OBSTETRICS & GYNECOLOGY

Placental Abnormalities  does not exceed 40mm

Dr. AJB
William’s Obstetrics 25th edition + Lecture Maternal Surface: Basal Plate
September 27, 2018  Divided by clefts into portions called cotyledons
 Clefts marked the site of internal septa that extend into the
intervillous space
HISTOPATHOLOGICAL EXAMINATION Fetal Surface: Chorionic Plate
 Where umbilical cord insert at chorionic plate’s center
 Maternal Indications  Large fetal vessels that originates from the cord vessels
 Abruption that spread and branch across the chorionic plate before
 Antepartum infection with fetal risk entering stem villi at placental parenchyma
 Anti CDE alloimunization  Fetal arteries almost invariably cross over veins
 Cesarean hysterectomy  Chorionic plate and its vessels are covered by thin
 Olgohydramnios or hydramnios amnion, and easily peeled from a postdelivery specimen
 Peripartum fever and infection
 Preterm delivery At term, the typical placenta weighs 470 g, is round to oval
 Postterm delivery with a 22-cm diameter, and has a central thickness of 2.5 cm
 Severe trauma (Benirschke, 20 1 2) . It is composed of a placental disc, extra
 Suspected placental injury placental membranes, and three-vessel umbilical cord. The
 Systemic disorders with known effects disc surface that lies against the uterine wall is the basal plate,
 Thick or viscid meconium which is divided by clefts into portions-termed cotyledons.
 Unexplained late pregnancy bleeding he fetal surface is the chorionic plate, into which the umbilical cord
 Unexplained or recurrent pregnancy complications inserts, typically in the center. Large fetal vessels that
originate from the cord vessels then spread and branch across
 Fetal and Neonatal Indications the chorionic plate before entering stem villi of the placenta
 Admission to an acute care nursery parenchyma. In tracing these, fetal arteries almost invariably
 Birth weight <10th or > or = 95th percentile cross over veins. he chorionic plate and its vessels are covered
 Fetal anemia by thin amnion, which can be easily peeled away from a postdelivery
 Fetal or neonatal compromise specimen.
 Neonatal seizures
 Hydrops fetalis
 Infection or sepsis SONOGRAPHICALLY
 Major anomalies or abnormal karyotype
 Multifetal gestation  Homogenous
 Stillbirth or neonatal death  Thickness is 2 – 4 cm
 Vanishing twin beyond the 1st trimester  Indents into the amnionic sac
 Lies against myometrium
 Placental Indications
 Gross lesions Retroplacental space:
 Marginal or velamentous cord inserion  Hypoechoic area
 Markedly abnormal placenta shape or size  Separates myometrium from placenta’s basal plate
 Markedly adhered placenta  1– 2 cm
 Term cord <32 cm or >100 cm
 Umbilical cord lesion As recommended by the American Institute of Ultrasound
in Medicine, placental location and relationship to the
internal cervical os are recorded during prenatal sonographic
examinations. As visualized ultrasonically, the normal placenta
NORMAL PLACENTA is homogenous and 2 to 4 cm thick, lies against the myome
trium, and indents into the amnionic sac.
GROSS The retroplacental space is a hypoechoic area that separates the
myometrium from
 470 g the basal plate and measures less than 1 to 2 cm. The umbilical
 Central thickness is 2.5 cm cord is also imaged, its fetal and placental insertion sites exam
 Diameter is 22 cm ined, and its vessels counted.
 Round to oval Many placental lesions can be identiied grossly or sono
 Chorionic plate normally extends to the periphery of the graphically, but other abnormalities require histopathological
placenta and has a diameter similar to that of the basal examination for clarification.
plate
ABNORMALITIES OF PLACENTA
COMPOSITION
Placental Calcification
 Placental disc  Calcium salts deposition maternal surface in basal plate
 Extraplacental membranes  Associated with:
 Three vessel umbilical cord o Nulliparity, smoking, higher socio – economic status,
increase maternal serum calcium

Hypertrophic Lesions of Chorionic Villi

RATE OF INCREASE OF PLACENTAL THICKNESS  Striking enlargement of the chorionic villi
 Associated with:
 1mm per week

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o Severe erythroblastosis, fetal hydrops, fetal hydrops,  Results to striking villous enlargment
maternal diabetes, fetal congestive heart failure,  Secondary to DM, severe maternal anemia, fetal hydrops,
maternal – fetal syphilis or syphilis, toxoplasmosis, or cytomegalovirus
 Partial mole or complete mole:
Placental Inflammation o Villi are enlarged and edematous and fetal parts are
 Characterized by degenerative and necrotic changes present
 Bacteria invade fetal surface of the placenta o Coexists with normal twin
 Associated with:  Placental mesenchymal dysplasia
o Preterm, prolonged membrane rupture o Has cystic vesicles
o Vesicles correspond to to enlarged stem villi
Syncytial Knot o There is no excessive torphoblast formation
 Clumps of syncytial nuclei project into the intervillous o Rare
space beginning after 32 weeks  Can also be due to collections of blood or fibrin
 Represents apoptosis o Causes:
 Massive perivillous fibrin deposition
 Intervillous or subchorionic thromboses
MICROSCOPE PLACENTAL ABNORMALITIES  Large retroplacental hematomas
Normal Maternal Fetal Disorders
Cytotrophoblastic cells - (+) numerous Of variants, placentas may infrequently form as separate, nearly
becomes progressively cytotrophoblastic cells in the equally sized discs. This bilobate placenta may also be called
reduced as pregnancy placenta bipartite placenta or placenta duplex. In these, the cord inserts
advances between the two placental lobes-either into a connecting
- associated with: Gestational chorionic bridge or into intervening membranes. A placenta
hypertension, diabetes, containing three or more equivalently sized lobes is rare and
erythroblastosis fetalis termed multilobate. Unlike this equal distribution, one or more
disparately smaller accessory lobes- succenturiate lobes - may
develop in the membranes at a distance from the main placenta
These lobes have vessels that course through the
membranes.
SHAPE AND SIZE
Of clinical importance, if these vessels overlie the
Bilobate placenta or Bipartate Placenta or Placenta Duplex cervix to create a vasa previa, dangerous fetal hemorrhage can
 Placenta form as separate, nearly equal sized discs follow vessel laceration. An accessory lobe can also be
 Cord inserts between the two placental lobes – either into retained in the uterus after delivery to cause postpartum uterine
a connecting chorionic bridge or into intervening atony and hemorrhage or later endometritis.
membranes
EXTRACHORIAL PLACENTATION
Multilobate Placenta
 Placenta with three or more equally sized lobes
 Rare Extrachorial Placentation
 Chorionic plate fail to extend to the periphery and leads to
Succenturiate Lobes or Small Accessory Lobes of the Placenta chorionic plate that is smaller than the basal plate
 Develop at a distance from the main placenta
 Have vessels that course through the membranes Circummarginate Placenta
 If these vessels overlie the cervix it may create VASA  Fibrin and old hemorrhage lie between the placenta and
PREVIA the overlying amniochorion
 Vasa previa
o If torn, can cause dangerous fetal hemorrhage Circumvallate Placenta
 Can be retained in the uterus after deliver and can cause  Assciated with antepartum bleeding and preterm birth
unterine atony and hemorrhage  Transient and benign
 Peripheral chorion is a thickened, opaque, gray – white
Placenta Membranacea circular ridge composed of a double fold of chorion and
 All or nearly all of the fetal membranes are covered with amnion
villi  Sonographically:
 May cause serious hemorrhage due to associated o Double fold is seen as thick, linear band of echoes
placenta previa or accreta extending from one placental edge to the other
 Ring Shaped Placenta  Cross – section:
o Variant of placenta membranacea o Appear as “shelf.”
o Placenta is annular, partial or complete ring of placental o Its location may help differentiate this shelf from
tissue amniotic bands and amniotic sheets.
o Associated with:
 Antepartum and postpartum bleeding; and  Most pregnancy with extrachorial placentation has normal
 fetal growth restriction outcome

Placenta Fenestra DEGENERATIVE PLACENTAL LESIONS

 Central portion of a placental disc is missing
 Some cases involves actual placentel hole
 Deposition of calcium salts
 Often, defect involves only villous tissue and chorionic
 Result from:
plate is intact
o Trophoblastic aging
 May prompt search for a retained placental cotyledon
o Infarction
 More extensive in smokers
Placentomegaly
 Increases as pregnancy progresses
 Placenta thicker than 40 mm

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Pathophysiology:
Calcium salts can be deposited throughout the placenta but  Slow maternal blood flow currents  blood stasis  fibrin
are most common on the basal plate. Calcification accrues deposition  decrease villous oxygenation 
with advancing gestation, and greater degrees are associated syncytiotrophobalst necrosis
with smoking and increasing maternal serum calcium levels). These
hyperechoic deposits can easily be seen sonographically, and a Maternal Floor Infarction
grading scale from 0 to 3 relects increasing calciication with  Deposition of dense fibrinoid layer on the placental basal
increasing numerical grade. Following this plate
scheme, a grade 0 placenta is homogeneous, lacks calcification,  Lesion is thick, white, firm, corrugated surface
and displays a smooth, flat chorionic plate. A grade 1 placenta  Impedes normal maternal blood flow into the intervillous
has scattered echogenicities and subtle chorionic plate undu space
lations. Grade 2 shows echogenic stippling at the basal plate. Associated with:
Large, echogenic comma shapes originate from an indented  Miscarriage
chorionic plate, bur their curve falls short of the basal plate.  IUGR
Last, a grade 3 placenta has echogenic indentations extending  Preterm deliveries
from the chorionic plate to the basal plate, which create discrete  Still births
components that resemble cotyledons. Basal plate densities also  Recur in subsequent pregnancies
increase.  Not well defined etiopathogenesis

Subchorionic Infarct
CIRCULATORY DISTURBANCES  Found underneath the chorionic plate
 Extend downward toward the intervillous space
 Disrupts maternal blood flow to or within the placenta
 Disturbs fetal blood flow through the villi
Intervillous Thrombus
Functionally, placental perfusion disorders can be grouped  Collection of a coagulated blood admixed with fetal blood
into: those in which maternal blood flow to or within the  Grossly round or oval, red if recent, white – yellow if older
intervillous space is disrupted, and those with disturbed  Causes elevated alpha – feto protein
fetal blood flow through the villi. These lesions are frequently
identified in the normal, mature placenta. Although they can Placental Infarctions
limit maximal placental blood flow, functional reserve within  Most common placental lesion
the placental prevents harm in most cases. Indeed, some esti  Normal or pathologic
mate that up to 30 percent of placental villi can be lost without  90% located at placental margin
untoward fetal effects. If extensive, however, these  due to occlusion of maternal uteroplacental circulation
lesions can profoundly limit fetal growth.  usually represent normal aging
Lesions that disrupt perfusion are frequently seen grossly Complications
or sonographically, whereas smaller lesions are seen only his  Ueteroplacental insufficiency
tologically. With sonography, many of these, such as sub  Placental abruption
chorionic fibrin deposition, perivillous fibrin deposition, and Associated with:
intervillous thrombosis, appear as focal sonolucencies within  Preeclampsia
the placenta. Importantly, in the absence of maternal or fetal  Lupus anticoagulant
complications, isolated placental sonolucencies are considered Histopath:
incidental findings.  Fibrinoid degeneration of trophoblast
 Calcification
 Ischemic infarction
Pathophysiology:
 Occlusion of decidual artery  interrupts blood flow to
intervillous space  ischemia  necrosis of villous Tissue
 Placental abruption

Placental Vessel Thrombosis

 Stem artery from fetal circulation in the placenta is
occluded producing a sharply demarcated area of
avascularity
Associated with:
 Normal pregnancy  (5%)
 Diabetic woman  10%
Will deprive 5% of villi with blood supply.
Placental Perfusion Disorders Complications:
 Common and found in normal mature  Fetal growth restriction
 Effect: limit maximal placental blood flow  Stillbirth
 Can lose up to 30% of its villi without untoward fetal
effects Hematoma
 Retroplacental Hematoma
Subchorionic Fibrin Deposition o Between placenta and its adjacent decidua
 Caused by slowing of maternal blood flow within the
intervillous space with fibrin deposition  Marginal Hematoma (AKA subchorionic haemorrhage)
 Lesions are white or yellow plaques on the fetal o Between chorion and decidua at the placental periphery
surface
 Subchorial thrombosis
Pervillous Fibrin Deposition o Breus mole
 Small, yellow – white nodules (normal part of placental o Along the roof of the intervillous space and beneath the
aging) chorionic plate

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ABNORMALITIES OF MEMBRANES
 Subamnionic
o Between placenta and amnion
o Complications Meconium staining
 Miscarriage, abruption, IUGR, preterm delivery,  Incidence is 12 – 20%
adherent placenta  Risk increases to 25 – 42% after 42 weeks
 ( + ) amnion stain  1 – 3 hours  then to chorion,
Fetal Blood Flow Disruption umbilical cord, and decidua
 Fetal thrombotic vasculopathy - affected portion of the  meconium passage cannot be timed or dated accurately
villous becomes infarcted and non-functional  Process:
 Subamnionic Hematoma  Meconium passage is prevented by tonic anal sphincter
contraction and lack of intestinal peristalsis
 Vagal stimulation produced by cord or head compression
PLACENTAL TUMORS in the absence of fetal distress
 Associated with:
 Fetal acidosis, non – reassuring fetal status, low APGAR
scores
 Fetal hypoxia produces anal sphincter relaxation and fetal
gasping  in utero aspiration of meconium  meconium
aspiration syndrome
 Complications:
 Meconium associated amniotic fluid embolism 
cardiorespiratory failure and consumptive coagulopathy 
maternal mortality
 4 fold risk of puerperal metritis

Chorioangioma (Hemangioma)
 Components resemble blood vessels and stroma of
chorionic villus
 Only benigh tumor of the placenta
 Incidence is 1%
 Increase maternal serum of alpha – fetoprotein
 Well circumscribed, rounded, predominantly hypoechoic
lesion near the chorionic plate amniotic cavity
 Increase blood flow is seen in color doppler
 5 cm is the cut – off size
 Tumor >5cm causes significant shunting which causes
fetal hydrops and anemia
o Other complication:
 antepartum hemorrhage, preterm delivery, amniotic Chorioamnionitis
fluid abnormalities, IUGR  Routes of infection:
 Ascending infection from the lower genital tract 
o Management: prolonged membrane rupture and long labor
 Decrease blood flow to the tumor by vessel occlusion  Hematogenous spread from maternal blood
and ablation  Direct spread from endometrium of FT
 Iatrogenic contamination
Tumor metastatic to the placenta  Process:
 Rare  Exclusion of vaginal bacteria from upper genital tract 
 Common: melanoma, leukemia, lymphoma, and breast entry of organism  initial infection of chorion adjacent
cancer decidua  full thickness involvement of membranes 
 Usually confined within intervillous space inflammation of chorionic plate and umbilical cord
 Melanoma can go to the fetus  Fetal Infections:
 Hematogenous, aspiration, swallowing, direct contact with
Maternal malignant tumors rarely metastasize to the placenta. infected Amniotic fluid
Of those that do, melanomas, leukemias and lymphomas, and  Gross:
breast cancer are the most common. Tumor  Infection characterized by clouding of membranes and foul
cells usually are confined within the intervillous space. As a odor (depends on bacterial species and concentration)
result, metastasis to the fetus is uncommon but is most often
seen with melanoma. Similarly, cases in which fetal Small Amnionic Cyst
malignancy metastasizes to  Due to fusion of amniotic folds, with subsequent fluid
the placenta are rare. These are predominantly retention
fetal neuroectodermal tumors, and only one case in the litera
ture describes transplantation of tumor to the maternal uterus. Amnion Noduosum
 Small, light tan nodules overlying the placenta
Embolic Fetal Brain Tissue  Hallmark of oligohydramnios
 Usually described with traumatic deliveries  Most common in:
 Location: placenta, fetal lungs  Fetal renal agenesis
 Prolonged PPROM
 Placenta of donor fetus
 Made up of:
 Vernix caseosa with hair

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 Sebum  Cocaine abuse

Amnionic Bands Single umbilical artery

 Formed from disruption of amnion  Incidence:
 Entrap the fetus and impair growth and development o Livebirths: 63%
 Consequence: fetal intrauterine amputation o Perinatal deaths: 1.92%
o Twins: 3%
Amionic Sheets  Most common aberration
 Normal amniochorion draped over preexisting uterine  Increased incidence is associated with:
synechia o Epilepsy
 Risk: preterm delivery and placental abruption o Preeclampsia
o Antepartum hemorrhage
o Amniotic fluid volume abnormalities
o Chromosomal abnormalities
ABNORMALITIES OF UMBILICAL CORD  Etiology:
o Secondary atrophy of a previously normal umbilical
NORMAL CORD artery
 Detected by routine UTZ (98% at 17 – 36 wks)
 Develops in close association with the amnion  Associated with:
 Susceptible to entanglement, compression, and occlusion o Spontaneous abortion
 Ave length: 40 – 70 cm o Renal aplasia
o Limb – reduction defects
Cord length is influenced by amniotic fluid volume, fetal mobility, o Atresia of hollow organs
heredity.  If an isolated sonographic finding: better prognosis
o No increased risk of aneuploidy
o Risk of IUGR
Association of short umbilical cords  If non – isolated sonographic finding:
 Oligohydramnios o Increase risk of aneuploidy
 Decrease fetal movement o Increase risk of structural abnormalities (renal agenesis,
 Fetal growth restriction imperforate anus, vertebral defects)
 Congenital malformation
 Intrapartum distress Hyrtlanastomosis
 Intrauterine fetal death (2 – fold risk)  Connection between the 2 umbilical arteries located 3 cm
of the placental inseetion of the cord
Long Cord  Acts as a pressure equalizing system between the
 Maternal systemic disease umbilical arteries  redistribution of pressure gradients
 Delivery complications and blood flow  improved fetal perfusion during unterine
 Cord entanglement contraction or umbilical artery compression
 Fetal distress  Fetuses with single umbilical artery lacks this safety valve
 Fetal anomalies  increase rate of unexplained IUFD in late pregnancy or
 Respiratory distress labor
 Perinatal mortality (3x)

Cord Diameter
 Used as predictive fetal marker
 Lean umbilical cord is linked with poor fetal growth
 Large dianmeter cords linked with macrosomia

Four vessel cord

( +) venous remnant  uncommon
increased risk of congenital anomaly
unknown significance
Cord Coiling
 Can be determined sonographically Fused Umbilical cord
 Umbilical coiling index (UCI) number of complete coils per  Occurs during embryological development  umblical
centimeter of cord length arteries fail to split (fused shared lumen)
 Hypercoiling  Associated with marginal or velamentous cord insertion
o Associated with:  No congenital fetal anomaly association
 Preterm birth Types:
 Fetal distress  Complete
 Meconium staining  Partial (typically found towards the cord insertion)
o Linked with fetal distress associated with:
 Fetal growth restriction
 Intrapartum fetal acidosis and asphyxia
 Preterm delivery

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ABNORMALITIES OF CORD INSERTION CORD ABNORMALITIES CAPABLE OF IMPEDING BLOOD FLOW

Marginal insertion False knots

 Battledore placenta  Knobs protruding from the cord surface
 Cord anchors at the placental margin  Focal redundancies of a vessel or wharton jelly
 Common in:  No clinical significance
 Multifetal pregnancy
 IVF True Knots
 Maybe associated with weight discordance  Caused by active fetal movement
 Incidence is 1%
Furcate Insertion  More common in monoamnionic twins
 Umbilical vessels separate from the cord substance before  Risk of stillbirth is increased by 5 – 10x
their insertion into the placenta  Causes heart rate abnormalities during labor
 Umblical vessels lose the protective wharton jelly shortly  Cord blood acid – base values are norma
before insertion  Covered by amnion
 Prone to compression, twisting, and thrombosis Loops
 Coiling of cord around portion of the fetus
 Nuchal cord  looped around the neck
 Incidence of nuchal cord:
o 1x  10 – 34%
o 2x  1.5 – 5%
o 3x  0.2 – 0.5%
 20% of fetuses with nuchal cord have moderate to severe
variable decelerations and with high incidence of lower
umbilical artery pH

Funic Presentation
 Uncommon: associated with fetal malpresentation
 Umbilical cord is the presenting part in labor
 May present with:
o Cord prolapse
o Fetal heart rate abnormalities

Umbilical Cord Stricture

Velamentous Insertion  Focal narrowing of the cord diameter
 Umbilical vessels spread in the membranes at a distance  Develops in the fetal umbilical insertion
from the placental margin  Characteristic pathological features:
 Increase risk of compression  fetal anoxia o Absence of wharton jelly
 Associated with: o Stenosis or obliteration of cord vessels at the segment
 Placenta previa
 Multiple gestation Hematoma
 Associated with:
Vasa Previa o Short cords
 Associated with velamentous insertion o Trauma
 Placental vessels lie between the cervix and the o entanglement
presenting fetal part  Causes:
o  vessel compression  fetal anoxia; and o Varix rupture (umbilical vein)
o  vessel laceration  fetal exsanguination o Umbilical vessel venipuncture
 Risk factors:
o Bilobate or succenturiate placenta Cysts
o 2nd trimester placenta previa ( with or without later  True and pseudocysts have similar sonographic
migration) appearance
o In Vitro fertilization  increased rates of abnormal cord  True cysts
insertion o Epithelium – lined remnants of the allantois
o Co – exist with a persistently patent urachus
 Anterpartum diagnosis results in improved fetal survival  Pseudocysts
rates o Local degeneration of wharton jelly
 Clinical diagnosis:  Single cord cysts in 1st trimester tend to resolve
o Palpation or direct visualization of a tubular fetal vessel  Multiple cord cysts portend miscarriage or aneuploidy
in the membranes overlying the presenting part  Pseudocysts persisting beyond 1st trimester can be
 Endovaginal sonography: associated with structural or chromosomal anomalies (18
o Identification of an echogenic, parallel or circular line & 13)
near the cervix
 ( +) hemorrage antepartum or intrapartum  check for
possibility of vasa previa and a ruptired fetal vessel Thrombosis
 Amount of fetal blood that can be shed without killing the  Rare event
fetus is relatively small  fetal death is instantaneous  Types:
o Venous  70%
o Venous and arterial  20%
o Arterial  10%
 Venous thromboses have lower perinatal morbidity and
mortalitty rates

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 Arterial thrombosis is associated with IUGR and IUFD

Vessel Dilatation
 Umbilical vein varix
o Marked focal dilatation
o Developed within the intra amnionic part of OR within
the fetal intra – abdominal portion
 Fetal intra – abdominal varix have increased rates for:
o IUFD
o Structural anomalies
o Aneuploidy
 Most common complications:
o Varix rupture
o Varix thromboses
o Compression of umbilical artery
o Fetal cardiac failure (high preload)

Cord hematomas are rare and generally follow rupture of an

umbilical vessel, usually the vein, and bleeding into the Whar
ton jelly. Hematomas have been associated with abnormal
cord length, umbilical vessel aneurysm, trauma, entanglement,
umbilical vessel venipuncture, and funisitis.
Most are identfiied postpartum, but hematomas are recognized
sonographically as hypoechoic masses that lack blood low.

Sequelae include stillbirth or intrapartum abnor

mal fetal heart rate pattern.
Umbilical cord vessel thromboses are rare in utero events and
seldom diagnosed antepartum. Approximately 70 percent are
venous, 20 percent are venous and arterial, and 1 0 percent are
arterial thrombosis. These all have high associ
ated rates ofstillbirth, fetal-growth restriction, and intrapartum
fetal distress. If
these are identified antepartum as hypoechoic masses without
blood low, data from case reports support consideration of
prompt delivery if of viable age

An umbilical vein varix can complicate either the intra-am

nionic or fetal intra-abdominal portion of the umbilical vein.
Sonographically and complemented by color Doppler, rare
intra-amnionic varices show cystic dilatation of the umbilical
vein that is contiguous with a normal-caliber portion. Of com
plications, an intra-amnionic varix may compress an adjacent
umbilical artery or can rupture or thrombose.
The rare umbilical artery aneurysm is caused by congeni
tal thinning of the vessel wall with diminished support from
Wharton jelly. Indeed, most form at or near the cord placental
insertion site, where this support is absent. These are associ
ated with single umbilical artery, trisomy 1 8, amnionic luid
volume extremes, fetal-growth restriction, and stillbirth. At least
theoretically, these aneurysms
could cause fetal compromise and death by compression of the
umbilical vein.

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