fritsch placenta part i 2012 compressed.pdf
TRANSCRIPT
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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
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GOALS – Placenta Lecture 1
Placental development.
Review normal histology.
Review gross pathology of placenta, membranes, and umbilical cord.
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PLACENTAL DEVELOPMENT
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Early Embryonic Development (Differentiation)
Modified from Keller G. Genes & Development 19:1129-1155, 2005
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From: Langman’s Medical Embryolgy 11th ed. TW Sadler
Early Placental Development – Day 7.5
31
2
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From: Langman’s Medical Embryolgy 11th ed. TW Sadler
Early Placental Development – Day 9
Embryonic Pole
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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.
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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
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From: Langman’s Medical Embryolgy 11th ed. TW Sadler
Villous Development
Archoring(primary) villi.
Branching to secondary and tertiary villi.
4th w 4th m
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From: Langman’s Medical Embryolgy 11th ed. TW Sadler
Formation of Membranes
8 w 12 w
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From: Langman’s Medical Embryolgy 11th ed. TW Sadler
Formation of the Umbilical Cord
5 w10 w
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NORMAL PLACENTAL HISTOLOGY
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Placenta Review
The Developing Human by Moore & Persaud
1
2
34
5
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Membranes
Amnion
Chorion
ExtravillousTrophoblast
Decidua
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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
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Nitabuch’sFibrinoid
Rohr’sFibrinoid
Extravillous Trophoblast
Decidua
Villi
Basal Plate
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Term Villi
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PLACENTAL PATHOLOGY
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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.
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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)
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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.
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AFIP PlacentalPathology byKraus et al. 2004
SUMMARY
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GROSS PLACENTAL PATHOLOGY
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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.
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SIZE AND SHAPE
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SHAPE
ACCESSORY LOBES
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Accessory Lobe
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Multilobed Placenta
Succenturiate (Multilobed) PlacentaFrom DB Singer
1 – 5%
2 – membrane vessels
3 – increased risk for:- bleeding- placenta previa- retained placenta
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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
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MEMBRANES & CHORIONIC PLATE
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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
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Membranes with remote parietalhemorrhages with hemosiderin.
When extensive consider the diagnosis ofdiffuse chorioamniotic hemosiderosis.
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Subchorionic Hemorrhages and Fibrin Thrombi
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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.
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Subchorionic Acute Hemorrhage Associated with Amniotic Fluid Infection
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Squamous Metaplasia of Amnion
From DB Singer
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Squamous Metaplasia
From DB Singer
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Amnion Nodosum (Oligohydramnios & Decreased
Movement)
From DB Singer
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Amnion Nodosum
From DB Singer
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Fetus Papyraceous
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Fetus Papyraceous
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SUBCHORIONIC CYST
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BASAL PLATE & PARENCHYMA
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Hemorrhages including abruption
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Abruption with Vaginal Hemorrhage
Abruptions (1-4%) are clinically significant retroplacental/marginal hemorrhages.From DB Singer
Retroplacental and Marginal Hemorrhages
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Marginal Abruption
From DB Singer
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Low Implantation- Praevia
From DB Singer
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Central Abruption
From DB Singer
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Central Abruption
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Adherent central clot 3.4 cmAdherent marginal clot 2.4 cm
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Retroplacental & marginal acute to subacutehemorrhages with intraparenchymal extensionconsistent with the clinical history of abruption.
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Compression of intervillous space near hemorrhages.
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MARGINAL HEMORRHAGE/ABRUPTION IN AFI
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Chronic Abruption
From DB Singer
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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.
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Intervillous Thrombus
Common (20%). Nonspecific.Associated with FMH, maternal thrombophilias, and preeclampsia.Usually fetal blood.
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Intervillous Thrombi
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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).
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Placental Infarcts
From DB Singer
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Acute Infarct with Inflammation
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Remote Infarct with DVH and SK
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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.
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Chorangioma with fibrosis
From DB Singer
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CHORANGIOMA
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CHORANGIOMA
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UMBILICAL CORD PATHOLOGY
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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.
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198 GM (23 W 133-211 GM)Marginal insertion 3v UC
Marginal Insertion
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Marginal and Velamentous Insertion
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Velamentous Cord Insertion
From DB Singer
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Velamentous Cord with Ruptured Vessel
From DB Singer
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Marginal and Furcate Insertion
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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.
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Marginal Insertion of Hypercoiled UC with Meconium
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Hypercoiled UC with Partial Loss of Wharton’s Jelly
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UNDERCOILED 2 VESSEL UC
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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.
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Long and Hypercoiled Cord
From DB Singer
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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.
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NORMAL UMBILICAL CORD SINGLE UMBILICAL ARTERY
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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.
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True Knot (Tight)
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Double True Knot
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False Knots (varices)
From DB Singer
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Salzburg Austria