fritsch placenta part i 2012 compressed.pdf

Dr. J. W. Ballantyne:

“… a diseased fetus without its placenta is an imperfect specimen and a description of a fetal malady, unless accompanied by a notice of the placental condition is incomplete… During intrauterine life, the fetus, the membranes, the cord and placenta form an organic whole and disease of any part must react upon and affect the other.”

Ballantyne, JW: Disease and Deformities of the Foetus: An Attempt to a System of Antenatal Pathology. Edinburgh, Oliver and Boyd, 1892-1895. From DB Singer

Maternal-Fetal-Placental Unit

PLACENTA – LECTURE 1Michael K Fritsch MD, PhD

Northwestern University and Ann and Robert H. Lurie Children’s Hospital of Chicago

GOALS – Placenta Lecture 1

Placental development.

Review normal histology.

Review gross pathology of placenta, membranes, and umbilical cord.

PLACENTAL DEVELOPMENT

Early Embryonic Development (Differentiation)

Modified from Keller G. Genes & Development 19:1129-1155, 2005

From: Langman’s Medical Embryolgy 11th ed. TW Sadler

Early Placental Development – Day 7.5

31

2

From: Langman’s Medical Embryolgy 11th ed. TW Sadler

Early Placental Development – Day 9

Embryonic Pole

From: Langman’s Medical Embryolgy 11th ed. TW Sadler

Early Placental Development – Day 13

1 – Completely embedded inendometrial stroma.

2 - Lacunae open into maternalspiral arteries – sinusoids. Utero-placental circulation established.

3 – Extraembryonic mesodermlayer forms and lines the cytotrophoblast layer (to becomechorion).

4 – Amnionblast (derived fromepiblast) will form separate layer

amnion later.

5 – Connecting stalk will become UC.

6 – Primary villi form.

7 – chorionic cavity forms.

From: Langman’s Medical Embryolgy 11th ed. TW Sadler

VASCULOGENESIS OF THE PLACENTA (Beginning day 14)

New vessels formed from mesodermic mesenchyme.

Cytotrophoblast cells invadethrough syncytiotrophoblast andresults in altered differentiationof extravillous trophoblast (EVT).

EVT

From: Langman’s Medical Embryolgy 11th ed. TW Sadler

Villous Development

Archoring(primary) villi.

Branching to secondary and tertiary villi.

4th w 4th m

From: Langman’s Medical Embryolgy 11th ed. TW Sadler

Formation of Membranes

8 w 12 w

From: Langman’s Medical Embryolgy 11th ed. TW Sadler

Formation of the Umbilical Cord

5 w10 w

NORMAL PLACENTAL HISTOLOGY

Placenta Review

The Developing Human by Moore & Persaud

1

2

34

5

Membranes

Amnion

Chorion

ExtravillousTrophoblast

Decidua

Chorionic Plate

Amnion

Chorion

Villi and Intervillous space

AmnionEpitheliumCompact layerAmnion mesoderm

Chorion with fetal vessels

Few trophoblast stem cells

Langhans fibrinoidInvasive cytotrophoblast

Syncytiotrophoblast

Intervillous space

Nitabuch’sFibrinoid

Rohr’sFibrinoid

Extravillous Trophoblast

Decidua

Villi

Basal Plate

Term Villi

PLACENTAL PATHOLOGY

Why examine the placenta?

Pros:Many neonatal diseases are associated with placentalpathology.

Placental pathology can give some insight into outcome.

Prediction for future pregnancy outcomes.

Cons:High false positive findings in placenta. Many normal neonates may have pathology in their placentas.

Pathology findings are not necessarily disease specific.

False negative findings not as great, but still significant.Fetuses with pathology may have a normal placenta.

Skill and efforts of pathologists vary tremendously.

Fetal Outcomes Associated with Singleton Placental Pathology

1) Normal

2) Preterm delivery (spontaneous abortion)

3) Fetal growth restriction (SGA - IUGR)

4) Hypoxic/ischemic CNS injury

5) Infection

1) Death (stillbirth)

2) Others (syndromes, tumors, gestational trophoblastic disease, recurrence, etc)

When does a placenta get sent to a pathologist?

From Embryo and Fetal Pathology by E. Gilbert-Barness

CAP guidelines (1997) and each hospital to establish their criteria based on above.

AFIP PlacentalPathology byKraus et al. 2004

SUMMARY

GROSS PLACENTAL PATHOLOGY

Placenta Review

Normal:

Size (at term) – 450-630 gm, 15-25 cm in diameter, up to 3 cm thick, ovoid to round, single lobe with 15-20 cotelydons.

Membranes – Clear and inserted at margins.

Placenta – Parenchyma beefy red without lesions. Chorionic plate clear with uniformly sized surface vessels.

Umbilical cord – Eccentric insertion of 3 vessel cord,

1-2 cm in thickness. Uniformly white surface and Wharton’s jelly.

SIZE AND SHAPE

SHAPE

ACCESSORY LOBES

Accessory Lobe

Multilobed Placenta

Succenturiate (Multilobed) PlacentaFrom DB Singer

1 – 5%

2 – membrane vessels

3 – increased risk for:- bleeding- placenta previa- retained placenta

SIZE

LGA (>10%) due to diabetes, hydrops, mesenchymal dysplasia, infections (syphilis),maternal obesity, genetic, others.

SGA (<10%) due to MVU (HTN, preeclampsia, infarcts), MPVFD/MFI, maternalchronic disease, chronic villitis, severe fetal thrombotic vasculopathy, genetic,others.

GESTATIONAL AGE (WEEKS)

WEIGHT(GM)

FETUS

PLACENTA

From DB Singer

MEMBRANES & CHORIONIC PLATE

Circumvallate Membrane Insertion

Cicumvallate – ridge present – associated with increased risk of bleeding and premature delivery.Circummarginate – no ridge – (common 25%) – significance uncertain.

We report both as % of circumference involved and widest amount of extrachorialis (cm).

From DB Singer

Membranes with remote parietalhemorrhages with hemosiderin.

When extensive consider the diagnosis ofdiffuse chorioamniotic hemosiderosis.

Subchorionic Hemorrhages and Fibrin Thrombi

Subchorionic Fibrin Thrombus

Common – 60%Associated with preterm birth, abortion, vaginal bleeding, IUGR, fetal demise.Frequent in placentas from mothers withsevere heart disease or thrombophilia.

Subchorionic Acute Hemorrhage Associated with Amniotic Fluid Infection

Squamous Metaplasia of Amnion

From DB Singer

Squamous Metaplasia

From DB Singer

Amnion Nodosum (Oligohydramnios & Decreased 

Movement)

From DB Singer

Amnion Nodosum

From DB Singer

Fetus Papyraceous

Fetus Papyraceous

SUBCHORIONIC CYST

BASAL PLATE & PARENCHYMA

Hemorrhages including abruption

Abruption with Vaginal Hemorrhage

Abruptions (1-4%) are clinically significant retroplacental/marginal hemorrhages.From DB Singer

Retroplacental and Marginal Hemorrhages

Marginal Abruption

From DB Singer

Low Implantation- Praevia

From DB Singer

Central Abruption

From DB Singer

Central Abruption

Adherent central clot 3.4 cmAdherent marginal clot 2.4 cm

Retroplacental & marginal acute to subacutehemorrhages with intraparenchymal extensionconsistent with the clinical history of abruption.

Compression of intervillous space near hemorrhages.

MARGINAL HEMORRHAGE/ABRUPTION IN AFI

Chronic Abruption 

From DB Singer

Summary Retroplacental and Marginal Hemorrhages:

1 – Do not correlate well with abruption (separation of basal plate from uterine walldue to intervening hemorrhage).

2 – Clinically significant (true abruption) acute hemorrhages associated with adverse outcomes: preterm delivery, IUGR, stillbirth, CNS injury.

3 – Etiologies – MVU, trauma, amniocentesis, uterine anomalies, placenta previa,cocaine use, nicotine, multiparity.

4 – Clinical triad – vaginal bleeding, pain, rigid abdomen.

5 – Histologic criteria: < 1h maybe nothingAcute (hours to a few days) – compression of villi and loss of intervillous spaces, increased perivillous fibrin focally, acute hemorrhage with neutrophils, associated decidual necrosis (arterial).Chronic (days to weeks) – above with infarcted villi, and hemosiderin (venous). Associated with multiparity, smoking, oligohydramnios, and deepimplantation, circumvallate insertion, preterm delivery, CP, neurologic impairment.

Intervillous Thrombus

Common (20%). Nonspecific.Associated with FMH, maternal thrombophilias, and preeclampsia.Usually fetal blood.

Intervillous Thrombi

Villous Infarcts

Due to diminished maternal perfusion with ischemic necrosis of affected villi.Associated with HTN and preeclampsia (MVU).

Histologic findings:Early – Loss of intervillous space and villous crowding.

Increased perivillous fibrin.Acute inflammation.

Later - Loss of nuclear basophilia.Ghosted villi +/- surrounding fibrin.Calcification.Surrounding villi with DVH and increased syncytial knots.

Adverse outcomes: IUGR, small placenta, death (>50% placenta infarcted).

Placental Infarcts

From DB Singer

Acute Infarct with Inflammation

Remote Infarct with DVH and SK

Chorangioma

Benign neoplasm of fetal capillaries.Associated with multiple gestations and congenital anomalies.

Grossly: a bulging white or red mass.

Histology:Proliferating fetal blood vessels (capillaries) with a cellular stroma.

Adverse outcomes: Rare unless large. Fetal hydrops, stillbirth, IUGR, anemia, thrombocytopenia, CHF, abruption, premature delivery, preeclampsia.

Chorangioma with fibrosis

From DB Singer

CHORANGIOMA

CHORANGIOMA

UMBILICAL CORD PATHOLOGY

Insertion Pathology:

Marginal (<1cm from margin): 7%; ? Clinical significance – associated withPreterm labor, neonatal asphyxia, abortions, malformed infants.

Velamentous (into membranes): 1% singleton (> in twins); prone to trauma, rupture, compression, thrombosis; associated with fetal thrombotic vasculopathy, low birth weight, low Apgar, abnormal fetal heart rate patterns, prematurity, cerebral palsy, early abortion, congenital anomalies, and death.

Furcate (vessels leave Wharton’s jelly before insertion): most normal, but weak association with stillbirth, thrombosis of fetal vessels, IUGR & hemorrhage.

198 GM (23 W 133-211 GM)Marginal insertion 3v UC

Marginal Insertion

Marginal and Velamentous Insertion

Velamentous Cord Insertion

From DB Singer

Velamentous Cord with Ruptured  Vessel

From DB Singer

Marginal and Furcate Insertion

Coiling Pathology:

Normal: 1-3 twists (coils) per 10cm of cord.

Hypercoiled: >3 twists/10cm

Undercoiled: <1twist/10cm

Both associated with increased risk of IUGR, fetal distress and perinatal death.

Marginal Insertion of Hypercoiled UC with Meconium

Hypercoiled UC with Partial Loss of Wharton’s Jelly

UNDERCOILED 2 VESSEL UC

Length:

Normal at term: 60 +/- 13 cm.

Excessively long cords (5%) are associated with cord accidents (stillbirth), entanglements, cord prolapse, true knots, excessive coiling, constricture,thrombi.Associated adverse outcomes include fetal distress, neurologic impairment,IUGR and IUFD.

Abnormally short cords (1-2%) are associated with cord hemorrhages, abruption, failure of descent, fetal distress, low Apgar, & congenital anomalies.

Long and Hypercoiled Cord

From DB Singer

Number of UC vessels:

Single umbilical artery (2 vessel cord) occurs in 1% of singleton pregnancies.

Most outcomes completely normal.

Associated increased risk of IUGR, antepartum hemorrhage, polyhydramnios and oligohydramnios.

Increased SUA in mothers with diabetes.

In autopsy studies SUA is associated with increased likelihoodof other congenital anomalies.

Accessory vessels: aberrant right umbilical vein or vitelline vessels.

NORMAL UMBILICAL CORD SINGLE UMBILICAL ARTERY

Knots:

Rare < 1%.

Classify as tight or loose.

Tight knots can result in umbilical vein compression.Tight knots associated with increased risk of IUFD and intrapartum demise(up to 10%) and poor neurologic outcome.

True Knot (Tight)

Double True Knot

False Knots (varices)

From DB Singer

Salzburg Austria