta in this picture is formalin fixed, hence the overall more gray-brown color.). The parenchyma gets its color from the fetal blood remaining in the villous trees at delivery, and is dependent upon the fetal hematocrit. In cases of fetal anemia, the placental parenchyma will be pale. In cases of fetal polycythemia, the placental parenchyma will be very dark red.

Because the villous trees are evenly spaced in the intervillous space, the parenchyma is uniformly spongy when palpated. Occasionally, there will be firm, tan-white nodules on the maternal surface. Such nodules may be infarcts, intervillous thrombi, chorangiomas or other lesion, elucidated only by microscopy.

Placental maternal surface microcalcifications

Placental maternal surface decidua basalis

The maternal surface of the term placenta also shows variable amounts of pin-point, yellow-white gritty granules of calcium salts. They usually appear after 29 weeks gestation, and increase progressively until term (the placenta in this picture is formalin fixed, hence the overall gray-brown color.) Although the quantity varies from placenta to placenta, immature placentas rarely have a significant amount of calcium, whereas postdates placentas may be densely gritty. It is an unreliable sign of maturity, and the quantity does not impact function and therefore it is of no clinical importance.




When the placenta separates from the uterus during the 3rd stage of labor, it does not split off evenly between maternal and placental tissue. In fact, the delamination occurs in the decidua basalis in an unequal plane. The more gray, residual decidua basalis is present on the maternal surface as a 1-3 mm variably thick layer over the more red placental parenchyma (the placenta in this picture is formalin fixed, hence the overall gray-brown color.) The quantity is unimportant. However, the decidua contains the maternal spiral arteries and is part of the most important and intimate contact zone between maternal and fetal tissues, the maternal surface.

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  1. Altshuler: Placenta Within the Medicolegal Imperative; Arch Pathol Lab Med, July 1991, 115:688-700.
  2. Altshuler, Deppish: 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, July 1991, 115:701-703.
  3. Benirschke: College of American Pathologists Conference XIX on the Examination of the Placenta: Summary; Arch Pathol Lab Med, July 1991, 115:720-721.
  4. Driscoll: Placental Examination in a Clinical Setting; Arch Pathol Lab Med, July 1991, 115:669-671.
  5. Gersell: ASCP Survey on Placental Examination; Am J Clin Path, Feb 1998, 109(2):127-142.
  6. Naeye: Disorders of the Placenta, Fetus and Neonate: Diagnosis and Clinical Significance; Mosby-Year Book, Inc., 1992.
  7. Schuler-Maloney, Lee: The Placenta: To Know Me Is To Love Me. A reference guide for gross placental examination; DSM PathWorks, Inc., 1998.

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