OBSTETRICS: Placental Abnormalities

Reference: Lecturer’s ppt and William’s OB 24th Edi

Transcriber: docdemetillo@icloud.com
“To toil and not to seek for rest... “

PLACENTAL ABNORMALITIES
Pp. 116 - 124

PLACENTAL ABNORMALITIES
I. Introduction
Always examine placenta after delivery Rate of Increase of Placental Thickness:
 1mm per week
 does not exceed 40mm
HISTOPATHOLOGICAL EXAMINATION
Maternal Surface: Basal Plate
II. Histopathological Examination  Divided by clefts into portions called cotyledons
Maternal Indications  Clefts marked the site of internal septa that extend into the intervillous space
 Abruption
 Antepartum infection with fetal risk Fetal Surface: Chorionic Plate
 Anti CDE alloimunization  Where umbilical cord insert at chorionic plate’s center
 Cesarean hysterectomy  Large fetal vessels that originates from the cord vessels that spread and branch
 Olgohydramnios or hydramnios across the chorionic plate before entering stem villi at placental parenchyma
 Peripartum fever and infection  Fetal arteries almost invariably cross over veins
 Preterm delivery  Chorionic plate and its vessels are covered by thin amnion, and easily peeled from
 Postterm delivery a postdelivery specimen
 Severe trauma
 Suspected placental injury Normal Placenta Sonographically:
 Systemic disorders with known effects  Homogenous
 Thick or viscid meconium  Thickness is 2 – 4 cm
 Unexplained late pregnancy bleeding  Indents into the amnionic sac
 Unexplained or recurrent pregnancy complications  Lies against myometrium

Fetal and Neonatal Indications  Retroplacental space:

 Admission to an acute care nursery  Hypoechoic area
 Birth weight <10th or > or = 95th percentile  Separates myometrium from placenta’s basal plate
 Fetal anemia  1 – 2 cm
 Fetal or neonatal compromise
 Neonatal seizures
 Hydrops fetalis ABNORMALITIES OF THE PLACENTA
 Infection or sepsis
 Major anomalies or abnormal karyotype IV. Abnormalities of the Placenta
 Multifetal gestation Shape and Size
 Stillbirth or neonatal death  Bilobate placenta or Bipartate Placenta or Placenta Duplex
 Vanishing twin beyond the 1st trimester  Placenta form as separate, nearly equal sized discs
 Cord inserts between the two placental lobes – either into a connecting chorionic
Placental Indications bridge or into intervening membranes
 Gross lesions
 Marginal or velamentous cord inserion  Multilobate Placenta
 Markedly abnormal placenta shape or size  Placenta with three or more equally sized lobes
 Markedly adhered placenta  Rare
 Term cord <32 cm or >100 cm
 Umbilical cord lesion  Succenturiate Lobes or Small Accessory Lobes of the Placenta
 Develop at a distance from the main placenta
NORMAL PLACENTA  Have vessels that course through the membranes
 If these vessels overlie the cervix it may create VASA PREVIA
III. Normal Placenta
Grossly:  Vasa previa
 470 g o If torn, can cause dangerous fetal hemorrhage
 Central thickness is 2.5 cm
 Diameter is 22 cm  Can be retained in the uterus after deliver and can cause unterine atony and
 Round to oval hemorrhage
 Chorionic plate normally extends to the periphery of the placenta and has a
diameter similar to that of the basal plate  Placenta Membranacea
 All or nearly all of the fetal membranes are covered with villi
Composition:  May cause serious hemorrhage due to associated placenta previa or accreta
 Placental disc  Ring Shaped Placenta
 Extraplacental membranes o Variant of placenta membranacea
 Three vessel umbilical cord o Placenta is annular, partial or complete ring of placental tissue
o Associated with:
 Antepartum and postpartum bleeding; and

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 OBSTETRICS: Placental Abnormalities
Reference: Lecturer’s ppt and William’s OB 24th Edi
Transcriber: docdemetillo@icloud.com
“To toil and not to seek for rest... “

 fetal growth restriction  Caused by slowing of maternal blood flow within the intervillous space with fibrin
deposition
 Placenta Fenestra  Lesions are white or yellow plaques on the fetal surface
 Central portion of a placental disc is missing
 Some cases involves actual placentel hole
 Often, defect involves only villous tissue and chorionic plate is intact  Pervillous Fibrin Deposition
 May prompt search for a retained placental cotyledon  Small, yellow – white nodules (normal part of placental aging)
 Pathophysiology:
 Placentomegaly o Slow maternal blood flow currents  blood stasis  fibrin deposition 
 Placenta thicker than 40 mm decrease villous oxygenation  syncytiotrophobalst necrosis
 Results to striking villous enlargment
 Secondary to DM, severe maternal anemia, fetal hydrops, or syphilis,  Maternal Floor Infarction
toxoplasmosis, or cytomegalovirus  Deposition of dense fibrinoid layer on the placental basal plate
 Partial mole or complete mole:  Lesion is thick, white, firm, corrugated surface
o Villi are enlarged and edematous and fetal parts are present  Impedes normal maternal blood flow into the intervillous space
o Coexists with normal twin  Associated with:
 Placental mesenchymal dysplasia o Miscarriage
o Has cystic vesicles o IUGR
o Vesicles correspond to to enlarged stem villi o Preterm deliveries
o There is no excessive torphoblast formation o Still births
o Rare  Recur in subsequent pregnancies
 Can also be due to collections of blood or fibrin  Not well defined etiopathogenesis
o Causes:
 Massive perivillous fibrin deposition  Subchorionic Infarct
 Intervillous or subchorionic thromboses  Found underneath the chorionic plate
 Large retroplacental hematomas  Extend downward toward the intervillous space

Extrachorial Placentation  Intervillous Thrombus

 Chorionic plate fail to extend to the periphery and leads to chorionic plate that is  Collection of a coagulated blood admixed with fetal blood
smaller than the basal plate  Grossly round or oval, red if recent, white – yellow of older
 Causes elevated alpha – feto protein
 Circummarginate Placenta
 Fibrin and old hemorrhage lie between the placenta and the overlying  Placental Infarctions
amniochorion  Most common placental lesion
 Normal or pathologic
 Circumvallate Placenta  90% located at placental margin
 Assciated with antepartum bleeding and preterm birth  due to occlusion of maternal uteroplacental circulation
 Transient and benign  usually represent normal aging
 Peripheral chorion is a thickened, opaque, gray – white circular ridge composed
of a double fold of chorion and amnion  Complications
 Sonographically: o Ueteroplacental insufficiency
o Double fold is seen as thick, linear band of echoes extending from one o Placental abruption
placental edge to the other
 Cross – section:  Associated with:
o Appear as “shelf.” o Preeclampsia
o Its location may help differentiate this shelf from amniotic bands and amniotic o Lupus anticoagulant
sheets.
 Histopath:
 Most pregnancy with extrachorial placentation has normal outcome o Fibrinoid degeneration of trophoblast
o Calcification
 Degenerative Placental Lesions o Ischemic infarction
 Deposition of calcium salts
 Result from:
 Pathophysiology:
o Trophoblastic aging
o Occlusion of decidual artery  interrupts blood flow to intervillous space 
o Infarction
ischemia  necrosis of villous Tissue  Placental abruption
 More extensive in smokers
 Increases as pregnancy progresses
 Placental Vessel Thrombosis
 Stem artery from fetal circulation in the placenta is occluded producing a sharply
Circulatory Disturbances demarcated area of avascularity
 Disrupts maternal blood flow to or within the placenta  Associated with:
 Disturbs fetal blood flow through the villi o Normal pregnancy  (5%)
o Diabetic woman  10%
 Placental Perfusion Disorders
 Common and found in normal mature
 Will deprive 5% of villi with blood supply
 Effect: limit maximal placental blood flow
 Complications:
 Can lose up to 30% of its villi without untoward fetal effects
o Fetal growth restriction
 Subchorionic Fibrin Deposition o Stillbirth

 Hematoma

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 OBSTETRICS: Placental Abnormalities
Reference: Lecturer’s ppt and William’s OB 24th Edi
Transcriber: docdemetillo@icloud.com
“To toil and not to seek for rest... “

 Retroplacental Hematoma o tunmor >5cm causes significant shunting which causes fetal hydrops and
o Between placenta and its adjacent decidua anemia
o other complication:
 Marginal Hematoma AKA subchorionic hemorrhage  antepartum hemorrhage, preterm delivery, amniotic fluid abnormalities,
o Between chorion and decidua at the placental periphery IUGR
o Management:
 Decrease blood flow to the tumor by vessel occlusion and ablation
 Subchorial thrombosis
o Breus mole  Tumor metastatic to the placenta
o Along the roof of the intervillous space and beneath the chorionic plate o Rare
o Common: melanoma, leukemia, lymphoma, and breast cancer
 Subamnionic o Usually confined within intervillous space
o Between placenta and amnion o Melanoma can go to the fetus
o Complications
 Miscarriage, abruption, IUGR, preterm delivery, adherent placenta  Embolic Fetal Brain Tissue
 Usually described with traumatic deliveries
 Fetal Blood Flow Disruption  Location: placenta, fetal lungs
 Fetal thrombotic vasculopathy
o Affected portion of the villous becomes infarcted and non functional
 Aubamnionic Hematoma ABNORMALITIES OF THE MEMBRANES

Abnormalities of the Placenta V. Abnormalities of the Membranes

 Placental Calcification Meconium staining
 Calcium salts deposition maternal surface in basal plate  Incidence is 12 – 20%
 Associated with:  Risk increases to 25 – 42% after 42 weeks
o Nulliparity, smoking, higher socio – economic status, increase maternal serum  ( + ) amnion stain  1 – 3 hours  then to chorion, umbilical cord, and decidua
calcium  meconium passage cannot be timed or dated accurately
 process:
 Hypertrophic Lesions of Chorionic Villi  meconium passage is prevented by tonic anal sphincter contraction and lack of
 Striking enlargement of the chorionic villi intestinal peristalsis
 Associated with:  vagal stimulation produced by cord or head compression in the absence of fetal
o Severe erythroblastosis, fetal hydrops, fetal hydrops, maternal diabetes, fetal distress
congestive heart failure, maternal – fetal syphilis
 associated with:
 Placental Inflammation  fetal acidosis, non – reassuring fetal status, low APGAR scores
 Characterized by degenerative and necrotic changes
 Bacteria invade fetal surface of the placenta  Fetal hypoxia produces anal sphincter relaxation and fetal gasping  in uteru
 Associated with: aspiration of meconium  meconium aspiration syndrome
o Preterm, prolonged membrane rupture
 Complications:
 Syncytial Knot  Meconium associated amniotic fluid embolism  cardiorespiratory failure and
 Clumps of syncytial nuclei project into the intervillous space beginning after 32 consumptive coagulopathy  maternal mortality
weeks  4 fold risk of puerperal metritis
 Represents apoptosis
Chorioamnionitis
 Microscope placental abnormalities  Routes of infection:
 Ascending infection from the lower genital tract  prolonged membrane rupture
Normal Maternal Fetal Disorders and long labor
 Hematogenous spread from maternal blood
Cytotrophoblastic cells becomes - (+) numerous cytotrophoblastic cells in
 Direct spread from endometrium of FT
progressively reduced as pregnancy the placenta
 Iatrogenic contamination
advances
- associated with: Gestational
 Process:
hypertension, diabetes, erythroblastosis
 Exclusion of vaginal bacteria from upper genital tract  entry of organism 
fetalis
initial infection of chorion adjacent decidua  full thickness involvement of
membranes  inflammation of chorionic plate and umbilical cord
 Placental Tumors
 Fetal Infections:
 Chorioangioma (Hemangioma)
 Hematogenous, aspiration, swallowing, direct contact with infected Amniotic fluid
o Components resemble blood vessels and stroma of chorionic villus
o Only benigh tumor of the placenta  Gross:
o Incidence is 1%  Infection characterized by clouding of membranes and foul odor (depends on
bacterial species and concentration)
o Increase maternal serum of alpha – fetoprotein
Small Amnionic Cyst
o Well circumscribed, rounded, predominantly hypoechoic lesion near the  Due to fusion of amniotic folds, with subsequent fluid retention
chorionic plate amniotic cavity
o Increase blood flow is seen in color doppler Amnion noduosum
 Small, light tan nodules overlying the placenta
o 5 cm is the cut – off size  Hallmark of oligohydramnios

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 OBSTETRICS: Placental Abnormalities
Reference: Lecturer’s ppt and William’s OB 24th Edi
Transcriber: docdemetillo@icloud.com
“To toil and not to seek for rest... “

 Most common in: o Perinatal deaths: 1.92%

 Fetal renal agenesis o Twins: 3%
 Prolonged PPROM
 Placenta of donor fetus  Most common aberration
 Increased incidence is associated with:
 Made up of: o Epilepsy
 Vernix caseosa with hair o Preeclampsia
 Sebum o Antepartum hemorrhage
 Desquamated squates (?) o Amniotic fluid volume abnormalities
Amnionic Bands o Chromosomal abnormalities
 Formed from disruption of amnion
 Entrap the fetus and impair growth and development  Etiology:
 Consequence: fetal intrauterine amputation o Secondary atrophy of a previously normal umbilical artery
Amionic Sheets  Detected by routine UTZ (98% at 17 – 36 wks)
 Normal amniochorion draped over preexisting uterine synechia  Associated with:
 Risk: preterm delivery and placental abruption o Spontaneous abortion
o Renal aplasia
ABNORMALITIES OF THE UMBILICAL CORD o Limb – reduction defects
o Atresia of hollow organs
VI. Abnormalities of the Umbilical Cord
Normal Cord:  If an isolated sonographic finding: better prognosis
 Develops in close association with the amnion o No increased risk of aneuploidy
 Susceptible to entanglement, compression, and occlusion o Risk of IUGR
 Ave length: 40 – 70 cm
 If non – isolated sonographic finding:
 Cord length is influenced by amniotic fluid volume, fetal mobility, heredity o Increase risk of aneuploidy
 Association of short umbilical cords o Increase risk of structural abnormalities (renal agenesis, imperforate anus,
o Oligohydramnios vertebral defects)
o Decrease fetal movement Hyrtlanastomosis
o Fetal growth restriction  Connection between the 2 umbilical arteries located 3 cm of the placental inseetion
o Congenital malformation of the cord
o Intrapartum distress  Acts as a pressure equalizing system between the umbilical arteries 
o Intrauterine fetal death (2 – fold risk) redistribution of pressure gradients and blood flow  improved fetal perfusion
during unterine contraction or umbilical artery compression
 Fetuses with single umbilical artery lacks this safety valve  increase rate of
 Long Cord
unexplained IUFD in late pregnancy or labor
o Maternal systemic disease
o Delivery complications
Four vessel cord
o Cord entanglement
 ( +) venous remnant  uncommon
o Fetal distress  increased risk of congenital anomaly(?)
o Fetal anomalies  unknown significance
o Respiratory distress
o Perinatal mortality (3x) Fused Umbilical cord
 Occurs during embryological development  umblical arteries fail to split (fused
 Cord Diameter shared lumen)
 Used as predictive fetal marker  Types:
 Lean umbilical cord is linked with poor fetal growth o Complete
 Large dianmeter cords linked with macrosomia o Partial (typically found towards the cord insertion)
 Associated with marginal or velamentous cord insertion
 Cord Coiling  No congenital fetal anomaly association
 Can be determined sonographically
 Umbilical coiling index (UCI) number of complete coils per centimeter of cord
length ABNORMALITIES OF THE CORD INSERTION
 Hypercoiling
o Associated with:
 Preterm birth VII. Abnormalities of the Cord Insertion
 Fetal distress Marginal insertion
 Meconium staining  Battledore placenta
o Linked with fetal distress  Cord anchors at the placental margin
o Associated with:
 Fetal growth restriction  Common in:
 Intrapartum fetal acidosis and asphyxia  Multifetal pregnancy
 Preterm delivery  IVF
 Cocaine abuse
 Maybe associated with weight discordance
 Single umbilical artery:
 Incidence: Furcate Insertion
o Livebirths: 63%

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 OBSTETRICS: Placental Abnormalities
Reference: Lecturer’s ppt and William’s OB 24th Edi
Transcriber: docdemetillo@icloud.com
“To toil and not to seek for rest... “

 Umbilical vessels separate from the cord substance before their insertion into the  Umbilical Cord Stricture
placenta  Focal narrowing of the cord diameter
 Umblical vessels lose the protective wharton jelly shortly before insertion   Develops in the fetal umbilical insertion
Covered by amnion  Characteristic pathological features:
 Prone to compression, twisting, and thrombosis o Absence of wharton jelly
o Stenosis or obliteration of cord vessels at the segment
Velamentous Insertion
 Umbilical vessels spread in the membranes at a distance from the placental margin  Hematoma
 Increase risk of compression  fetal anoxia  Associated with:
o Short cords
 Associated with: o Trauma
 Placenta previa o entanglement
 Multiple gestation  causes:
o varix rupture (umbilical vein)
 Vasa Previa o umbilical vessel venipuncture
 Associated with velamentous insertion
 Placental vessels lie between the cervix and the presenting fetal part  Cysts
o  vessel compression  fetal anoxia; and  True and pseudocysts have similar sonographic appearance
o  vessel laceration  fetal exsanguination  True cysts
o Epithelium – lined remnants of the allantois
 Risk factors: o Co – exist with a persistently patent urachus
o Bilobate or succenturiate placenta  Pseudocysts
o 2nd trimester placenta previa ( with or without later migration) o Local degeneration of wharton jelly
o In Vitro fertilization  increased rates of abnormal cord insertion
 Single cord cysts mpted in 1st trimester tend to resolve
 Anterpartum diagnosis results in improved fetal survival rates  Multiple cord cysts portend miscarriage or aneuploidy
 Clinical diagnosis:  Pseudocysts persisting beyond 1st trimester can be associated with structural or
o Palpation or direct visualization of a tubular fetal vessel in the membranes chromosomal anomalies (18 & 13)
overlying the presenting part
 Endovaginal sonography:
o Identification of an echogenic, parallel or circular line near the cervix  Thrombosis
 ( +) hemorrage antepartum or intrapartum  check for possibility of vasa previa  Rare event
and a ruptired fetal vessel  Types:
 amount of fetal blood that can be shed without killing the fetus is relatively small o Venous  70%
 fetal death is instantaneous o Venous and arterial  20%
 o Arterial  10%
 Venous thromboses have lower perinatal morbidity and mortalitty rates
Cord abnormalities capable of impending blood flow:  Arterial thrombosis is associated with IUGR and IUFD
 False knots
 Knobs (?) protruding from the cord surface  Vessel Dilatation
 Focal redundancies of a vessel or wharton jelly  Umbilical vein varix
 No clinical significance o Marked focal dilatation
o Developed within the intraamnionic part of OR within the fetal intra –
 True Knots abdominal portion
 Caused by active fetal movement
 Incidence is 1%  Fetal intra – abdominal varix have increased rates for:
 More common in monoamnionic twins o IUFD
 Risk of stillbirth is increased by 5 – 10x
o Structural anomalies
 Causes heart rate abnormalities during labor
o Aneuploidy
 Cord blood acid – base values are norma

 Loops  Most common complications:

 Coiling of cord around portion of the fetus o Varix rupture
 Nuchal cord  looped around the neck o Varix thromboses
 Incidence of nuchal cord: o Compression of umbilical artery
o 1x  10 – 34% o Fetal cardiac failure (high preload)
o 2x  1.5 – 5%
o 3x  0.2 – 0.5%
#JourneytoClerkship
 20% of fetuses with nuchal cord have moderate to severe variable decelerations
and with high incidence of lower umbilical artery pH +
AMDG
 Funic Presentation Gloria in Excelsis Deo
 Uncommon: associated with fetal malpresentation
 Umbilical cord is the presenting part in labor
 May present with:
o Cord prolapse
o Fetal heart rate abnormalities

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