The Continuous Textbook of Women\'s Medicine Series ISSN: 1756-2228; DOI 10.3843/GLOWM.

409323 15/09/2022
This chapter should be cited as follows:
Nzioka A, Okiro P, Glob. libr. women's med.,
ISSN: 1756-2228; DOI 10.3843/GLOWM.409323

The Continuous Textbook of Women’s Medicine Series – Obstetrics Module

Volume 10
COMMON OBSTETRIC CONDITIONS
Volume Editor: Professor Sikolia Wanyonyi, Aga Khan University Hospital, Nairobi, Kenya

Chapter

Pathology of the Placenta

First published: February 2021

AUTHORS

Ancent Nzioka, MBChB(Moi), MMed Anat Path (AKUH,N), PhD (Cytopathology), FCPath-ECSA
Consultant Surgical Pathologist and Senior Lecturer, Mount Kenya University, Nairobi; Department of Health and
Emergency Services, Machakos County Government, Kenya

Patricia Okiro, MBChB (UON), MMed Anat Path (AKUH,N), MPhil Paed Path (UCT)
Consultant Surgical Pathologist and Assistant Professor of Pathology, Aga Khan University Hospital, Kenya

INTRODUCTION
The placenta is a maternofetal organ responsible for nutrition, waste elimination and gaseous exchange between the
developing fetus and mother. The placenta also produces a number of hormones that are important during pregnancy.
The placenta has two components: the fetal placenta, which develops from the same blastocyst that forms the fetus,
and the maternal placenta, which develops from the maternal uterine tissue. The placenta begins to develop upon
implantation of the blastocyst into the maternal endometrium. The outer layer of the blastocyst becomes the
trophoblast, which forms the outer layer of the placenta. This outer layer is divided into two further layers: the
underlying cytotrophoblast layer and the overlying syncytiotrophoblast layer. The syncytiotrophoblast is a multinucleated
continuous cell layer that covers the surface of the placenta. The syncytiotrophoblast contributes to the barrier function
of the placenta.

PLACENTAL PHYSIOLOGY

Maternal placental circulation

After ovulation, the uterine endometrium undergoes decidualization in preparation for implantation, due to
progesterone secretion. This change can be seen as early as day 23, roughly 10 days following peak of luteinizing
hormone.

Spiral arteries in decidua are remodeled so that they become less convoluted and their diameter is increased. Spiral
artery remodelling begins in the rst few weeks of pregnancy and modi es the arteries to high- ow low-resistance
vessels capable of meeting the demands of the developing fetus. Remodelling of the spiral arteries probably begins in
the late rst trimester and is completed by 18–20 weeks of gestation. There is relatively high pressure as the maternal
blood lls the intervillous space through these spiral arteries, and bathes the fetal villi in blood, allowing an exchange of
gases to take place. As the pressure decreases between pulses, the deoxygenated blood ows back through the
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endometrial veins. Maternal blood ow is approximately 600–700 ml/min at term.

Fetoplacental circulation
Deoxygenated fetal blood passes through umbilical arteries to the placenta. At the junction of umbilical cord and
placenta, the umbilical arteries branch radially to form chorionic arteries. Chorionic arteries, in turn, branch into
cotyledon arteries. In the villi, these vessels eventually branch to form an extensive arterio-capillary-venous system,
bringing the fetal blood extremely close to the maternal blood; but no intermingling of fetal and maternal blood occurs.
The human placenta performs the following physiological functions: respiratory, nutritive, excretory, production of
enzymes, production of pregnancy associated plasma proteins, barrier and endocrine functions.

PLACENTAL ENDOCRINOLOGY

The human placenta and fetal membranes secrete a large number of hormones. 1 These hormones are identical or
similar in structure and function to hormones secreted by the hypothalamus, pituitary and ovaries. These hormones
include the following.

Steroid hormones estrogens and progesterone

Estrogens are secreted initially by the corpus luteum and later by the fetoplacental unit (fetal adrenal cortex and the
placenta). The syncytiotrophoblast produces estrogen in large quantities under hCG stimulation. Progesterone is initially
produced by the corpus luteum and prepares the endometrium for implantation. Between week 5 and 8 postovulation,

progesterone production is taken over by the placental syncytiotrophoblast.2 Progesterone hormone maintains a non-
contractile uterus and champions development of an endometrium conducive for the pregnancy. By the end of the rst
trimester, placental production of estrogen and progesterone hormones replaces the corpus luteum.

Peptide hormones
Activin and inhibin are produced by the trophoblasts and regulate hCG production.

Cytokine growth factors (transforming growth factor (TGF)-alpha, TGF-beta, epidermal growth factor (EGF)) are
produced by trophoblasts. They stimulate proliferation of trophoblast and production of bronectin.
Human chorionic adrenocorticotropin (hACTH) is produced in small amounts. It is thought to have similar functions
ACTH.
Human chorionic gonadotropin (hCG) is a glycoprotein similar in structure to pituitary luteinizing hormone. It is
primarily synthesized by the villous syncytiotrophoblasts. Synthesis begins before implantation and is detectable 7–10
days after implantation. This forms the basis for early pregnancy tests. Peak levels are reached at 8–10 weeks'
gestation. Its role is to maintain maternal corpus luteum that secretes progesterone and estrogens.
Human chorionic thyrotropin (hCT) is produced in small amounts by the syncytiotrophoblast. Its function is believed
to be similar to thyroid stimulating hormone (TSH).

Human placental growth hormone has a similar structure to pituitary growth hormone except for 13 amino acids. It
regulates maternal blood glucose levels so that the fetus has adequate nutrient supply.
Human placental lactogen (hPL) is a polypeptide similar to growth hormone synthesized by the villous
syncytiotrophoblast. First detectable by 4 weeks with peak levels at end of third trimester. It acts as an insulin
antagonist to in uence growth, maternal mammary duct proliferation and lipid and carbohydrate metabolism.

Insulin-like growth factors stimulates proliferation and di erentiation of cytotrophoblasts.

Placental alkaline phosphatase (PLAP) is an alkaline phosphatase normally produced by syncytiotrophoblast and
primordial germ cells. May be involved in migration of primordial germ cells in developing fetus.

Relaxin is produced by the villous cytotrophoblast. It softens the cervix and pelvic ligaments in preparation for
childbirth.
Pregnancy speci c beta-1 glycoprotein (SP1) is present in syncytiotrophoblast and extravillous trophoblast.

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PLACENTAL ANATOMY

Placental mean weight

As the fetus grows, the placental weight also increases as indicated in Table 1 below. 3

Table 1 Mean placental weight by gestational age.

Gestational age (weeks) Mean placental weight (g)

Prior to 28 253

28–32 314

33–36 391

37–40 456

>40 496

Parts of the placenta

The human placenta is composed of the following parts (Figure 1): 4

1. Disc composed of the fetal portion known as the chorionic plate and the maternal portion known as the basal plate
decidua. The disc is divided into cotyledons from the primary stem villi and into lobules from secondary stem villi. The
average size of the disc at term is 22 cm in diameter, 2.0–2.5 cm in thickness and 470 g in weight.
2. Membranes composed of the amnion, exocelomic space, chorion and decidual capsularis. Membranes usually insert
directly onto the placental edge:
a. Amnion is the innermost lining of the amniotic cavity. It is composed of flat epithelial cells that rest on a thin
basement membrane with underlying thin band of loose connective tissue. It may show squamous metaplasia,
especially near cord or in pregnancies complicated by oligohydramnios.
b. Exocelomic space is the potential space between the amnion and chorion that allows the membranes to slide
against each other without friction.
c. Chorion is a connective tissue membrane containing fetal vessels. It is internal to the amnion and external to the
villi.
d. Membranous chorion (chorion laeve) formed by the collapse of the intervillous space during development. It is
composed of mononuclear, sometimes vacuolated, trophoblasts and scattered atrophic chorionic villi.
e. Decidual chorion (chorion frondosum) located in the placenta proper.
3. Umbilical cord which is the twisted cable that connects the fetus to the placenta and carries the two umbilical arteries
and a single umbilical vein. The vessels branch out over the fetal surface to form the villous tree. The average size of the
umbilical cord is 55–60 cm long and 2.0–2.5 cm in diameter.

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Figure 1 Gross placenta and umbilical cord.

PLACENTAL EXAMINATION
Placental pathology continues to be an underutilized and inadequately handled surgical subspecialty. No evaluation of a
sick or demised neonate is complete without placental examination. Pathology of the placenta, umbilical cord, and/or
placental membranes is causally ascribed for between 11% and 65% of stillbirth cases.5 Placental examination is a useful
adjunct in de ning etiology, prognosis, and risk of recurrence of pregnancy disorders, and is aided by the provision by
the clinician of pertinent history to guide this process. Placental injury can result at di erent points in placental
development and function. Early injury often results from abnormalities in maternal blood supply during developmental
processes of placentation. Later insults result from compromise of fetal blood supply and external insults.
In 1997, the College of American Pathologists outlined clinical indications for placental pathological examination,
highlighting maternal, fetal-neonatal and placental indicators of placental pathology, 6 and highlighting the importance of
relevant clinical history to accompany placentas submitted for pathological evaluation (Table 2). The minimum
information required for placental evaluation are the gestational age, obstetric index, maternal history, baby weight,
Apgar score, malformations and other pertinent ndings.

Table 2 Summary of the indications for comprehensive gross and microscopic placental examination by a pathologist. 6

Maternal indications Fetal/neonatal indications Placental indications

Preterm delivery at 36 weeks or less Intrauterine fetal demise or early Umbilical cord
neonatal death abnormalities
Fever or suspected infection
NICU admission (e.g. prematurity, Abnormal insertion site
Abnormal antenatal testing (abnormal fetal
hyaline membrane disease,
movements, stress and non-stress tests, Short or long umbilical cord
infections, congenital anomalies)
sonographic tests, amniocentesis tests triple
Other ndings
and quadruple blood tests) SGA/LGA (<10th or >90th centile)
(hypercoiling, true knots,
Severe oligohydramnios/polyhydramnios Birth depression (pH <7.0/Apgar <7; parenchymal masses,
assisted ventilation >10 min; hemorrhages, abnormal
Hypertension/diabetes
Abnormal tone/neonatal seizures) shape)
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Vaginal bleeding Suspected infection
Maternal indications Fetal/neonatal indications Placental indications
Chronic diseases (cardiovascular, renal, Hydrops fetalis
autoimmune)
Multiple pregnancy
Thick meconium with fetal distress)
Congenital abnormalities
Unfavorable obstetric outcomes (de ned as
one or more previous stillbirths, spontaneous
abortions, or premature births)

Maternal history of substance abuse

SGA, small for gestational age; LGA, large for gestational age

GROSS PLACENTAL LESIONS

Several gross placental lesions are described, with variable clinical signi cance. These are summarized in Table 3 below. 7

Table 3 Description of gross placental lesions.

Umbilical cord Membranes Parenchyma

Color: (yellow: infection; greenish: meconium; Color: (yellow: infection; Weight: (fetal-placental weight
brown: hemosiderin) greenish: meconium; brown: ratios; small – FGR; heavy –
hemosiderin) hydrops placentalis, delayed
Coiling: (hypocoiled: reduced activity/poor
villous maturation)
growth; hypercoiled: fetal distress) Surface: (amnion nodosum)
Dimensions and appearance:
Insertion site: (velamentous/furcate – into Insertion: (marginal: normal;
(FGR, infarcts, hemorrhages;
membranes; marginal – risk of circummarginate/circumvallate
maternal oor
hemorrhage/compression) – see text below)
infarction/perivillous brin
Length: (short: reduced fetal deposition)
activity/malformations; long: multiple poor
Placental variants:
outcomes)
(succenturiate (accessory lobe),
Knots: false/true membranacea (chorionic sac
covered by placental tissue),
Vessels: (single umbilical artery: congenital
duplex (bilobed), bipartite,
malformations)
tripartite (incompletely
Neoplasms: (cysts, teratomas, angiomyxomas) separate discs)
Hematomas

FGR, fetal growth restriction

STORAGE AND PROCESSING OF PLACENTA FOR PATHOLOGICAL EVALUATION

Placentas should never be frozen. Freezing distorts the villi, obscures meconium, and compromises diagnosis. For
xation, the specimen should be placed at least 10 times its volume of 10% neutral bu ered formalin. If samples are
taken fresh for xation before trimming, they should be no more than 2 cm thick. The rest of the processing is similar to
other tissue specimen.

CLASSIFICATION OF PLACENTAL PATHOLOGIES

Major pathologies are evaluated by both gross examination and placental histopathology. Below, the major
pathologically signi cant lesions are described. In the evaluation of lesions a ecting the placenta, they are often outlined
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as those resulting from maternal/trophoblastic abnormalities, fetal vascular/stromal abnormalities and postplacental
lesions. These may result from maldevelopment, malperfusion, loss of integrity, or secondary lesions.8,9

1. Maternal maldevelopment/malperfusion lesions

Historically, emphasis was placed on gross placental abnormalities, including abnormal shape, size, and weight. This has
remained an important indicator of placental function, especially in combination with other fetal parameters, such as
fetoplacental weight ratios.10 More recently, the description of other lesions includes defective arterial remodeling and
superficial implantation.11 These are the described pathogenetic mechanisms of disorders such as pre-eclampsia, and
reflect maternal malperfusion of the placental bed. These lesions are marked grossly by placental hypoplasia (weight
<10th centile; thin umbilical cord <8 mm), infarcts and hemorrhages (abruptio placenta, marginal/chronic abruptio) and
microscopically by villous infarcts and accelerated villous maturation.9
2. Fetal stromal-vascular lesions
Similar to maternal lesions, these can be divided into fetal maldevelopmental/malperfusion lesions, loss of integrity and
secondary or extrinsic factors.11 Maldevelopmental lesions include delayed villous maturation, villous capillary lesions
and dysmorphic villi. Malperfusion may be global or partial, highlighted by the lesions previously known as fetal
thrombotic vasculopathy, and can affect a segment of or the entire placenta.12 Loss of integrity results in fetomaternal
hemorrhages and villous edema, and secondary insults including meconium effects.
3. Inflammatory, infectious lesions
This category of disorders accounts for a large proportion of placental pathologies. It includes preterm deliveries and
recurrent pregnancy losses.13,14 The spectrum of acute infections includes chorioamnionitis, acute villitis and acute
intervillositis. Chronic lesions (chronic villitis, intervillositis, and deciduitis) and idiopathic lesions (villitis of unknown
etiology (VUE), fetal eosinophilic/T cell lymphoplasmacytic vasculitis, and chronic histiocytic intervillositis (CHIV)) account
for the remainder of lesions.15
4. Others lesions
A final category includes lesions the pathogenesis of which remains incompletely understood. These include perivillous
fibrin deposition, as well as other lesions such as placental malformations/deformations, placental disruptions,
heterotopias, hydrops placentalis and genetic or chromosomal abnormalities.11

The major components of these lesions are described brie y below.

Maternal vascular malperfusion

Following the consensus of the Amsterdam placenta working group that aimed to standardize the reporting of placental
pathologies, maternal vascular malperfusion is the preferred term for these lesions.9 It encompasses inadequate spiral
artery remodeling and pathology, with resultant abnormal spiral artery ow. Its e ects include fetal growth restriction
and fetal demise.16 The clinical syndromes associated with these lesions are preeclampsia and preeclampsia-like
syndromes (thrombophilia, renovascular disease) and diabetes mellitus.17,18 The gross ndings resulting from these
lesions are:

1. Small placentas (weight less than 10th centile for gestation)

2. Placental infarcts involving more than 5% of placental volume at term, away from the margin, or any infarcts in a preterm
placenta
3. Indenting retro placental hemorrhages (abruptio placenta).19

The resultant structural abnormalities include accelerated villous maturation and distal villous hypoplasia in partial or
global obstruction, and infarcts in segmental/complete maternal vascular malperfusion, with areas overlying occluded
spiral arteries showing ischemic necrosis.11 The molecules described to be involved in these lesions include, but are not
limited to pro-angiogenic factors such as vascular endothelial growth factor (VEGF) and placental growth factor (PIGF), as
well as anti-angiogenic factors, such as soluble fms-like tyrosine kinase 1 (sFlt-1/VEGFR-1), which are produced by the
developing placenta.20,21 This is an area of ongoing research for biomarkers to predict risk of preeclampsia. Decidual

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arteriopathy, which is a lesion described in the basal plate of pre-eclamptic placentas, is an associated nding that
includes acute atherosis of spiral arteries, brinoid necrosis with or without foamy macrophages, muscularized spiral
arteries and chronic perivasculitis.19 Rupture of these poorly remodelled/artheromatous vessels results in loss of
maternal vascular integrity, and can present acutely as abruptio placenta.22,23 Other etiologies include vasoactive drugs,
trauma and uterine rupture. 24 This lesion is distinguished from marginal abruption, a more chronic process resulting
from rupture of decidual veins in a background of premature rupture of membranes, cervical insu ciency, low lying
placentation, anatomical abnormalities and chorioamnionitis,19,20 resulting in recurrent marginal hemorrhages and
circumvallation/circummargination of placental membranes and chorioamnionic hemosiderosis.

Fetal vascular malperfusion

Previously termed fetal thrombotic vasculopathy (FTV), this is an uncommon but signi cant lesion that is likely secondary
to obstruction due to cord lesions, hypercoagulable states and fetal cardiac dysfunction.12 It has been associated with
signi cant neurological impairment and adverse fetal outcome.25 Three forms of obstruction have been described:8

1. Thrombosis of chorionic plate and stem villous vessels leading to degeneration and eventual loss of capillaries in
downstream villi12
2. Mechanical obstruction (recurrent or intermittent cord compression)
3. Vessel wall damage. 26

Multiple histologic ndings have been described, including thrombosis of the fetal chorionic plate or umbilical cord
vessels which may be visible grossly, mural organizing thrombosis with lamination, with or without muscular
degeneration and ectasia of the vessel walls, and calci cation of older thrombi.26 Distal avascular villi can be seen.
The Amsterdam consensus group suggested a grading system with low and high grade lesions, representing segmental
and global forms of fetal vascular malperfusion, respectively, and possibly better predicting subsequent clinical outcome
and complications.9,26

In ammatory/infectious lesions
Acute chorioamnionitis accounts for a large proportion of this group of lesions, and is a frequent forerunner of preterm
birth and a major contributor to neonatal complications.13 Infections commonly occur in early gestation (23–24 weeks) as
compared to term,14,27 and are characterized by neutrophilic in ltrates of the fetal membranes and chorionic plate. A
three-tier staging and two-tier grading system has been proposed by the Amsterdam group, as indicators of duration
and intensity of in ammation. An equally important component is the fetal in ammatory response, which is an indicator
or adverse neonatal outcomes.8 Other patterns of acute in ammation are acute villitis, commonly seen in E. coli and
group B streptococcal infections, and acute intervillositis with intervillous microabcesses, as exempli ed by Listeria
monocytogenes infections. A host of other organisms from the gastrointestinal, genitourinary, oral and skin have been
implicated in causation of acute chorioamnionitis.13 The described routes of infection are most often ascending, rarely
hematogenous and transamniotic. Chronic chorioamnionitis is an infrequent nding and is often seen with other
in ammatory lesions, including villitis of unknown etiology (VUE) and longstanding ascending in ammation (see below).28
Chronic infection, characterized by lymphohistiocytic in ltrates, presents as chronic villitis (associated with TORCH
(toxoplasmosis, rubella cytomegalovirus, herpes simplex, and HIV) infections) and/or intervillositis (described in
malaria).29 Other forms of in ammation of uncertain etiology include VUE, a cause of recurrent pregnancy loss thought
to represent a graft versus host disease (GVHD) type of reaction,30 chronic histiocytic intervillositis (CHIV), also associated
with recurrent pregnancy loss and fetal growth restriction31 and eosinophilic/T cell vasculitis, an in ammatory lesion of
fetal origin and uncertain clinical signi cance.32
Finally, other important lesions include:

1. Delayed villous maturation (previously villous maturation defect or villous dysmaturity), seen often in placentas of

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diabetic mothers and characterized by large placentas, with abundant villus stroma and poor formation of
vasculosyncytial membranes between fetal capillaries and maternal blood.33
2. Fetal hydrops/hydrops placentalis, also resulting in large placentas, which may be immune (ABO/Rhesus incompatibility)
or non-immune (cardiovascular, fetal anemias).34
3. Perivillous fibrin deposition/maternal floor infarction: rare, related idiopathic lesions characterised by deposition of
fibrinoid material in the placental resulting in fetal growth restriction, and risks of recurrence with fetal death.35,36

PLACENTAL MALARIA
Malaria in pregnancy is substantial cause of morbidity and mortality for the pregnant woman and her fetus and
newborn. The general immune suppression during pregnancy makes women more susceptible to malarial infection
especially during rst trimester. Initially low cell-mediated immune response in placenta makes it a preferred site for the
malaria parasites to hide from host immune responses. However, as malarial infection progresses, there is an increase in
cell-mediated immune response resulting in massive recruitment of macrophages to intervillous spaces of placenta
causing oxidative stress and apoptotic cell death in placenta. This can lead to poor pregnancy outcome, such as
abortions, still birth, IUGR, and LBW.37
Placental microscopic (histologic) ndings in malaria include:

1. Active disease shows free and intraerythrocytic parasites in intervillous space with minimal amounts of coarse hemozoin
brown pigment.
2. Chronic infection shows intervillositis with trophoblast basement membrane thickening and increased syncytial knots
has been noted. In chronic infections, parasites coexist with pigment covered with fibrin.
3. In inactive infections, only pigment is identified. Half of the patients with parasites in placenta have no parasites in
peripheral blood. 38

PRACTICE RECOMMENDATIONS

• Placental examination is a significant part of evaluation a sick or demised neonate.

• Adequate and relevant history is mandatory for placental evaluation and generation of a clinically useful
report.
• Certain gross lesions are indicators for possible significant microscopic lesions.
• Placental pathologies may originate preplacentally (maternal vascular malperfusion/maldevelopment),
intraplacentally (fetal vascular malperfusion) or postplacentally (infection, inflammation), and may be
predictors of long-term life outcomes of the affected infants.
• Certain significant but rare conditions result in recurrent pregnancy loss, and should be born in mind in
patients with poor obstetric histories.

CONFLICTS OF INTEREST
The author(s) of this chapter declare that they have no interests that con ict with the contents of the chapter.

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The Continuous Textbook of Women\'s Medicine Series ISSN: 1756-2228; DOI 10.3843/GLOWM.409323 15/09/2022

STUDY ASSESSMENT
Question 1

Which of the following statements relating to the placenta are correct? Please select all that apply.

(a) The placenta nourishes the fetus by establishing a dialysis pattern for exchange between the maternal and fetal
circulations True

(b) The placental barrier is very thin and freely permeable to glucose and amino acids
True
(c) The PO2 of the blood of the umbilical vein is the same as that in the maternal arterial blood
True
(d) The placenta secretes about ten times as much progesterone as the corpus luteum
True
(e) The estrogens secreted by the placenta tend to increase uterine excitability during late pregnancy
True

Question 2

Spiral arteries supply blood to the ________ side of the placenta.

(a) Fetal True

(b) Maternal True

Question 3

The fetal umbilical ______ carries deoxygenated blood to the placenta.

(a) Artery True

(b) Vein True

Question 4

The average length of umbilical cord is:

(a) 25 cm True
(b) 40 cm True
(c) 55 cm True
(d) 75 cm True
(e) 125 cm True

Question 5

Obstetrics - V10 - Common obstetric conditions - Chapter - Pathology of the Placenta Page 10 of 11
The Continuous Textbook of Women\'s Medicine Series ISSN: 1756-2228; DOI 10.3843/GLOWM.409323 15/09/2022

The mean placental weight at term is:

(a) 235 grams True

(b) 314 grams True

(c) 391 grams True
(d) 456 grams True
(e) 496 grams True

Question 6

The umbilical vein carries:

(a) Deoxygenated fetal blood away from the placenta True

(b) Deoxygenated fetal blood to the placenta True

(c) Deoxygenated maternal blood away from the placenta True

(d) Oxygenated fetal blood away from the placenta True
(e) Oxygenated maternal blood to the placenta True

Obstetrics - V10 - Common obstetric conditions - Chapter - Pathology of the Placenta Page 11 of 11