Williams Obstertics, twenty- second edition

- page 619 ~ 630 -

 Placental Abnormalities

 Abnormalities of the Membranes

 Umbilical cord Abnormalities

 Pathological Examination
 Abnormal Shape or Implantation

 Degenerative Placental Lesions

 Circulatory Disturbances

 Hypertropic Placental Abnormalities

 Placental Inflammation

 Tumors of the Placenta

 Normal placenta (term placenta )
 diameter : 22 cm
 thickness : 2.0 ~ 2.5 cm
 weights : approximately 470 g (about 1 lb).

 Placental and fetal size and weight roughly correlate in a linear

fashion

 Fetal growth depends on placental weight which is less with

small- -for- gestational age infants
-Heinonen and colleagues, 2001-
Abnormality Definition Clinical significance
Multiple  Placenta bipartita or bilobata
Placentas - the placenta is separated into lobes
with a single - division is incomplete and the vessels
fetus
of fetal origin extend from one lobe to
the other before uniting to form the
umbilical cord
 Placenta duplex, triplex Bilobed placenta
- two or three distinct lobes are separated

entirely and the vessels remain distinct.

Succenturiate  small accessory lobe ≥1, develop in  retained in the uterus
lobes the membranes at a distant from the after delivery and may
periphery of the main placenta, to cause serious hemorrhage
which they usually have vascular  accompanying vasa previa
connections of fetal origin - dangerous fetal hemorrhage at
 incidence : 5% delivery
 Abnormality Definition Clinical significance
Membranaceous  all of the fetal membranes are serious hemorrhage d/t
Placenta covered by functioning villi and the associated placenta previa or
placental develops as a thin accreta
membranous structure occupying
the entire periphery of the chorion

Ring – shaped  Placenta is annular in shape and Antepartum & postpartum

Placenta sometimes a complete ing of placental bleeding and fetal growth
tissue restriction
 Variant of membraceous placenta
- tissue atrophy in a portion of the
ring a horseshoe shape in more
common
 Incidence : < 1/6000 deliveries
 Diagnosis Definition Clinical significance
Fenestrated Placenta  Central portion of a discoidal placenta mistakenly considered to
is missing indicate that a missing
 In some instances, there is an actual portion of placenta
hole in the placenta but more often
the defect involves only villous tissue
with the chorionic plate
Placenta  serious variations in which Torrential hemorrhage
Accreta trohpoblastic tissue invade the
Increta myometrium to varying depths
Percreta  much more likely with placenta
previa or with implantation over a
prior uterine incision or perforation
 Abnormality Definition Clinical significance
Extrachorial  When the chorionic plate, which is on the
Placentation fetal side of the placenta, is smaller than
the basal plate, which is located on the
maternal side, the placental periphery is
uncovered
 Circumvallate
Placenta  Fetal surface of such a placenta presents  Antepartum hemorrhage
a central depression surrounded by a - from placental abruption
thickened, grayish-white ring. and fetal hemorrhage
 Ring : composed of a double fold of  Preterm delivery
amnion and chorion with degenerated  Perinatal mortaliy
decidua and fibrin in between  Fetal malformations
 Within the ring, the fetal surface presents
the usual appearance, except that the
large vessels terminate abruptly at the
margin of the ring
Circummarginate
placenta  Ring dose not have the central depression  less well defined
with the fold of membranes
 Causes
: trophoblast aging or impairment of uteroplacental circulation
with infarction
 Deposition of calcium salts is heaviest on the maternal surface in
the basal plate.
→ further deposition occurs along the septa and both increase as
pregnancy progresses
 Calcification : 10 - 15% of all placentas at term
* By GA33wks : some degree of calcification ≥ ½ of placentas
- Spirt and colleagues ,1982 -
 Diagnosis : Sonography
Placental calcification
 Placental perfusion may be impaired by disruption of
uterine vessels, placental vessels or the intervillous
space
Placental infarctions
 m/c placental lesions
 Etiology : continuum from normal changes to extensive and
pathological involvement
 Incidence : 10% of 500 consecutive placentas from
uncomplicated
term pregnancies
 Several types (by lesion sites )
- located at the placental margin (90%) , size <1cm(90%)
- underneath the chorionic plate - Subchorionic infarct
: downward with their apices the intervillous space
- Intercotyledonary septa
: meet and form a column of cartilage – like material
extending
from the maternal surface to the fetal surface
 Placental infarction
A: placental infarction, B: fibrin deposit, C: normal placenta
 Placental margin (90%)
sites Placental margin
cause occlusion of the maternal uteroplacental circulation
normal aging
finding around the edge of nearly every term placental : dense yellowish-white
fibrous ring representing a zone of degeneration and necrosis
- incidental finding
Associated  normal
Lesion  numerous – development of placental insufficiency
 thick, centrally located and randomly distributed
: preeclampsia or lutus anticoagulant
 these conspicuous lesions arise after occlusion of decidual artery
interrupts blood flow to the intervillous space
: necrosis of villous tissue develops from ischemia
 decidual a. occlusion : placental abruption
Histopathologic Fibrinoid degeneration of the trophoblast, calcification and ischemic
feature infarction
Materal Floor infarction
 Uncommon lesion
 Incidence : 6/1000 deliveries - by Adams-Chapman and colleagues, 2002-
 Etiopathogenesis : not well defined
associated with thrombophilia (in some cases)
 Sites : not large areas of villous infarction
massive net-like fibrin deposition throughout the placenta
– Benirschke and Kaufmann , 2000 -
 Fibroid deposition occurs within the decidua basalis
(usually confined to the placental floor)
→ fibrin can extend into the intervillous space to envelop the villi
which then atrophy
 associated outcome
: fetal restriction, abortion , stillbirths, increased incidence of CNS
injury and neurodevelopmental sequelae in these infants

not associated with preeclampsia, placental abruption

Placental Vessel Thrombosis

 When a stem artery from the fetal circulation in the placenta is

occluded, it produces a sharply demarcated area of avascularity
 Single a thrombosis : 5% of placentas in normal pregnancies
10% of diabetic woman
 Thrombosis of a single stem artery will deprive only 5% of the
villi of their blood supply
 associated with fetal growth restriction and stillbirth
- Benirschke and Kaufmann, 2000
-
 skriking enlargement of the chorionic villi is commonly seen in
association with
 severe erythroblastosis
 fetal hydrops.
 maternal diabetes
 fetal CHF
 maternal-fetal syphilis
 Syncytial knots: clumps of syncytial nuclei are found to project
into the intervillous space
- begining after 32wks
 The number of cytotrophoblastic cells becomes progressively
reduced as pregnancy advances.
 By term, such cells are few and inconspicuous
 In some maternal or fetal disorders, numerous cytotrophobalstic
cells are found in placentas
- Gestational hypertension , diabetes and erythroblastosis fetalis
 Changes that are now recognized as various forms of degeneration and
necrosis were formerly described under the term placentitis
e.g.) Small placental cysts with grumous contents were formerly
thought to be abscesses.

 Nonetheless, especially in cases of preterm and prolonged membrane

rupture, bacteria invade the fetal surface of the placenta
→ chorioamnionitis
 Gestational Trophoblastic Disease

 Chorioangioma(Hemangioma)

 Tumors Metastatic to the Placenta

 Embolic Fetal Brain Tissue

Chorioangioma (Hemangioma)
 The resemblance components to the blood vessels and
stroma of the chrionic villus
 Benign tumors of placenta
 Incidence : 1%
 Hamartomas of primitive chorionic mesenchyme
 Diagnosis
: larger chorioangiomas – sonographic findings
 Associated symptome
- small growths : asymptomatic
- large tumors : hydramnios or antepartum hemorrhage
 Complication
: associated with low birthweight
: fetal death and malformations are uncommon
 Siller and Skafish (1986 )
: Multiple placental chorioangiomas in which a blood group A
fetus bleed acutely into her O group mother
→ The mother showed evidence of acute hemolysis without
anemia
and the fetus developed a sinusoidal heart rate pattern
frequently
seen with we severe anemia
 Severe iron deficiency anemia in the neonate as the consequence
of chronic fetal-to-maternal bleeding from multiple small
chorioangiomas
 Large tumors provide an arteriovenous shunt that can lead to
fetal heart failure
Tumor Metastatic to the Placenta
 Malignant tumors rarely metastasize to the placenta
 Melanoma (1/3), leukemias and lymphomas 1/3
 Tumor cells usually are confined within the intervillous space
- the fetus : metastases (¼)
 Malignant cells seldom proliferate to cause clinical disease

Embolic Fetal Brain Tissue

 Fetal brain tissue occasionally is seen embolized to the placenta
or fetal lungs
 Usually has been described with “traumatic” deliveries
 This phenomenon is not without precedent because brain tissue
has been found in pulmonary veins following head trauma in
older children and adults
 Meconium Staining

 Chorioamnionitis

 Other Abnormalities
 Incidence : remarkably constant
20% of almost 250,000women delivered during the
past 20years - in Parkland Hospital
 Preterm fetuses seldom pass meconium.
 <38 wks : uncommon
>42 wks : increase to 25~30%
 Staining of the amnion can be obvious within 1~3hours after
meconium passage
 Although more prolonged exposure results in staining of the the
chorion, umbilical cord and decidua, meconium passage cannot
be timed or dated accurately – Benirschke and Kaufmann(2000)
Study Meconium Passage(%)
Eden and associates(1987)
39weeks 14
40weeks 19
42weeks 26
>42weeks 29
Usher and colleagues(1988)
39-40 weeks 15
41 weeks 27
42 weeks or greater 32
Steer and co-workers(1989)
<36 weeks 3
36-39 weeks 13
40-41 weeks 19
42 weeks or greater 23
 Clinical significance
: perinatal morbidity and mortality↑
- by Nathan and co-workers in Parkland Hospital, 1994-
- perinatal mortality - 1.5 : 0.3 per 1000
- severe fetal acidemia (cord arterial pH < 7.0) - 7 : 3 per
1000
- cesarean delivery : doubled (14% : 7%)
: neonatal morbidity and mortality ↑
- meconium aspiration syndrome (10% of exposed infants)
: serious maternal risk ↑
- associated with amnionic fluid embolism
→ increases maternal mortality from cardiorespiratory failure
and consumptive coagulopathy
- Puerperal metritis : 4 times
 Imflammation of the fetal membranes is usually manifestation of
imtrauterine infection
 Associated with prolonged membrane rupture and long labor
 Characteristic
: clouding of the membranes
foul odor (depending on bacterial species and concentaraion )
 Definition
: mono-and polymorphonuclear leukocytes infiltrate the chorion,
the resulting microscopical finding - cells origin : maternal
 Leudocytes are found in amnionic fluid (amnionitis) or the
umbilical cord(funisitis) - cell origin : fetus
 < 20 wks almost all polymorphonuclear leukocytes : maternal
origin
> 20 wks: Inflammatory response : maternal & fetal
 Preterm deliveries : m/c
 Accordign to some investigators these findings of
inflammation may be nonspecific and are not always
associated with other evidence of fetal or maternal
infection

 Management
: antimicrobial administration and expedient delivery

 Explanation for many otherwise unexplained cases of

ruptured membaranes, preterm labor or both
 Abnormalities Definition & causes Clinical significance
Amnionic cyst  lined by typical amnionic epithelium
 fusion of amnionic folds with
subsequent fluid retention

Amnion nodosum  tiny, light tan , creamy nodules in the Found in

amnion made up of vernix caseosa  fetuses with renal agenesis
with hair, degenerated squames and  prolonged preterm ruptured
sebum membranes
 Oligohydramnios  the placenta of the donor
fetus with twin-to-twin
transfusion syndrome
Amnionic band  caused when disruption of the amnion  Intrauterine amputation
leads to formation of bands or strings
that entrap the fetus and impair growth
and development of the involve
structure
 Length
 Cord Coiling
 Single Umbilical Artery
 Four-vessel cord
 Abnormalities of cord insertion
 Cord Abnormalities capable of impeding blood flow
 Torsion and Strictures
 Hematoma
 Cysts
Length

: appreciable variation, extremes range

- no cord(achordia) ~ lengths<300cm
- mean length : 37cm
- excessively long cords : ≥ 70cm ( ≥2 SD )
 Short umbilical cords
: associated with adverse perinatal outcomes such as fetal growth
restriction, congenital malformations, intrapartum distress and
risk of death (doubled) - Krakowiak and associates,2004 –

 Excessively long cords

: associated with
- maternal systemic disease and delivery complications such as
prolapse, cord entanglement, fetal distress, fetal anomalies and
respiratory distress
- perinatal mortality : increased nearly threefold, albeit with
borderline statistical significance
 Determinants of cord length
- concept that cord length is influenced positively by both the
volume of amnionic fluid and fetal mobility
- heredity

 Miller and associates identified the cord to be shortened

appreciably when there had been either chronic fetal constraint
from oligohydramnios or decreased fetal movement, such as with
Down syndrome or limb dysfunction

Long cord Short cord

 Umbilical vessels : in a spiraled manner

 Hypocoiled cords
: increase in various adverse outcomes in fetuses
- meconium staining, preterm birth and fetal distress

 Hypercoiled cords
: higher incidence of preterm delivery and cocaine abuse in
one
with hypercoiled cords
- Rana and associates (1995) -
 The umbilical cord
: typically contains two arteries and a single vein

 Risk factors
: in women with diabetes, epilepsy, preeclampsia, antepartum
hemorrhage, oligohydramnios and hydramnios
→ increased incidence

 ¼ of all infants with only 1artery have associated congenital

anomalies
- two-vessel cords were identified in 1.5% of 879 fetuses aborted
spontaneously
: serious malformation, most associate with chromosomal
abnormalities >1/2 of these - Byrne and Blane,1985-
 Diagnosis
: routine ultrasound screening
- GA 17~36wks : 98% of cases

 Prognosis
- fetal prognosis
: depends on whether the two-vessel cord is associated with
other
abnormalities or whether it is an isolated finding
- Perinatal prognosis
: two-vessel umbilical cord is an isolated sonographic finding
→ better
 Budorick and co-workers (1995)
: no abnormal karyotypes and only one echocardiographic
abnormality in 31 fetuses with a two-vessel cord

 Gossett and associates (2002)

: 74 such fetuses all had normal echocardiography

 Catanzarite (1995)
- two of 46 fetuses : lethal chromosomal abnormalities
- 1/3 of 46 fetuses : tracheoesophageal fisrula
 When a two vessel cord is a nonisolated finding
- aneuploid ≥ ½ - Budorick and associates (2001) –
- renal aplasia, limb-reduction defects, atresia of hollow organs
in such fetuses, suggesting a vascular etiology
- Pavlopoulos and colleagues (1998) –

 Goldkrand and associates (2001)

: growth restriction did not occur in anatomically normal
fetus with a single artery
 Venous remnant in 5%

 Significance : unknown
Cord insertion
: usually inserted at or near the center of the fetal surface of the
placenta

 Furcate insertion

 Marginal insertion

 Velamentous insertion

 Vasa Previa
 Anomalities Definition incidence Significance
Furcate insertion Umbilical vessels separate from the Rare
cord substance before their
insertion into the placenta
Margnial Inserion Battledore placenta 7% at term Cord being pulled off
: cord insertion at the placental during delivery of the
margin placenta

Velamentous  Umbilical vessels separate in 1.1%  more frequently

Insertion the membranes at a distance with twins
from the placental margin  28% of triples
 Reach surrounded only by a
fold of amnion
Vasa Previa
 Associated with velamentous insertion when some of the fetal
vessels in the membranes cross the region of the cervical os below
the presenting fetal part
 Incidence : 1/5200 pregnancies
- ½ : associated with velamentous inserion
- ½ : marginal cord insertions and bilobedor, succenturiate-lobed
placentas
 Risk factors
- bilobed , succenturiate or low-lying placenta
- Multifetal pregnancy
- Pregnancy resulting from in vitro fertilization
 Diagnosis
: color Doppler examination (low sensitivity with ultrasound)
- Perinatal diagnosis : associated with increased survival (97:44)
- Antenatal diagnosis : associated with decreased fetal mortality
compared with discovery at delivery
 Hemorrhage antepartum or intrapartum
: vasa previa and a ruptured fetal vessel exists
 Detecting fetal blood
- Apt test
- Wright stain : to smear the blood on glass slides stain the smears
with Wright stain and examine for nucleated RBC
- normally are present in cord blood but not maternal blood
 - risk of low lying placenta : 80%
  Knots
false Result from kinking of the vessels to
accommodate to the length of the cord
True  Result from active fetal movements Incidence : 1.1%
 Venous stasis Stillbirth incidence : 6%
→ mural thrombosis and fetal esp)
hypoxia, high incidence : monoamnionic twins
causing death or neurological
morbidity

False knot(Lt), true knot (Rt)

 Loops
: Coiled around portions of the fetus, usually the neck.
longer cords

- one loop of nuchal cord : 20~34%

- Two loops in 2.5 ~ 5%
- three loops : 0.2~0.5%
 coiling of the cord around the neck is an uncommon cause of
antepartum fetal death or neurological damage
 Entwined cords cause intrapartum complications
 As labor progresses and there is fetal descent, contractions may
compress the cord vessels
→ fetal heart rate deceleration that persist until the contraction
ceases
 In labor 20% of fetuses with a nuchal cord have moderate to
severe valiable heart rate deceleration
→ have a lower umbilical artery pH
 Torsion
 Incidence : rare
 Result from fetal movements during which the cord normally
becomes twisted
 fetal circulation is compromised

Stricture
 More serious
 Most infants with this finding are stillborn
 Associated with an extreme focal deficiency in Wharton jelly
 In monoamnionic twinning, a significant fraction of the high
perinatal mortality rate is attributed to entwining of the
umbilical cords before labor
 accumulations of blood are associated with short
cords, trauma and entanglement

 result from the rupture of a varix, usually of the

umbilical vein with effusion of blood into the cord

 caused by umbilical vessel venipuncture

: found along the course of the cord and are designate true and false
according to their origin
True false
Size Small Considerable size

Causes Derived from remnants of the Result from liquefaction of Wharton jelly
umbilical vesicle or the
allantois
 Placenta and cord – including the number of vessels-
should be examined grossly following all deliveries

 Decision to request pathological examination will

depend on clinical and placental findings
 Pathological placental examination in the following
circumstances

 Perinatal death
 Preterm delivery
 Fetal growth abnormalities
 Fetal malformations
 Hydrops
 Any other fetal disorders
 Multiple pregnancy
 Maternal disorders
 Gross placental lesions
Circumvallate(left) and cricummarginate(right) variaties of extrachorial placentas
Anomaly of Placental site
Velamentous Insertion
Internal cx os