Our group has been closely involved in community hospital placental pathology since
Dr. Shaw attended Dr. Doug Shanklin's groundbreaking CME course in Gatlinburg, Tenn.
in 1978. We have given focused attention to placental pathology
since then and consider that we have an actual "placenta program" concerning
placenta evaluation for our patients (HERE). Our hospital now has the second largest delivery volume in S. C. We tend to examine all placentae from gestations of abnormal (1) pregnancies and/or (2) L&D experiences. We have a "placenta green sheet" requisition which comes down with each case & contains a check list of valuable factors which may have applied to the case prior, during, and after delivery. For example, it is quite unwise to entertain a pathological diagnosis of placenta accreta in the absence of an indication of "difficult placental delivery". A main and valuable goal of the pathology exam of the placenta is to show that it was free of any currently-known abnormality. Should an abnormality be discovered, physicians are then provided "heads up" information that they can consider as they evaluate the progress of the baby's developmental milestone markers. That is, it is valuable to know that your baby's placenta was normal. Even if antepartem & L&D seemed normal, a disaster such as toxic shock syndrome can happen some days after discharge (L12-6661).
Because a significant percentage of placental abnormalities turn out to have unknown clinical significance in that mother's particular case, it is a real problem for the obstetrician, nurse practitioner, certfied nurse midwife, nurse, or pediatrian to discuss the placental findings unless they are CRUCIAL to the family understanding the situation with their newborn(s).
PATIENTS: HERE is sort of a lay person's page which includes info from our four month study of ALL placentae delivered. It incudes warnings about YOU trying to "read" too much into a placenta pathology report.
ANATOMY: To the naked eye, one sees the umbilical cord dangling through remnants of the ruptured amnionic sac and attached to the placental disc (chorionic plate). Surrounding the entire maternal-surface perimeter of the intact sac and plate/disc unit is a thin layer of maternal decidual tissue (decidua capsularis coating the sac and decidua basalis coating the plate/disc). This thin line or interface layer of decidual cells surrounds the sac and disc structure and stands between those elements and the inner or interior uterine surface and represents a potential-space cleavage plane for the sac and plate/disc
to physiologically loosen free and be easily delivered vaginally.
Scattered small areas that were uncleaved at delivery and the placenta tugged free can appear to be patches of placenta accreta (this artifactually amplified during C-section delivery. When delivered intact & normal, this decidual layer is seen grossly as a faintly shiny maternal-surface which is always spmewhat marred by the trauma of delivery. If abnormal patches or zones are present (especially noticed in placentae removed at C-section prior to normal lytic cleavage within that decidual layer), sections for histology are best if they represent normal and abornal surface junction. Between that decidual layer & endometrial layer, one sometimes sees a thin fibrin layer (Nitabuch's fibrin).
[common] ACUTE CHORIOAMNIONITIS (ACA): As an aid to our neonatologists dealing with possible neonatal sepsis cases, 2010 found us instituting rapid assessment with next-day diagnosis when requested. We also offer classical frozen section diagnosis
(almost never ordered) and have developed a means to do frozen sections on partially or completely formalin fixed tissue (utilized about 2-4 times a year). By the end of
2010, we had reorganized the placenta requisition sheet so that we might be tipped off & able to proactively expidite what could be ACA cases, to include:
- CLINICAL SUSPICION:
- newborn CBC abnormals: bandemia, leukocytosis, thrombocytopenia.
- newborn fever (febrile): since there are scant other reasons for a febrile newborn, This demands an unusually careful scrutiny of the histology because it may be a case of maternal GBS positivity on antibiotic therapy which can deliver a placenta without evidence of ACA [L10-14413].
- mother is GBS positive.
- premature rupture of membranes (PROM): when the membranes are ruptured (amniorrhexis) more than one hour prior to delivery.
- prolonged rupture of membranes (PPROM): when the membranes have been ruptured 12 hours or more pre-term and 18 hours or more at term, prior to delivery.
- foul smelling fluid at delivery.
- ROUTES OF PLACENTAL INFECTION17:
- ascending: the vast majority are by this route and affect the extraplacental membranes (maternal component) first!
- hematogenous: these uncommon cases are by way of maternal blood & generally show up first in the chorionic tissue; In other instances, the ACA fetal component is exclusively (L11-2986) or predominantly involved & maternal component uninvolved or positive to a much lesser degree; you might find it in the placenta of an IUFD case (A10-15) reflected in the placenta as fetal leukocytosis which may demonstrate some secondary vascular invasion by polys or, if intrachorionic thrombi are present, as dirty, septic-type intrachorionic thrombi (L11-14552).
- other (rare): from endometritis; from pelvis via fallopian tubes; from percutaneous procedures (even intrauterine fetal transfusion).
- HISTOPATHOLOGY: In the 21st century, pregnant mothers are monitored for group B Strep. (GBS). There is a formalin fixation, H&E staining artifact sometimes seen in loose amnion stroma that appears to be copious cocci (not so [L12-11343]). Polys may marginate (even copiously) noninfiltratively beneath the fibrin layer underneath the chorionic roof membrane (maybe starting at the peripheral amnion-sac refflection angle [L12-16297]) without
necessarily implying clinical significance (but maybe worth mentioning). I (EBS) think that the below grade & stage system is interesting but doubt the clinical utility.
THEREFORE, lets always note (1) whether either or both of the maternal or fetal components are histologically activated (polys infiltrating), as well as (2) the
distribution of activation and (3) intensity of infiltration.
More ACA notes on this page HERE. Below Staging (duration) Grading (intensity)after 16 of ACUTE CHORIOAMNIONITIS (ACA):
- MATERNAL component inflammatory response10, 15:
- Stage (duration):
ACA (polys in of roof & membranes)
- uncertain significance: scant or focal groups of subchorionic fibrin pre-diffusely marginated polys are infiltrating subchorionic fibrin; polys infiltrate the decidua capsularis & not amnion stroma.
- Stage 1 (early): acute subchorionitis (diffuse polys infiltrating subchorionic-roof marginated fibrin that is layered beneath roof stroma & amnion and chorion tissues are negative) or acute peripheral chorionitis (polys in chorionic roof membrane stroma at lateral junction with decidua capsularis/basalis). Grade = mild, moderate, severe.
- Stage 2 (intermediate): ACA (polys infiltrate actual chorionic roof stromal connective tissue). Grade = mild, moderate, severe.
- Stage 3 (advanced/late): necrotising ACA (hypereosinophilia of amnion basement membrane, heavy accumulation of polys, poly karyorrhexis [nuclear dust], something like >25% amniocyte [amnion epithelial cell] necrosis). Grade = mild, moderate, severe.
- Grade (intensity):
- Grade 1 (mild–moderate).
- Grade 2 (severe) severe acute chorioamnionitis or with subchorionic microabscesses (or septic intrachorionic thrombi [A10-15]).
- Other: acute villitis;
acute intervillositis (with intervillous abscesses); chronic (or subacute) chorioamnionitis; microfocal necrotizing acute deciduitis is often seen with ascending ACA & significance uncertain when ACA is absent [L12-1882]; eye-catching decidual plasma cells may be significant but scattered, loose groupings of lymphocytes are likely physiological.
- FETAL component inflammatory response10, 15:
- Stage 1 (Early): chorionic roof vasculitis or umbilical cord phlebitis (funicular phlebitis).
- Stage 2 (Intermediate): umbilical arteritis or umbilical panvasculitis (& maybe a few polys stray into Wharton's jelly).
- Stage 3 (Advanced): necrotizing funisitis (polys filling into Wharton's) or concentric umbilical perivasculitis.
- Grade 1 (Mild–moderate)
- Grade 2 (Severe) severe fetal inflammatory response or with intense chorionic (umbilical) vasculitis.
- Other Associated: fetal vessel thrombi.
- Other specific features:
- More detail (HERE) as to histopath & sampling.
- INTERPRETATION CAVEAT: the neonatal-sepsis-inducing threat of ascending ACA to the baby is heralded (an implicit threat) by polys in the the amnion sac component & becomes a real-live threat when polys infiltrate the chorionic roof stroma. At birth with placenta showing ACA, if the baby does not have bandemia by CBC and is afebrile, then this is more likely the group that would have an increased incidence of "late sepsis".
CAUTION: The finding of one or more "severe" placental
abnormalities does not doom your child to any definite adverse
consequences at all. There were severe abnormalities in placentae
of two of my (EBS) grandchildren (severe ACA) and one of my partner's
children (HEV). All have developed normally...their doctors were able to be
forewarned as they made decisions and gave advice as these children
grew up. [back to placenta table of contents
(TOC)] Dr. Virginia Apgar, anesthesiologist, devised the Apgar score in 1953; and an abnormal Apgar score is a good general reason for a pathology
exam of the placenta.
On our placenta exam requisition sheet, you might find that the L&D providers indicate an abnormal AFI or BPP [L10-9388](a web site).
- AFI = amnionic fluid index, a measure of the volume. Done by ultrasound, fluid depth is measured in 4 uterine quadrants and the 4 measurements summed. Sum less than 5cm is oligohydramnios and equal to or greater than 25cm is polyhydramnios.
- BPP = biophysical profile is a detailed in-office type ultrasound measuring 5 factors (4 fetal activity factors and the amount of amnionic fluid. Score each of the 5 a 0 if abnormal and a 2 if normal...10 is the highest score (10 is maximally normal).
- Placental size: Most of the weight is due to the meaty chorionic plate and a minority due to the cord and the amniotic sac. On
the basis of numbers alone, placentomegaly can be diagnosed when
the weight is greater than 600 grams or the fetal:placental (F/P) weight ratio is 3:1
or lower. Interpret abnormal ratios as you do WBC differentials:
absolute or relative increases or decreases of "F" or "P" as
reason for altered ratio. Weigh after removal of
membranes, cord, and attached clot (std. weight tables don't
include membranes & cord & attached clot).
- small placenta (placenta diminutivata): An unusually
small (less than the 10th weight for dates percentile?) or diminutive placenta [L09-2617, L09-4211, L09-4852, L12-15945] may have clinical significance and is seen with some frequency. Low maternal
pregravid weight, low pregnancy weight gain, and the absence
of hand and facial edema in the gravida were all associated
with small placentas. All these factors are associated
with low maternal gestational blood volume expansion with
resulting low blood flow from the uterus to the placenta.
The most important risk factor is fetal growth retardation
(SGA/IUGR). Other factors associated with small placentas
include accelerated placental maturation and major fetal
malformations. Unevenly accelerated placental maturation
is the characteristic consequence of pre-eclampsia and
chronic maternal hypertension (which reduce blood flow
from the uterus to the placenta). Many of the major autosomal
disorders are associated with placental growth retardation.
Trisomy 21 is an exception, the fetus often being more
growth-retarded than the placenta. Excessive obstruction
of the villous chamber can cause small placenta.
Small placentae are said to be associated with increased frequency
of stillbirths and mental retardation at 7 yrs of age, independent
of the size of the fetus, malformations in the child, and
the disorders that chronically reduce uteroplacental blood
flow. The association with stillbirths raises the possibility
that small placentas are sometimes functionally inadequate
to supply all of the needs of the fetus for oxygen and nutrients.
Maternal cigarette smoking during pregnancy is a well-known
cause of fetal growth retardation; it does not cause a parallel
retardation of placental growth, so the ratio of fetal to
placental growth reduces.
large placenta (placentomegaly): Common causes
of unusually large placenta are villous edema, maternal
diabetes mellitus, severe maternal anemia, fetal anemia,
congenital syphilis, large intervillous thrombi, and a
large blood clot beneath the chorioninc (fetal surface)
roof of the placenta (pathologist often cannot identify the specific cause [L09-3132]). Rare causes of unusually large placentae
include toxoplasmosis, congenital fetal nephrosis, idiopathic
fetal hydrops, and multiple placental chorioangiomata.
Placental enlargement with diabetes mellitus and chronic
fetal and maternal anemia are usually related to abnormally
large villi. Villous edema is said to be the most frequent cause of a preterm
placenta being overweight. Recognizing placental villous
edema is important because when its widespread and severe
it makes fetuses hypoxic with resulting low Apgar scores,
difficulty in resuscitation at birth, neonatal respiratory
distress, a high neonatal mortality, and an increased frequency
of long-term neurologic abnormalities. A weight of 700 grams or higher at term (or earlier) is large; and greater than the 90th percentile weight for dates might be considered large. The term placentomegally may be technically correct in a case of fetal macrosomia (baby larger than 90th percentile) but could be an overuse of the term [L11-1124].
- Placental shape:
- Unusually thin placenta: The antecedents of thin
placentas are a placenta that was subnormal in weight, the
gravida being short, and major fetal malformations. An unusually
thin placenta increases the risk fro both fetal growth retardation,
and for neonatal death, raising the possibility that very
thin placenta are sometimes functionally insufficient. A
thin placenta does not increase the risk for long-term neurological
- Unusually thick placenta: They are usually an indication
of health rather than of disease. They are associated with
lower than expected frequencies of fetal growth retardation
and neonatal death.
- odd shapes:
- other: one will sometimes note thin spots along an edge which might suggest a low-lying implantation. Or there may be pocket-like indentations from the maternal aspect due to submucous maternal uterine nodules such as a myoma [L10-10256].
- Other-than-ACA life-threatening (IUFD) placental lesions4 (majority
visible & interpretable by naked eye exam):
- placental abruption, extensive
- placental infarction, extensive [L11-12949]
- truly knotted cord
- tight nuchal cord (usually cases of long cords)
- umbilical vascular thrombosis
- ruptured vasa previa
- chorionic vascular thrombosis,
- giant chorangioma (chorioangioma) [&/or
diffuse, severe chorangiosis or high volume chorangiomatosis]
- other cord lesions such as coarctations [L11-12886], furcations, thromboses, and velamentous situations.
- terminal villus deficiency, severe: terminal villi are capillary extrusions which are covered by a little stroma
and with the capillaries intimately beneath the outer covering by trophoblasts, that thin peripheral aspect being
referred to as a vasculsycytial membrane [L11-3589; L11-12819].
- Placental implantation: The
mid-zone of a normally thick decidua basalis at the villo-decidual interface usually lyses over time at term to create a plane of potential space & release the placenta with the baby's delivery.
The lytic process may be the basis for fetal fibronectin (an adhesive glycoprotein at the maternal-fetal interface) detection by testing to separate false from true labor. When decidua basalis is of developmentally deficient thickness or completeness of interface coverage, the placenta removes/delivers with difficulty.
The normal term placenta maternal surface, upon careful gross exam, has a faintly shiny "icing" or glaze over the cotelydon surfaces that is the remaining cotyledon-side, interface decidua basalis component still attached to the chorion. When there are dull patches are patches or zones remindful of the texture of suede or even disrupted or focal absence of the cotyledon surface, such distortions reflect the stripping that happens with the stubborn, sometimes desperate,
clinical attempts to remove the adherent placenta at time of
delivery. Post-partum bleeding can follow in accreta cases & even lead to emergency hysterectomy [L10-8875]. So, even very early and patchy instances of accreta may be detected
in cases labeled "manual removal of placenta" or "difficult
placenta delivery" [L10-10512,L11-5115] . (Most common cause of disrupted normal maternal surface is the manual delivery of C-section, usually in non-term cases which had not yet begun the physiological process of decidua basalis lysis...L11-4373). So, pathologists & PAs should look on the maternal cotyledonal
for areas where the smooth, barely shiney decidual surface is absent, especially at edges of disrupted cotyledons, & take
sections at any transition between smooth (slightly shiney) and non-smooth ("dull")
surfaces. I speculate that normal term placentae have several small accreta-type patches to keep the term placenta "tacked" in place so that the placenta does not prematurely dislodge prior to infant delivery [L11-4259].
- placenta creta: tends
to be variably expressed & starts with loss of basal decidua.
- placenta accreta: villous
adherence to internal myometrial surface (attenuated &/or absent decidua [L08-1044]).
- placenta increta: villous
adherence into myometrium
- placenta percreta: villous
adherence to through the myometrium
- placenta previa: placenta is situated
too close to, maybe even partially or totally over, the internal
cervical os & has poor development of decidua.
- The cord18: is more liable
to torsion or kinking if the diameter is too small, segmentally (coarctation) or diffusely, due to insufficient
Wharton's jelly; a term birth with cord less than 32 cm long (less
than 40 cm6)
is short (too short for normal, uneventful vaginal delivery?[L11-3400]) or greater than 100 cm long (>/= 70 cm prob. too long; >75
cm6) is too long & either short or long can be
a problem. Cord normally tends to be about the crown-heel length
Since cutting of the cord leaves a portion of unknown length on the baby, and since a cord segment is sometimes sent for blood gas determination, surgical pathology diagnosis of "short cord" may be overly sensitive (but we do it).
- Length: Short cord implies little fetal movement
(hypokinesis or akinesis) & is occasionally associated with premature
separation & hemorrhage...may impede fetal descent & may be
associated with uterine inversion (as to fetal-movement history, a thin, attentive mother may report lots of movement, yet the cord be short [L12-15945, 30 cm]). Associations with IUGR, increased
perinatal mortality, neurological abnormalities (CNS damage6),
decreased IQ, and seizures4. If vaginal delivery does occurr, the baby can be compressed too long tethered in the birth canal or even pull loose & have depressed Apgar upon delivery (L11-3400). Long cord implies excessive
fetal movement (nuchal cord danger) & may lead to congestion & thrombosis...associated
with hyperactivity syndromes.
- Insertion: 360 degree movement: is there anything
about cord insertion that is restrictive and could lead to kinking (as can
narrowing...coarctation...at the anterior abdominal wall)? Insert as a tri-cornered twirl
or as a three-pronged fork? Inserts with cord coarctation or furcation?
Inserts centrally, eccentrically, paramarginally, marginally, or velamentously?
birth hole in amnion sac is partly encircled by a large vessel...vasa
previa...from closely velamentous cord). Velamentous insertion
has 4x increased associations with multiple gestations or congenital
syndromes, 4x associations with diabetes mellitus, 2x association with
advanced maternal age &/or smoking, neurological disorders, and
2-3x assoc. with hyperactive syndromes4.
- Vessels: Is the artery (2) and vein (1) number
normal? A one artery cord frequency is 1% of deliveries & associated
with twice the incidence of renal anomalies, 4x the incidence of stillbirth,
2x the incidence of IUGR, and 2x the incidence of preterm delivery4.
- Twins have increased incidence of abnormal umbilical
cord; twin chorionicity is routinely stated in our reports but does
not determine identical vs. fraternal (that is done with DNA testing).
- Nuchal cord: pathologists have to rely on being giventhe history of cord around the neck (nuchal cord); nuchal cord usually due to a long cord but can be due to a short cord
[L07-7915]; ifthere is stillbirth, the presence of fetal erythroblastosis will be evidence that it was not a sudden death...fetus went through a stage of at least
subacute severe hypoxia [L07-7915].
- Knots or other evidence of nuchal or other compression,
torsion, or stricture; true knots in 1% of deliveries and inconsequential
unless they are an "occlusive true knot" (look for indentation
when untied and/or edematous segment toward placenta due to vein obstruction)4.
Too many helical turns per unit length (hypertwisted) may be abnormal, see below. Don't mistake
a false knot (an aneurysm) for a real knot.
- Membranous cord insertions: velamentous cord...look
for torn vessels in these insertions; liable to cord entanglements causing such as fetal demise of both twins, both having vel. insertion [L10-11996].
- Look for thrombi [L-05-8676], hematomata (watch out for clamp
and other delivery artifacts) or other compressive lesion. Thrombi
likely reflect a genetic thrombophilia from such as Protein C deficiency.
- Look for lacerations (from, say, C-section).
- "Cooked macaroni" segment: necrotizing
vasculitis - [check serology-RPR].
- Edema: may indicate maternal diabetes, B. strep
infection, Rh/HDN disease, fetal demise6
- Thin, skinny, diameter (coarctation; stricture): associated with IUGR. Is it entirely
thin [L09-2859] or just segmentally thin or multisegmentally thin?;
the 5 cm @ insertion is 50% thinner than rest of cord in this 2-vessel
cord). Thin segments can tortion & cause fetal death [L09-2296]; thin zones can tear during interventions such as C-section [L09-4109]. Coarctation may be coincidental &, at first glance, seem to be the cause of a demise until one checks the record and finds, for example, that the demise was delivered by C-section and had a near-complete abruption [L10-10256].
- Massive diameter: Beckwith-Wiedemann macrosomy
- Thrombi involving veins are more important because
can fragment to embolize to fetal CNS. See 3g, above. [artery L07-5096] Additional venous
thrombosis risk with maternal lupus anticoagulant and with maternal
- Furcate cord: (as in "bifurcation" or "trifurcation") = absent or severly deficient Wharton's (usually at @ insertion)
to the point of the vessels beginning to separate.
example) [some other cases are LMC-02-3467; LMC-03-1187
twins; LMC-03-8751; L07-11588 & L07-11588 stillbirth].
- Battledore placenta: oval shape with marginally (toward one of the poles) inserted
- Barber-pole, candy-cane-striped cord: suppurative
- Premature division of vessels at insertion: see furcate cord,
- Hypertwisted (hypercoiled) cord </= 40 cm may
be functionally too short for vaginal delivery...probably indicated
fetal hyper-movement. Normally have 1 twist per 5 cm.; hypertwisting assoc. with
- Few or no twists (hypocoiled...achirality5)
= hypo-movement. High assoc. with IUFD5.
- [common] Acute chorioamnionitis (ACA) & funisitis:
stageing details on this page HERE.
- Frozen section of cord and fetal surface
of placenta for rapid diagnosis (in our lab, we even have a technique on formalin fixed tissue.
- Routine blocks: Permanent section
roll of membranes to include the edge of the birth rupture
hole; section of cord at both ends and the middle; placental
sampling to include two or more blocks reflecting the villi
and the fetal surface membrane layers (any degree of polys
in vessel wall of cord is diagnostic; more than a few polys
into the fibrin layer underneath the fetal chorionic surface of the placenta is possibly significant & when diffusely so, is significant). Beyond cord vessels & into Wharton's jelly is "funisitis".
- Intense ACA protocol: if the requistion indicates a clinical finding or seeting on the requisition "green sheet" that implies an increased risk or likelihood that the placenta is ACA, we put extra sections of cord, membrane roll and chorionic roof surface focused on some vessels.
- Organisms: If a placenta is unfixed,
air-dried touch preps or smears from the under surface of
the placental roof of the fetal surface of the placenta
can be used for diagnosis of various organisms (the same
site for obtaining cultures)
- Extent of cord involvement:
- is it segmental, regional,
total? [degree or severity of ACA]
- vein only - phlebitis...funicular
phlebitis (vein drains placenta back into fetus).
- one artery, two arteries = funicular arteritis (hematogenous from fetus?...arterial
blood from fetus to placenta).
- Wharton's-jelly stroma
involved = funisitis.
- "funisitis" implies
vessel/vessels plus Wharton's stromal involvement (see above).
- cord segmental inflammation...with
negativity for inflammation in the several centimeters
at both insertion ends...likely reflects cord prolapse
ahead of the head and over the endocervix.
- yellowish dots/nodules
on surface indicate candida; longstanding can calcify;
lymphoplasmacytic assoc. with lues or HSV4.
Because predisposing factors likely to remain, recurrence risk
of ACA is high in next pregnancy.
- Acute inflammatory cell infiltrate at less than 18 weeks gestation is from the mother; after 18 weeks, may be from the mother and infant.
- Fetal death by other causes, followed by postmortem acute chorioamnionitis will show exudate in a maternal pattern only (no cord or chorionic vasculitis).
- Acute chorioamnionitis ascends through intervillous space whether it originates through the cervix, hematogenously from the mother, or from the underlying endometrium.
- If there is a slight acute villitis in association with a severe acute chorioamnionitis, then this suggests that the fetus is septicemic from septic amnionic fluid.
- Prominent acute villitis associated with a much less impressive chorioamnionitis is said to suggest origin from maternal hematogenous routes.
- Characteristic pattern of cervical-ascending-induced fetal chorionic vasculitis is with the perivascular infiltrate more eccentrically pronounced toward the direction of the amniotic cavity.
- If amnionic fluid is rapidly populated with organisms, then ingested by fetus, one may see funisitis predominating in umbilical arteries and the chorionic roof membranes only little if any involved.
- If only a single segment of cord shows funisitis not associated with acute chorioamnionitis, then "infected" prolapsed cord is highly likely.
- Route: Whether infection is hematogenous,
ascending from birth canal, or from endometritis/myometritis,
exudate progresses through decidua, to intervillous space,
to chorionic roof, through stroma to involve vessels & then fetus or
to fetus and then to vessels.
Vasculopathies (blood flow obstruction or hypo-oxygenation in fetal blood "supply line"11):
- extrusions of squames: fetal squamous debris extruded between amnion and either decidua parietalis or chorionic roof during L&D or postpartum placental manipulation [L09-894] is not to be confused with "amnion Nodosum".
Chorangiosis of villi: Major congenital malformations
found in 28% of chorangiosis births [L07-5499]; 27% of chorangiosis diagnoses
are associated with neonatal death. We are usually alerted
to this diagnosis by microscopic visual inspection (don't be fooled
by instances of capillary congestion); if you suspect it, the convention
for diagnosis is: 10X power exam of three different blocks (the
sites in no way related to any infarcts) and eval. of 10 or more
micro fields in each block site, with each field averaging 10 or
more villi in which there are 10 or more vascular channels per
villous (very rarely diagnosed). In practice I usually "eyeball" screen
rather than count fields. If screen is suspect, then count. As
the attached article reveals, this diagnosis prompts a careful
exam of the live baby and alerts to ischemic or diabetic problems
for subsequent pregnancies.
Intra-villous trophoblastic inclusions in stroma: when greater than four trophoblastic incusions (endophyic...inverted...intrusions can be found on an H&E slide of 2 square centimeters of placental plate microscopic cut surface, the specificity of the finding indicating increased risk that the baby has Autism Spectrum Disorder (ASD) is 92%20 but the sensitivity is less than 50% (less than a coin toss).
Villous edema: Dr. Naeye thinks any degree of villous
edema might, in the future, be found to be associated with significant
findings in the child and should be searched for. True edema
makes Hofbauer cells more obvious. Hydrops is now most often
non-immunological in etiology.
villitis: Alone, it may or may not be significant,
but should alert one for further clinico-pathologic case
- Hemorrhagic endovasculitis (HEV): Also called "fetal thrombotic vasculopathy". As
high as 86% of HEV placentae are stillborn; HEV = 50% recurrence rate (and 1/3 of those will be stillbirths);
as many as 40% of HEV live births will have some developmental
retardation (especially if associated with pregnancy-induced
hypertension and chronic villitis)...very important for pediatrician
to know this and to pick up on any developmental retardations
and manage as soon as begin to be manifest. I (EBS) have
seen "early" HEV change in one stillbirth definitely
caused by a true cord knot [LMC-05-6783]. So, there is a pseudo-HEV:
some have speculated that some HEV is the viable-endothelial-cell reaction
attempting to organize the stagnant blood in the circulation
following a fetal death [L08-11493] & not the cuase of it. I believe those cases are the pseudo-HEV cases, and I see pseudo-HEV in some stillbirths [L09-2016].
- vasculitis as part of ACA, either or both as chorionic roof vessel vasculitis or funicular (cord) vessel vasculitis or
funisitis = fetal participation.
- VUE cases with obliterative fetal vasculopathy (vasculitis & perivasculitis with downstream avascular terminal villi)
11. See more VUE info, below
- meconium-induced vasospasm as evidenced by vascular myonecrosis (myo-apoptosis).
- chorionic vessel thromboses, otherwise, of uncertain etiology: [L07-5508].
- terminal villus deficiency: see above [L11-3589]
Chronic hypoxic...low flow...villous changes: While very uncertain,
an increase in syncytial knots with some cytotrophoblastic proliferation [LMC-05-6232] is
thought by some to reflect decreased...low flow...villous chamber perfusion
(one is required to find greater than 125 to 150 knots per 100
terminal villi) [LMC-06-1557]. BM thickening in central placenta possibly
reflects hypoxia. Villous "hypermaturity" (thin & fibrous-like) may be a (more sustained & chronic ?) low flow hypoxic
change. These changes suggest retarded flow in the maternal vascular supply line11. And one finds it in midtrimester stillbirths due to poor flow following the demise & not causing the demise [L09-2016]. "Tenney-Parker" changes of the
terminal villi, an increase in syncytial nuclear clumping and basophilia, are common in cases of chronic uteroplacental malperfusion, whether fetal
flow or maternal . Expected in patients with sickle cell
Brownish to pale subchorial "thrombi" just beneath
the fetal surface *(chorionic roof) of the placenta: are related to increased
fetal movement; associated with longer cords; reflect stasis
Solid cut-surface, intraparenchymal lesions:
- Specific villitis: infection associated variety; "diffuse
sclerosing villitis" (DSV)...uniform villous involvement.
- Nonspecific villitis: Villitis of uncertain etiology
(VUE); patchy villitis. Apparently not infection-associated,
appears to be associated with (1) disorders which decrease maternal
flow to placenta (such as eclampsia) and (2) those of unknown etiology. Because
of former, isolated finding could herald recurrence in subsequent pregnancy.
Meconium: Hardly ever sufficient rectal accumulation
prior to 28-30 weeks & likely that membrane pigmentation prior
to then is hemosiderin6. Can often be found as
macrophage pigmentation in the stroma of the fetal surface amnion
and chorion stroma. Meconium expulsion can be cleared in
2-3 weeks so fluid becomes clear again. Location of pigmented
macrophages not yet reliably relatable to time after meconium expulsion. Stillbirth placentae with some greenish color grossly may have undergone compacting of the usually loose subamnionic stroma and rendering the meconium macrophages harder to visualize [L09-2016]. Don't
confuse with hemosiderin which is abnormally present prior to near
term. Look for amnion cell necrosis and vessel muscle necrosis
in cord...assoc. with poor fetal outcome.
Vasculo-syncytial membrane (V-S membranes): The
normal term placenta has syncytial trophoblasts with nuclear knots
and attenuated cytoplasm over the villous surface. Terminal
villous cross-sections typically show most of the cross-section
occupied by capillary profiles (1-6) and with one or more peripheral
ones bulging under attenuated trophoblastic cytoplasm with essentially
no stroma between maternal and fetal blood may produce chronic
hypoxia and fetal death.
Infarcts & thrombi of parenchyma: DDX also includes chorangioma & nodular chorangiomatosis [L-07-2053]. If, in every other respect,
the maternal blood supply to the placenta appears to be adequate,
then the fetus is likely to survive infarction of up to 20-30%. If it
involves over 10-15% of the placenta [L09-628 25%], it is almost invariably confined
to patients with hypertensive disease in pregnancy...look for PIH-associated "acute
atherosis" in membrane-roll decidua capsularis vessels. In 5-15% of placentae;
and, specially if infarcts are more central, they tend to be associated
with pre-eclampsia, diabetes, SLE, and utero-placental (maternal flow circuit) insufficiency [L07-11588]...may
see consequences such as IUGR, fetal distress, or IUFD4.
You have to
decide whether there is enough residual normal placenta and intervillous chamber space to support fetus. "Maternal
floor infarction" and/or "massive perivillous fibrin" can cause stillbirth and can recur; and such are most often associated
with pre-eclampsia, particularly the HELLP syndrome variety (hemolysis,
elevated LFTs, low platelets with RBC fragments). When volume of
infarcts is over 50% of placental volume, think of lupus anticoagulant
Presence of infarcts implies acute vascular occlusion by some process.
- Intrachorionic thrombi: may think it is an infarct on gross exam; indicate
feto-maternal hemorrhage but may be insensitive [LMC-01-5295,
term/near-death fetal demise, Hb2.0, K-B test 3%, fetal RBCs & not
any intrachorionic thrombi. LMC-03-2803 6-8cc of intrachorionic
thrombi.]. These may tip off to testing the mother with
such as the K-B test for circulating fetal
RBCs in mother's blood. Identifying these thrombi helps the obstetrician be forewarned
to the possible generation of maternal antibodies against one or
more fetal RBC, WBC, or Platelet antigens then detectable in a subsequent pregnancy. Fresh ones are more red, while old ones are pale.
- "Massive" or "excessive" perivillous fibrin deposition: This type of grossly massive deposition may result from immune rejection and lead to intervillous space occlusion and hypoxic fetal injury, IUGR [LMC-92-7437; LMC-94-1458; LMC-03-4820; LMC-04-6078; LMC-04-11106] or SGA, or death if affects enough volume. It may be associated with recurrent fetal problems in subsequent pregnancies. A variant where deposition is at maternal-aspect base is "maternal floor infarction"; avoid having too high of a diagnostic threshold (we have offered the warning of possible maternal thrombophilia with as low as about 5% floor involvement...LMC-06-5615; or atypical excessive involvement [L08-12153]). It can look like "marbled" beef or be as plaques or nodules resimbling older thrombi or infarcts. Implies maternal thrombophilia or hypercoagulation state10 (from such as "lupus anticoagulant" or protein C or S deficiency).
- Infarcts & thrombi of parenchyma: see below.
- chorangioma (chorioangioma) or chorangiomatosis placentae:tends to be a red color (multiple chorangiomata) [L09-3796].
- X-cell island: these sometimes become cystic
- septal cyst: of the inter-cotyledonous septae.
- Central and floor infarcts more important than peripheral perimeter infarcts.
- Infarcts of same (one episode) or variable (chronic
on-going problem) ages?
- Infarcts are geographic, sharply delineated, reddish (fresh) to pale brown to yellowish white (older).
- Subchorial or intervillous (intrachorionic) thrombi
are brownish, firm, and more vague. Intrachorionic [LMC-04-891],
if space occupying, probably reflect feto-maternal hemorrhage (a
baby has about 70cc blood). Can be grossly mistaken for infarcts.
- Breus' mole (massive subchorionic hematoma) is a rare
entity associated with IUGR.
- Intervillous/perivillous fibrin thrombosis: normally
involves all term placentas, can be seen grossly on cut surface as
faint laciness of a paler color in 25%, & excessive when more
obvious grossly on cut surface as definitely lacy or "marbled" with
paleness; & massive lesions are heavier & pale & may
rim & outline a cotyledonous lobule ("gitterinfarct")9.
Villitis may have a lacy or marbled cut surface9.
- "X cell island" nodules caused by island expansion as fibrin accumulates in island centers rather than centers becoming cystic [L07-6650].
- Intraplacental vascular thromboses give softer, tan,
slightly outlined foci.
Placental masses: teratoma or teratomatous gestation[L11-2523] vs. acardiac twin; chorangioma; blighted fetus absorbed into chorion; thrombi; infarcts; hematoma; venous lake (usually best noted by ultrasound; other benign or malignant tumors.
Focal amnion surface lesions: over placenta or
cord (must very carefully examine so as not to miss):
- amnionic: protrude from amnion surface into cavity.
- placental surface cysts: at maternal surface & often associated with subchorial fibrin & lined by subchorial trophoblasts & when numerous or larger,
tend to be associated with IUGR13 [L08-13515].
- chorionic (cystic cavitation of X cell islands): round to oval by U/S and contain a gelatinous fluid & can be just beneath the chorionic
roof (subchorionic) or intrachorionic (septal) cysts [LMC-06-4298]. Subchorionic ones may impinge on blood flow of a roof vessel or may impinge
on flow of blood at cord insertion site.
Amnion bands and loss of amnion membrane: infant
abnormalities such as loss of finger should always have high intensity
search for bands in placenta.
Fetal & maternal RBCs & WBCs: there should be very few NRBCs in
villous circulation of a normal term birth; if found, consider causes
of hypoxia, alpha Thal., hemolytic problems. Sickle cells [LMC-03-1535;
LMC-04-1866 trait; L13-1442 odd trait], spherocytes and possibly other abnormal
RBCs [LMC-03-8791], when in sufficient number, may be
discernable in fetal villous circulation or maternal intervillous chamber blood [L10-14472]. Congenital leukemia [L06-8166] with a WBC count of nearly
200,000 is surprisingly deceptive...WBC clumps most readily noted in larger fetal vessels (therefore, placenta not pale).
Decidual changes in basal decidua:
- Whitish dots:
squamous metaplasia (insignificant)
- Amnion nodosum (AN): absolutely means
severe oligohydramnious; always seen in renal agenesis
cases (superficial lanugo debris & squames form amnion surface stromal nodules that displace amnion surface epithelium). Associated
with poor fetal lung development. AN is not fetal squamous debris extruded between amnion and either decidua parietalis or chorionic roof during L&D or postpartum placental manipulation [L09-894].
- Yellowish dots:
Placenta previa: very hard for pathologist to diagnose;
maybe see some micro-organization of exposed basal placental surface
(and admixed WBCs) with elsewhere more normal. A membranous (very
thin toward one edge) zone is nearly always a placenta previa6.
Abruption of placenta: in a variable percentage
of cases it leaves its pathological mark as a retro-placental hematoma,
fresh to variably organized. Careful histological exam to be sure not an intrachorionic thrombus.
Lobation: placenta is normally a round to oval disc.
- Acute inflammatory cells are abnormal, though
significance depends on quantity and presence elsewhere
(see ACA, above).
- If lucky enough to see efferent ends of spiral
arterioles, retention of muscular wall, perivascular acute
cells, atherosis, and thrombi are always abnormal and imply
a reduction in uterine-to-placenta maternal blood flow.
- Lymphocytes probably simply reflect a fetal-maternal
immunological battle and are of no significance unless so prominent
as to extend through floor to involve basal villi.
- Lymphocytes plus plasma cells (with or without
eosinophiles) probably not normal but of uncertain significance.
- Can offer "compatible with" or "suggestive
of" placenta accreta (in a placenta which was clinically
abnormally tightly attached) if see basal decidua absent
or only 1-3 cells thick or with some attached strands of
myometrium. Cannot flatly diagnose accreta
on a delivered placenta. Placental floor infarction
as well as severe basal villitis are two additional causes of
difficult placental separation.[LMC-03-2618]
- succenturiate lobation: an extra lobation still
based on the placenta proper (can be a reflection of an abnormal
uterine cavity...septation or fibroid, etc.)6.
- accessory lobation: an extra lobation totally detatched
from the placenta proper and associated with risk of vasa
previa6 situation (as the vessels connecting
the accessory lobe to placenta proper course through the
interconnecting membranes, which zone might overly the uterine
exit through the cervix).
Ultrasound grades and gross path correlates:
- Langhan's Cytotrophoblast = cuboid, polyhedral
or ovoid with well marked borders; clear to slightly granular
cytoplasm; pale, finely granular nucleus; PAS + ; and can
be in stroma; mature villi = compressed between syncytial
trophoblast and BM.
- Hofbauer = round, ovoid or reniform; 25 micro
diameter; eccentric nucleus; usually coarsely vacuolated
cytoplasm; they are tissue macrophages; is alpha-1 antichymotrypsin
& CD68 positive. Can be stellate shaped.
- Syncytial trophoblast = differentiated multinucleated.
- Stromal cell = stellate, fibroblast-like.
- Lymphocyte = as identified in any other tissue.
- Mast cell = in small numbers and identified
as in other tissues.
- Plasma cell = coarse nuclear chromatin and
- Decidual cell = large epithelioid cell and
ID by location external to trophoblast.
Villous maturity retardation or acceleration:
: u/s diagnosis as early as 12 weeks and
is c/w 1st and 2nd trimesters (suspect diabetes if >4cm
- I: most often 30-32 weeks but can be seen
- II: doesn't bracket so well and can also
be seen at term.
- III: term placenta and gross exam reflected
by deep clefting around cotyledons and/or presence of calcium
speckling over cotyledon basal surfaces.
- thin placentas - IUGR, juvenile diabetic
mothers with retinopathy.
- thick placentas - > 4 cm often normal
but see it with gestational diabetes, non-immune hydrops, & congenital
- Retarded = "maturitas retardata placentae"[L08-13363]:
see very widespread and obvious lack of histological maturity
for gestational age.
- in some diabetics
- in some HDN
- in some luetic
- in some Down's; in
- in some apparently
- Accelerated = "maturitas praecox placentae":
see very widespread and obvious histological maturity for
- in some pre-eclamptics
- in some essential
hypertension and PIH cases: may reflect an attempt
to increase villous oxygen-grabbing efficiency in cases of
low or reduced intervillous maternal blood flow [LMC-06-1557; L09-7698].
- skinny terminal villi with exaggerated syncytial trophoblasts look hypermature and indicate reduced utero-placental blood flow (low
flow) in the sense of the fetal load demanding more blood than the uterus can supply14 (as in large fetuses, multiple gestation
pregnancy, preterm delivery, and PIH).
= hemolytic disease of newborn
= small for gestational age
= intrauterine growth retardation
PIH = pregnancy induced hypertension (is this a maternal compensatory
attempt to pressure over-ride obstructive deciduo-placental
lesions which have given rise to decreased intervillous blood flow from
mother?): uneven villous maturation, decidual lesions of acute atherosis, increased prevelance of intravillous fibrinoid (normally 3% or less of villi), infarcts, and "Tenney-Parker" changes of the terminal villi (an increase in syncytial nuclear clumping and basophilia).
= chorionic villous sampling
- uneven maturation = tends to recur and suggests
higher risk pregnancy [LMC-05-6232].
Cardinal Rule: don't stop your diagnostic evaluation
on discovery of one type of lesion. It's fairly common to
have multiple placental abnormalities.
- Large: macrosomia...child of diabetic; a large for
gestational age (LGA) baby.
SGA...IUGR; lesions associated with IUGR:
- placental surface cysts (multiple or large13).
- acute atherosis, even if not PIH case.
- chronic villitis (both DSV & VUE).
- small placenta; thin placenta.
- short cord; thin cord; hypertwisted cord.
- definitely excessive or massive perivillous fibrin deposition.
- central infarcts sufficient to cause uteroplacental insufficiency.
- massive subchorial (under fetal surface) hematoma (Breu's mole).
Importance of placental exam?
- ultrasound of high quality can detect fetal
sex, multiple fetuses, even differentiate monochorionic
(thin) from dichorionic (thicker) septum, congenital anomalies,
uterine and placental shape and placental location abnormalities,
placental maturity, etc.
- doppler of high quality can detect intervillous
space flow reductions.
- we should look for lesions of any invasive
procedures such as amniocentesis.
- fetal heart rate and uterine contraction
- scalp electrodes.
- cord blood gases.
- if we detect lesions prone to recur, the
obstetrician will be able to monitor the subsequent pregnancy
- perinatal morbidity can be reduced when neonatologists
and pediatricians know of such as chorioamnionitis.
- discovery of placental lesions (such as HEV)
portending risk of developmental retardation need to be
known by the pediatrician because better outcomes follow
early detection and management as they manifest in the
- amazingly, stillbirth cases are "worth" much
less than a damaged child or cerebral palsy case, and these are practically
un-winnable by plaintiff if the placental exam is abnormal.
- damaged child cases have about a 20 year
statue of limitations.
- for plaintiff to win a lawsuit [societal adverse impact of lawsuits], there must
Villous surface area: (fetal weight tends to be
- a damaged patient.
- negligent acts .
- cause of damage
must be the negligent act or acts; therefore, it is very
difficult, EVEN IF the doctor commits negligent acts, to
win a suit for a damaged infant if abnormalities are found
in the placenta!
- Normal surface area data:
- Planimetric method,
6.5-14.7 sq. m.
- Point counting method,
mean of 11 sq. m.
- Associated with decreased surface area:
- placentae with infarcts associated with
maternal hypertension (cases ave.
8.4 sq. m.).
- Normotensives with
SGA babies (ave
6.4 sq. m.).
Increased in HDN and not merely due to edema.
examination of the placenta is really complete without measurement
of the placental volume, the chorionic villous surface area,
and the volume proportions of the intervillous space, villous
tissue, and villous capillaries." This is, of course, an exam which cannot be done in the usual pathology lab.
HELLP Syndrome: no placental findings other than possible
PIH acute atherosis lesions [L-01-1457].
Amnion Nodosum = results from oligohydramnious and presence
somewhat predictive of degrees of pulmonary hyperplasia. AN is not fetal squamous debris extruded between amnion and either decidua parietalis or chorionic roof during L&D or postpartum placental manipulation [L09-894].
Acute atherosis lesion in membrane-roll arterioles in
decidua vera is highly suggestive of PIH/eclampsia/pre-eclampsia
but can be seen in IUGR, lupus anticoagulant syndrome, and maternal renal
The affected vessels have hyaline occlusion of some decidua vessels...more likely to be seen in the decidua capsularis vessels.
PIH: look for "low flow" skinny terminal villi (villous hypoplasia) with increased space around them (accelerated looking maturation), acute atherosis of decidual vessels, and an increased percentage of terminal villi with subtrophoblastic fibrin.
- pre-term = <37 weeks
("very pre-term" = <32 weeks).
- normal term range 37-40 weeks.
- post-dates, post term= >40 & up to 42
- post-dates, post mature= >42 weeks
Amnion sac: The amnion and chorion layers fuse early in pregnancy. But, they can separate and lead to amnion bands. When there are multiple gestations (twins, etc.), look for inequality of sac size and then compare each sac subdivision with the associated cord and cord vascular radiation across the placental disc surface. A twin placenta can have 50%-50% cord vascular distribution, but one sac might attach to the plate and circumscribe 90% of the fetal-surface surface area if the other cord has a marginal insertion [L12-262]. Usually, in twins, if one draws an axis line between the two cord insertions, the non-peripery insertion of the dividing sac membrane runs along an axis 90 degrees to that cord-insertions axis.
Our placentae from unusual cases: L14-419 (Bannayan-Riley-Ruvalcaba Syndrome [BRRS]);.
- Look for increased NRBCs (especially at >7500/mm3)11 or WBCs.
- Look for
sickled RBCs [L02-1805] or other dysmorphic RBCs.
Acute features: Acute features might include focal miliary collections of polys with fibrin and leukpcytoclasis.
That acute might have gradations to include a histiocytic & subtley granulomatous look. These may hint at TORCH or other infectious etiologies.
But, extensive studies and even attempts at culture might all come up negative [L12-12853].
Chronic features: Chronic villitis can be seen as a very minor, inconsequential
finding or rarely, with a more important degree of villous involvement. When
essentially all villi are involved and include a prominent histiocytic
component, the variety of chronic villitis is DSV (diffuse-sclerosing
villitis), DSV implying an infectious etiology (TORCH and luetic
infections). The mother tends to present somewhat ill, possibly
with IUGR, IUFD, or evidence of NIFH. The other, more common
variety of chronic villitis is villitis of undetermined etiology
(VUE) which is marked by a sub-total involvement of villi, >10%
of villi being affected signifying a severe degree of involvement. A
chronic villitis placenta does not usually look abnormal on casual
gross inspection. Some feel that the VUE reaction reflects
a graft-versus-host reaction with the inflammatory response halting
the maternal reaction against fetal antigens at the level of the
placenta. Mother tends not to be ill; and VUE has been associated
with recurrent reproductive failure, IUGR, and mid-trimester elevations
of maternal AFP.
Future pregnancies (obstetrical view):
When there is a prominent degree of involvement (greater
than focal, one grading scheme denoting as "patchy" or "diffuse"),
there is an uncertain but known risk of VUE recurrence in subsequent
pregnancies. Assuming that any treatable TORCH/luetic infection
was treated and resolved in the mother, recurrence of the DSV variety
is said to be rare.
Sequelae in the newborn (pediatric view):
In the case of the VUE variety, there is a relatively
infrequent association with TORCH/luetic etiology; therefore, any
newborn sequelae would be (as in the DSV variety) relative to any
actual such infection. If the VUE is extremely prominent
and with evidence of chronic vascular insufficiency (prominent
villous edema; significant erythroblastosis; newborn polycythemia)
or association with additional lesions suggesting subacute or chronic
vascular compromise, then sequelae are possible. Newborn polycythemia asociated with tachypnia and followed by hyperbiliruninemia may reflect
placental transfusion of the newborn due to delayed cord clamping greater than 2 minutes. Since IUGR
can be seen in both VUE and DSV varieties, when IUGR is present,
possible sequelae are at least related to the fact of IUGR.
If the newborn appears to have neurologic injury,
then management is by standard methods. If there is no apparent
abnormality, then care should be taken (all cases DSV; severe cases
VUE) that the baby is seen at typical and standard times throughout
childhood development in order to detect any milestone delays in
order to allow early corrective intervention should delays be encountered.
TWINS & ZYGOSITY
By 2015, genetic and molecular methods most precisely determine zygosity details. But morphology helps initially...especially if there is no serious legal question. Fetal and neonatal death are several times more frequent
in twins and triplets than in single-born (singleton) infants. Multiple gestattions are easily detected with ultrasound. Expert ultrasound can sometimes see the insertion of the dividing membrane and detect the "twin-peak sign" indicative of a dichorionic-diamniotic twin gestation19. Mortality
and preterm birth are more frequent in monozygous (usually identical...one
egg) than in dizygous (2 egg) twins. Chorionicity determination is
a relatively quick means to "get an idea" of likelihood of zygosity. Twins of different sex are essentially always dizygous
(except for monozygote that becomes XO/XY). The examining
pathologist usually examines twin placentae without knowledge of
the sex of the babies. A macroscopic and microscopic examination
of the membranes between the two fetal sacs usually indirectly establishes
the "working diagnosis" of zygosity of same-sex twins:
if chorionic cell layers are absent in the middle of this
dividing membrane, the twins are monochorionic (and the dividing membrane will seem thick and opaque). And all monochorionic
twins are monozygous (except as above). If chorionic cell
layers are present in the middle of the dividing membrane, the
twins are diamnionic, dichorionic (and zygosity is uncertain). In a small percentage of cases, the chorionic cellular stripe is markedly attenuated/thinned & very subtley visualized, maybe even focally absent [L10-10637]. Approximately
8% of same-sex dichorionic twins are monozygous (one egg), the
rest dizygous. So, a determination of dichorionicity of the
twin placenta means that the odds are 12 to 1 that the twins
are from two eggs, fraternal. Entirely separate twin placentae are dichorionic. Blood group identification,
enzyme markers, HLA, genetic typing, and DNA matching have been
or are occasionally utilized early (or some families may desire
to know with certainty early) to truly & accurately document
the zygosity of phenotypically similar, same-sex dichorionic-placenta
twins (most families just wait to see if they look alike). Sometimes
such further non-DNA testing is not definitive because the parents
have a similar distribution of antigens. For the same reason,
an analysis of multiple-restriction enzyme site polymorphisms with
DNA probes can produce a false-positive diagnosis of monozygosity. In
the final analysis, if push comes to shove (say for organ transplant),
experts with the physician team making the important decision may
need to consider many evidence parameters in order to be sure of
The axis of the fused dividing membranes is usually at right angles to the axis between the two cord insertion sites and reasonbly situated along the line between the periphery of the vascular radiation from each cord. When the insertion of the joined dividing membranes is obviously different from this, it is referred to as "irregular fusion" [l11-10311]. And, this situation may include the finding of sac volumes which vary considerably, one from another [L12-262].
section of the dividing membranes:
CHORIONIC-ROOF-PERIPHERY FIBRIN RINGS & EXTRACHORIAL
Trace peripheral change & no extrachorial
|The placental disk...the chorion...is geographically
divided into: (1) the membraneous chorion (the chorionic roof ...the
shiny fetal surface..."chorion laeve"); and (2) the villous chorion...the
basal plate...the red, meaty component. As the umbilical cord vessels
radiate across the fetal surface of the placenta toward the periphery,
they finally turn downward into the substance of the plate at a
point a cm or so short of the absolute periphery of the villous
plate (basal plate...chorionic plate..."chorion frondosum"). That
peripheral zone of the membraneous chorion beyond the vascular down-turn
is called the "subchorial closing ring", tending to be
about 1 cm wide, fairly often being perceptible as a slightly more
pale yellowish peripheral zone. Older German placental terminology
referred to this peripheral ring as the "schlussring." When
any placental tissue is beyond the roof membrane (chorion laeve) reflection/insertion
(when the reflection is not inserting on the perimeter rim of the
basal plate), there is a chance of antepartum hemorrhage...vaginal
bleeding (this finding may explain episodes of vaginal bleeding).
EXTRACHORIAL PLACENTA (EP): this common finding7 is
when the chorionic villous plate is larger than the chorionic roof,
and the membranes reflect off of the chorionic roof prior to (short
of) the periphery of the placental villous-plate edge. If that
is the only abnormality, then it is "__% extrachorial placenta",
see below. Additionally, one can fairly frequently note cases wherein a part of the chorionic plate extends beyond the limit of the
chorionic roof and membrane reflections to a very mild degree.
Some say that all EPs are either PM or PV or mixed (see below).
EP frequency is 5-20% of placentae. EPs found more commonly in
multigravidas; EP conventionally thought of as of no clinical significance7.
CHORIONIC ROOF FIBRIN RING ENHANCEMENT (CRFRE): As
that (see above) peripheral subchorial closing ring becomes more
enhanced with underlying subchorionic fibrin, it is first known
as "yellowish enhancement of the peripheral subchorial closing
ring of the fetal surface" (if one would like to dictate it
into a SP gross) (PM may or may not have enhanced subchorial fibrin
deposition, see below). CRFRE does not have any extrachorial placenta;
it is of no known clinical significance.
PLACENTA MARGINATA (PM): is when there is
impressive extrachorial placenta (lets say, a third or more of
the periphery being clearly beyond the point of membranes insertion).
And circummarginate (placenta circummarginata...PCM) placenta is
when the entire placental periphery is extrachorial. Lets say that
there is impressive extrachorial placenta, but only 90%...that
could be called "subtotal circummarginate placenta".
Some would, alternatively, call any placenta with extrachorial
component & negativity for membrane plication a "partial
placenta marginata". PM is an EP...EPs found more commonly
in multigravidas; EP conventionally thought of as of no clinical
PLACENTA VALLATA (PV): This is the condition
(always with a prominent fibrin ring) of a non-marginal...placenta circumvallata (PCV) when essentially
100% extrachorial placental periphery...membrane insertion so that
there is (1) significant extra-membranous placental plate tissue
around part or all of the periphery, plus subchorial
fibrin variably depositing beneath that intramembraneous roof ...and
causing a toward-the-cord folding over and tacking
together (plication) of membranes so as to encroach on the
area of the fetal surface as if there is an extramembraneous "drawstring" of
fibrin clot pulling membranes cordad and forming a (2) perceptible & palpable
shelf ("vallate" = having a ridge) on the amnionic cavity aspect of the fetal surface of the
plate [LMC-04-5297]. As with incontestable
PM/PCM, incontestable placenta circumvallata (PCV) is a 100% circumferential
abnormality. One can have mixed PM & PV [A-03-4] and
have the mix involve 100% of the circumference. We have also had a case with a 50% arc of thick CRFRE plus definite partial plication but only a
few millimeters of EP (L06-4997]...therefore, odd PV vs. a very marked example of CRFRE. Frequency of PV is reported
from 0.5%-6%. The complete form of PCV is the only variant of EP
with significant association with antepartum bleeding and/or preterm
delivery3, 7; and it is associated with SGA6,
(posted August 2002;
latest addition 15 January 2014; a link added 29 July 2015)
Perrin EVDK, Pathology of the Placenta, 1984.
Naeye RL, Disorders of the Placenta, fetus,
and Neonate: Diagnosis and Clinical Significance, 1992.
Silverberg SG, Principals and Practice of Surgical
Pathology and Cytopathology vol 3, 1997 p.2593-2628.
Lange JM, Placenta lecture at MUSC, Charleston,
SC 3/03 [KRM]
Singh V, et. al., Umbilical Cord Lesions in
Early Fetal Demise, Arch. Path. & Lab. Med. 127(7):850-853,
Spark RP, The Placenta: the Rebirth of the
Afterbirth, a Critical Assessment & Clinicopathologic
Correlation Lecture, AAPA workshop handout, September 2003
Gersell DJ, May 1997 ASCP CME OB-Gyn Course,
Savannah, Ga....handout. (EBS's office)
The Cedars-Sinai Medical Center in L. A., California, website in
neonatology, placenta, as of 29 Sept. 2004.
Schuler-Maloney, Doris, The Placenta: To
Know Me is to Love Me, spiral-bound 175 page manual
and/or 400 photo CD, DMS
Pathworks, Inc. (website has a nice introduction to
placental exam triage).
Kraus FT, Redline RW, Gersell DJ, Nelson DM,
Dicke JM, Atlas of Nontumor Pathology: Placental Pathology,
AFIP, 331 pages 2004 [EBS's office].
- Redline WR, "Severe fetal vasular lesions in term infants with neurologic impairment ", AJ Ob & Gyn 192:452-457, 2005.
- Yetter JF, Examination of the Placenta, American Family Physician 57(5):16 pages, 1 March 1998, online as of 7/17/2006.
- Brown DL, et. al., "Placental Surface Cysts Detected on Sonography", J. Ultrasound Med. 21:641-646, 2002.
- Kaplan CC, "Placental Examination", LABMEDICINE 38(10):624-628, October 2007.
- Redline WR Microsoft Powerpoint with excellent photos: http://pathology.bsd.uchicago.edu/PedsPath/files/REDLINE%20SNOWMASS%20PLACENTAL%20INFLAMMATION%20LECTURE%20(NXPowerLite).ppt.
- Kraus FT, Redline RW, Gersell DJ, Nelson DM, and Dicke JM, Atlas of Nontumor Pathology: Placental Pathology, AFIP First Series, Fascicle 3, 331 pages, 2004.
- Fox H., Pathology of the Placenta, 2nd Ed., 488 pages, 1997.
- eMedicine write-up on cord problems: http://emedicine.medscape.com/article/262470-overview.
- ultrasound diagnosis HERE.
- Autism Spectrum Disorder sentinel marker, Dr. Kliman at Yale, HERE. Kliman Labs, HERE.