placental investigation: patterns and clinical outcomes fileplacental investigation: patterns and...
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Placental investigation:
patterns and clinical outcomes
Raymond W. Redline
Case Western Reserve University
Cleveland OH, USA
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Maternal supply line: the “extended” placenta
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Failure of Arterial
Remodeling
Brosens, Robertson, Dixon,
Pijnenborg, Khong
Persistent
muscularization
of basal plate arteries
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Maternal vascular malperfusion
GJ Burton 2009
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BIPHASIC VILLOUS ARCHITECTURE IN
MATERNAL MALPERFUSION
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Increased syncytial knots
Agglutination Increased intervillous fibrin
Paucity
Global/ partial obstruction: accelerated villous maturation
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Area of paucity >40% = Distal villous hypoplasia correlates with absent end-diastolic flow by doppler
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Segmental/ complete obstruction: villous infarction
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Decidual Arteriopathy
Atherosis
Mural Hypertrophy
Chronic perivasculitis
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Maternal vascular: loss of integrity
Spiral arteries:
Abruptio placenta
Decidual veins:
Marginal
abruption
(retroplacental hemorrhage)
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Findings consistent with Abruptio Placenta
Ruptured spiral artery
Central hematoma with indentation
Predisposing factors:
Preeclampsia, vasoactive drugs, trauma
Presentation:
vaginal bleeding, uterine rigidity,
abdominal pain, hypotension
Pathogenesis:
Ruptured spiral artery:
sheer stress or ischemia-reperfusion
Adverse outcomes:
Preterm delivery
Neurodisability
IUFD
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Distended marginal vein
Acute peripheral separation/ Marginal abruption
Marginal retroplacental hemorrhage
Predisposing factors:
Low implantation, PROM,
chorioamnionitis
Presentation:
Vaginal bleeding,
Precipitous delivery
Pathogenesis:
Abnormal marginal anatomy
Inflammation of marginal decidua
Adverse Outcomes:
Preterm delivery
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Chronic abruption/ peripheral separation
•Circumvallation and green staining
Chorioamnionic hemosiderosis
Predisposing factors:
multiparity, abnormal
implantation
Presentation:
chronic vaginal bleeding,
oligohydramnios
Pathogenesis:
abnormal marginal anatomy
Outcomes:
Preterm delivery
FGR
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Clinical consequences of maternal
vascular/ trophoblastic lesions
Symptoms:
preeclampsia, impaired fetal growth, abnormal doppler studies, oligohydramnios, pregestational diabetes. obesity, thrombophilia
Outcomes:
Fetal growth restriction (FGR), Preterm delivery (PTD), Abruptio placenta: IUFD, CNS injury, Long term cardiovascular risk
Recurrence risk:
5-10%
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Fetal stromal vascular
placenta: umbilical cord,
chorionic plate, villous
stroma
CNS
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Fetal stromal vascular
placenta: proximal and
distal villi
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Normal vasculo-syncytial membranes)
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Normal term villi Delayed villous maturation
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Delayed villous maturation
(AKA distal villous immaturity/ maturation defect)
Pathology:
- Increased villous stroma with central capillaries
- Thick trophoblast layer lacking vasculo-syncytial membranes
- Placentomegaly with decreased fetoplacental weight ratio
Associations:
- Diabetes (increased fetal insulin)
- Maternal obesity
- UC obstruction
- IUFD
- Subset of FGR
Physiology:
- Increased demand (increased fetoplacental mass)
- Decreased placental function (increased diffusion distance)
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Fetal stromal-vascular maldevelopment:
fetal villous capillary lesions
• Chorangioma (single/ multiple)
(1-2% of all placentas)
• Chorangiosis
(5-10% of term placentas)
• Multifocal chorangiomatosis
(<1% of all placentas)
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Definition: 10 capillaries/villus in
> 10 villi several different areas
(some with 15-20 capillaries)
Pathophysiology: Angiogenic GF
response to excessive glucose or
hypoxemia
Clinical: High altitude, smoking,
excessive air pollution, maternal
anemia, diabetes
Villous chorangiosis
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Chorangioma (placental hemangioma)
• GA: 32-36 weeks
• Increased in:
– Multiple pregnancies
– Preeclampsia
• Possible genetic predisposition
• Complications (rare):
• Sequestration of platelets
• A-V shunt with hydrops
• Fetal growth restriction
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Multifocal
chorangiomatosis
Pathology: Multiple foci of
excessive capillary growth
affecting immature intermediate
and stem villi
Pathogenesis: Adaptive
response to oxygen deprivation
and reduced fetal blood flow
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FETAL VASCULAR MALPERFUSION BY SITE
Global/ partial: Chronic partial intermittent
UC obstruction
Segmental/
complete: Fetal
thrombosis
Stem vessel
obliteration
UMBILICAL CORD
CHORIONIC PLATE
PROXIMAL VILLI
Avascular villi/
Villous stromal
Vascular
karyorhhexis
CORD OBSTRUCTION
Courtesy of Theonia Boyd, Boston Children’s Hospital
DISTAL VILLI
Fetal blood flow
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Fetal vascular malperfusion
• Global/ partial-intermittent: fetal-umbilical vessels • Venous dilation, chorionic/ stem villi
• Intramural fibrin deposition, recent or remote
• Scattered small foci, avascular villi and/or stromal vascular
karyorhexis
• Segmental/ complete: chorionic-proximal villous vessels • Chorionic/ stem villous thrombi
• Stem vessel obliteration (fibromuscular sclerosis/ loss of lumina)
• Large foci, avascular villi and/or stromal vascular karyorhexis
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Global/ partial-intermittent: obstructive UC lesions
Dilated veins, chorionic plate
(diameter > 4x artery)
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1. Increased fetal venous pressure - ? UC occlusion
2. ? Old thrombi incorporated into vessel wall
3. ? Fibrin or myofibroblast-derived matrix
Recent Remote
Intramural fibrin deposition (“intimal fibrin cushions”)
chorionic plate or large stem villi
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Scattered small foci of avascular villi
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Fetal vascular malperfusion
• Global/ partial-intermittent: fetal-umbilical vessels • Venous dilation, chorionic/ stem villi
• Intramural fibrin deposition, recent or remote
• Scattered small foci, avascular villi and/or stromal vascular
karyorhexis
• Segmental/ complete: chorionic-proximal villous vessels • Chorionic/ stem villous thrombi
• Stem vessel obliteration (fibromuscular sclerosis/ loss of lumina)
• Large foci, avascular villi and/or stromal vascular karyorhexis
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Courtesy of Theonia Boyd, MD
Segmental/ Complete: Large Vessel Thrombi
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Secondary lesions: stem vessel obliteration,
(fibromuscular sclerosis and loss of lumina)
Recent Remote
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Large foci of
hyalinized avascular villi
Secondary lesions: distal villi (avg >15/ slide = FTV)
Villous stromal
vascular karyorrhexis
Sander 1980 Redline 1994
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Clinical consequences of
fetal stromal-vascular/ lesions
Presentation:
UC entanglement, ↓ fetal movement, abnormal BPP/ NRFHR, gestational diabetes, obesity
Outcomes:
IUFD, CNS injury, less commonly FGR
Recurrence risk:
Low, with rare exceptions
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Acute Chorioamnionitis
Pathogenesis: Infection: ascending,
hematogenous, contiguous
Predisposing factors: ROM, Abnormal cervix,
Pathogenic flora
Presentation: PTL, PROM, Fever, WBC
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Histologic Chorioamnionitis Maternal Inflammatory Response
Stage = Duration
1. Subchorionitis/ chorionitis
2. Chorioamnionitis (amnion + chorion)
3. Necrotizing chorioamnionitis (>25% amniocytes)
Grade = Intensity
1. Mild-moderate (subchorionic PMN)
2. Severe (subchorionic PMN abscesses)
Redline et al, Pediatr Devel Pathol 2003
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Early acute subchorionitis
(Maternal Stage 1/3)
*Diffuse
infiltration
of neutrophils
from intervillous
space into
subchorionic
fibrin
*chorionic
plate and
amnion-
negative
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Acute chorioamnionitis (stage 2)
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Necrotizing acute chorioamnionitis
(Maternal Stage 3/3)
*Neutrophil
karyorrhexis
*amniocyte
necrosis
*amnion BM
thickening/
eosinophilia
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Severe acute chorioamnionitis (subchorionic
microabscesses, Maternal Grade 2/2)
Confluent Neutrophils (> 20 cells in max extent) below chorion
Membranes Chorionic plate
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Histologic Chorioamnionitis Fetal Inflammatory Response
Stage = f (Duration x Fetal Maturity)
1. Chorionic Vasculitis/ Umbilical Phlebitis
2. Umbilical Arteritis
3. Concentric Umbilical Perivasculitis
Grade = Intensity (chorionic vessels)
1. Mild-Moderate (PMN)
2. Intense (confluent PMN)
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Umbilical phlebitis
(Fetal Stage 1/3)
Umbilical arteritis
(Fetal Stage 2/3)
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Concentric umbilical perivasculitis
(Fetal Stage 3/3)
Neutrophils
(+ associated
debris) in
concentric
bands-halos
around one
or more
umbilical
vessels
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Severe chorionic vasculitis (Fetal Grade 2/2)
Confluent-near confluent intramural neutrophils in chorionic
vessels with degenerative changes in VSMC
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Chronic Villitis
Definition: Lymphocytes and increased macrophages in
placental villi
Subtypes:
• Chronic villitis, infectious
• Chronic villitis, idiopathic
(AKA “villitis of unknown etiology” = VUE)
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Chronic villitis (idiopathic) = graft versus host reaction
Fetoplacental
Antigens Maternal
Immune Response
Maternal T cells
(Blue with two
X-chromosome signals)
Scott Hyde
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Location: Basal/ Parenchymal/ Both
Extent: Low Grade (<10 villi/ focus) focal:> 1 focus,1 slide
multifocal: >1 slide
High Grade (>10 villi/ focus) patchy: >1 focus
diffuse: >5% of all villi
Associated lesions: decidual plasma cells
extensive perivillous fibrin
fetal vascular involvement
Chronic villitis: idiopathic/ (“VUE”) Classification scheme
Kraus et al, 2004
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<10 villi/ focus
Low grade VUE High grade VUE
> 10 villi/ focus
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High Grade VUE involving fetal vessels
Avascular distal villi Obliterative fetal vasculopathy
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Cerebral Palsy at Term vs. Placentas Routinely
Submitted to Pathology Department
Placental Lesions CP Group Routine 1 Routine 2
(1992-2010) (2003) (2010)
N= 205 250 100
Fetal malperfusion: global/partial 32(16) 11(4) 5(5)
Meconium associated vascular necrosis 28(14) 8(3) 0(0)
Fetal malperfusion: segmental/complete 24(12) 6(2) 0(0)
VUE, high grade 23(11) 7(3) 3(3)
Histologic ACA, severe fetal response 10(6) 8(3) 1(1)
Meconium, without vascular necrosis 73(36) -- 29(29)
Histologic ACA, mild-mod fetal response 26(13) 15(6) 16(16)
Maternal malperfusion 23(11) 34(14) 6(6)
VUE, low grade 13(6) 10(4) 8(8)
Chronic abruption 8(4) 7(3) 1(1)
Redline, 2008