Placental Abnormalities

Slide 1 · Placental Abnormalities

Structural, vascular, inflammatory and implantation-related mechanisms of fetal compromise

Dr Abu Suraih Sakhri

MBBS, MD (Pathology)

www.abusuraihsakhri.com

Slide 2 · Learning outcomes

Explain how placental function determines fetal growth in late gestation.

Distinguish maternal from fetal vascular malperfusion and their morphology.

Relate implantation, cord and infectious lesions to pregnancy outcomes.

Interpret selected placental patterns in fetal growth restriction.

Slide 3 · The placenta is a critical growth organ

Third-trimester fetal growth places major demands on uteroplacental flow.

Placental growth during the mid-trimester determines subsequent exchange capacity.

Reduced delivery of nutrients or oxygen may constrain fetal growth.

Slide 4 · Functional placental architecture

Chorionic plate — fetal vascular branches

Decidua basalis — maternal vascular interface

Chorionic villi with fetal vessels

Maternal blood surrounds villi in intervillous spaces

Slide 5 · Maternal and fetal circulations are distinct

Maternal compartment

Fetal compartment

Maternal arteries supply blood to intervillous spaces

Umbilical vessels connect fetus to vessels in chorionic villi

Intervillous blood surrounds villous surfaces

Fetal blood remains within fetal vascular channels

Defective spiral arteries compromise maternal inflow

Cord obstruction compromises fetal-side perfusion

Slide 6 · Exchange requires two functioning pathways

Adequate maternal inflow

Intervillous perfusion

Viable exchange villi

Patent fetal vessels

Delivery to the fetus

Sequential mechanism (schematic)

Slide 7 · Fetal growth restriction is not synonymous with prematurity

Premature infants may be small yet appropriate for gestational age.

Fetal growth restriction (FGR) denotes failure to achieve expected fetal growth.

Small-for-gestational-age (SGA) is a size description; Etiologic assessment remains necessary.

Slide 8 · Three broad origins of growth restriction

Maternal

Impaired maternal placental flow; Vascular disease and other maternal exposures.

Fetal

Intrinsic restriction of growth potential; Chromosome anomalies and infection.

Placental

Inadequate placental development, perfusion or exchange.

Slide 9 · Why timing matters

Placental growth in mid-gestation

Increasing fetal demands

Insufficient perfusion reserve

Relative nutrient / oxygen limitation

Fetal growth restriction

Sequential mechanism (schematic)

Slide 10 · Placental insufficiency is a functional concept

An inadequate placenta cannot consistently meet fetal metabolic demands.

Perfusion abnormalities and primary villous disease can both limit exchange.

Placental size alone does not identify every underlying mechanism.

Slide 11 · Placental etiologies named

Umbilical–placental vascular anomalies, thrombosis and infarction.

Placental abruption or placenta previa.

Chronic villitis, placental infection and multiple gestations.

Some small placentas have no identifiable cause.

Slide 12 · Placental FGR: Central physiologic sequence

Reduced placental capacity

Limited oxygen / nutrient availability

Down-regulation of later fetal growth

Asymmetric growth pattern

Relative brain sparing

Sequential mechanism (schematic)

Slide 13 · Patterns of growth restriction

Predominantly placental

Predominantly fetal

Usually asymmetric (disproportionate)

Usually symmetric (proportionate)

Relative preservation of brain growth

Many organ systems similarly restricted

Reflects supply limitation in later pregnancy

Reflects intrinsically reduced fetal growth potential

Slide 14 · Brain sparing: Interpretation of the pattern

Asymmetric FGR implies unequal effects on organ growth.

Relative sparing of the brain in placental FGR.

The morphologic pattern supports—but does not prove—a placental cause.

Slide 15 · From a growth pattern to a working differential

Observed pattern

Etiologic direction

Asymmetric small fetus

Consider limited placental nutrient / oxygen supply

Proportionately small fetus

Consider intrinsic fetal causes or congenital infection

Mixed or indeterminate pattern

Assess maternal, fetal and placental factors together

Slide 16 · Maternal vascular disease can affect the placenta

Chronic hypertension and preeclampsia may reduce uteroplacental flow.

The fetus may be intrinsically normal yet receive inadequate placental supply.

Maternal vascular insufficiency and placental lesions often coexist.

Slide 17 · Intrinsic fetal disorders can mimic placental FGR

Chromosomal disorders and structural anomalies can limit fetal growth.

Congenital infections may restrict growth through fetal mechanisms.

Symmetric growth restriction prompts evaluation beyond perfusion lesions.

Slide 18 · Anatomic sites of placental dysfunction

Maternal inflow

Spiral artery remodeling; Decidual vasculopathy; Abruption.

Exchange tissue

Placental hypoplasia; Infarction; Inflammatory villous injury.

Fetal outflow

Cord compromise; Fetal vascular thrombi; Avascular villi.

Slide 19 · Maternal vascular malperfusion: Definition

Maternal vascular malperfusion (MVM) signifies inadequate maternal blood supply to intervillous spaces.

Abnormal implantation, placental development or maternal vascular disease may initiate it.

Effects extend from growth restriction to severe placental ischemia.

Slide 20 · Maternal malperfusion causal map

Abnormal vascular remodeling / disease

Restricted intervillous supply

Villous ischemia

Placental structural changes

Possible FGR or severe compromise

Sequential mechanism (schematic)

Slide 21 · Placental hypoplasia: One MVM feature

Robbins specifies placental weight below the tenth percentile for gestational age.

Reduced placental mass may reduce the available exchange surface.

Hypoplasia is one element of the MVM pattern, not its sole feature.

Slide 22 · Placental infarcts

Infarcts are areas of ischemic placental injury.

Large or numerous infarcts are described in maternal malperfusion.

Functional significance depends on the cumulative loss of viable exchange tissue.

Slide 23 · Villous consequences of ischemia

Small villi

Distal villi may appear shrunken.

Syncytial knots

Ischemic villous changes include increased syncytial knotting.

Expanded intervillous space

Distal villous hypoplasia includes relatively increased maternal vascular space.

Slide 24 · Distal villous hypoplasia

The distal villi are abnormally small in affected regions.

The proportion of surrounding maternal vascular space increases.

The finding belongs to a constellation of ischemic villous alterations.

Slide 25 · Syncytial knots as an ischemic sign

Increased syncytial knotting is described in placental MVM.

Interpret knotting alongside placental age and other structural findings.

It is not a standalone proof of a specific maternal condition.

Slide 26 · Normal versus poorly remodeled spiral arteries

Physiologic remodeling

Large-caliber

Low-resistance vessel

Incomplete remodeling

Persistently narrow

Higher-resistance vessel

Conceptual vessels; Not a histologic image

Slide 27 · Failure of spiral artery remodeling

Normal extravillous trophoblast transforms spiral arteries into low-resistance vessels.

Incomplete remodeling retains features of high-resistance maternal vessels.

The resulting placenta is less able to accommodate late-gestational demand.

Slide 28 · Decidual arteriopathy in maternal malperfusion

Affected vessels may lack expected physiologic remodeling.

Other possible findings include thrombi, fibrinoid necrosis and acute atherosis.

These changes support maternal vascular disease in the appropriate context.

Slide 29 · Placental abruption

Abruption represents premature separation of the placenta from the uterine wall.

Retroplacental bleeding can destabilize uteroplacental perfusion.

Abruption among placental causes of growth restriction and prematurity.

Slide 30 · Abruption: Why fetal injury can follow

Maternal–placental interface bleeds

Placental separation / unstable vessels

Less effective maternal perfusion

Acute compromise or chronic growth limitation

Sequential mechanism (schematic)

Slide 31 · Maternal vascular malperfusion: Integrated lesion set

Gross or macroscopic clues

Microscopic clues

Small placenta for gestation

Distal villous hypoplasia

Infarcts; possibly large or numerous

Increased syncytial knots

Retroplacental hematoma

Abnormal decidual arteries; thrombi / atherosis

Slide 32 · Case: Small placenta and infarcts

CLINICAL SCENARIO

A fetus shows late-gestation growth restriction. The placenta is small and contains multiple infarcts.

Which primary functional compartment is likely compromised?

Interpretation: Maternal uteroplacental perfusion; Interpret as a pattern of maternal vascular malperfusion.

Slide 33 · Fetal vascular malperfusion: Concept

Fetal vascular malperfusion (FVM) involves diminished perfusion of placental villi from the fetal side.

Cord obstruction and fetal-side vascular lesions are important upstream abnormalities.

Thrombi and avascular villi provide morphologic clues.

Slide 34 · Fetal malperfusion causal map

Umbilical cord or fetal-vessel obstruction

Impaired flow within villous fetal vessels

Villous vascular thrombosis / injury

Avascular villi

Fetal compromise

Sequential mechanism (schematic)

Slide 35 · Umbilical cord obstruction

Tight knots, kinks, nuchal or body cords and prolapse may interrupt flow.

Marked acute obstruction can be fatal yet leave few placental morphologic clues.

Chronic or intermittent obstruction can produce fetal vascular malperfusion.

Slide 36 · Why a true knot matters

Constriction of umbilical vessels reduces fetal-side blood delivery.

The downstream placenta may develop avascular villi and vascular thrombi.

A gross cord lesion and a downstream villous lesion support a causal interpretation.

Slide 37 · Avascular villi

Chorionic villi normally contain fetal capillaries.

Loss or absence of vessels within involved villi characterizes avascular villi.

The finding is illustrated in the setting of fetal vascular malperfusion.

Slide 38 · Villous vascular thrombi

Thrombosis in fetal placental vessels may interrupt flow to dependent villi.

Thrombi and endothelial damage are described in second-trimester losses.

Evaluate thrombi together with cord abnormalities and villous changes.

Slide 39 · Maternal versus fetal malperfusion

Maternal vascular malperfusion

Fetal vascular malperfusion

Maternal blood reaching intervillous space is limited

Fetal blood flowing into villous vessels is limited

Placental infarcts; decidual arteriopathy

Avascular villi; fetal vascular thrombi

Small villi and syncytial knots may occur

Cord lesions or compression may be found

Slide 40 · Single umbilical artery as a placental vascular anomaly

A single umbilical artery among potential placental causes of FGR.

The cord must be assessed together with placental perfusion and fetal findings.

A vascular anomaly does not alone establish the cause of restricted growth.

Slide 41 · Abnormal cord insertion

Abnormal umbilical insertion is included among placental contributors to FGR.

It identifies a structural abnormality of the placental vascular connection.

Interpret its clinical significance in the context of the complete placenta.

Slide 42 · Case: Knot and avascular villi

CLINICAL SCENARIO

A tight, complex true umbilical-cord knot is accompanied by extensive avascular villi.

What is the mechanistic diagnosis suggested by these findings?

Interpretation: Umbilical vascular obstruction with downstream fetal vascular malperfusion.

Slide 43 · Placenta previa: Low implantation

The placenta implants in the lower uterine segment and covers the cervix partially or completely.

Clinically significant bleeding may occur in the third trimester.

Previa among placental abnormalities contributing to poor pregnancy outcomes.

Slide 44 · Placenta accreta spectrum

Loss of decidua allows chorionic villous tissue to contact or invade myometrium.

Depth and extent of abnormal attachment vary within the spectrum.

Failure of normal placental separation creates a risk of major postpartum hemorrhage.

Slide 45 · How placenta accreta spectrum develops

Focal or extensive decidual absence

Direct villous contact with myometrium

Abnormal placental attachment / invasion

Failure of placental separation

Severe postpartum bleeding risk

Sequential mechanism (schematic)

Slide 46 · Previa, accreta and abruption are not interchangeable

Placenta previa

Placenta accreta spectrum

Placental abruption

Low implantation over cervix

Abnormally adherent / invasive placenta

Premature placental separation

Third-trimester bleeding risk

Retained placenta / postpartum bleeding

Retroplacental bleeding; impaired perfusion

Location-related abnormality

Implantation-interface abnormality

Separation-related abnormality

Slide 47 · Multiple gestations increase placental vulnerability

Twins may differ in growth, malformations and placental pathology.

Monochorionic twins share a placenta and vascular connections.

Multiple gestations appear among placental settings associated with FGR.

Slide 48 · Twin placentation: Chorion and amnion

Placentation

Anatomic feature

Dichorionic diamniotic

Separate chorions and amniotic sacs; placentas may be fused

Monochorionic diamniotic

Single chorion; two amniotic sacs

Monochorionic monoamniotic

Single chorion and one shared amniotic cavity

Slide 49 · Chorionicity determines vascular sharing

Monochorionic placentas imply monozygotic twins.

Shared placental vasculature allows anastomoses between fetal circulations.

Dichorionic placentation can occur in monozygotic or dizygotic pregnancy.

Slide 50 · Twin-to-twin transfusion: Vascular imbalance

Monochorionic vascular anastomoses

Unbalanced transfer across shunts

Donor: Underperfusion

Recipient: Volume overload

Severe fetal consequences

Sequential mechanism (schematic)

Slide 51 · Twin-to-twin transfusion syndrome

Donor twin

Recipient twin

Relatively underperfused

Receives excess transferred blood flow

Disadvantaged by unbalanced shunt

Subject to fluid overload

May experience severe compromise

May experience severe compromise

Slide 52 · Case: Discordant monochorionic twins

CLINICAL SCENARIO

Monochorionic twins are substantially discordant; One appears underperfused and the other fluid overloaded.

What placental connection explains this pattern?

Interpretation: Intertwin vascular anastomoses causing unbalanced twin-to-twin transfusion.

Slide 53 · Two principal routes of placental infection

Ascending microorganisms enter via the birth canal and involve the membranes.

Hematogenous maternal spread can seed villous tissue through the circulation.

Route of spread predicts the dominant tissue compartment affected.

Slide 54 · Ascending infection sequence

Ascending bacterial exposure

Chorioamniotic inflammation

Maternal neutrophilic response

Possible fetal vascular response

Membrane rupture / preterm delivery

Sequential mechanism (schematic)

Slide 55 · Acute chorioamnionitis: Membrane pathology

Ascending infection is most often bacterial.

Maternal neutrophils infiltrate chorion–amnion membranes.

Inflammation can accompany premature membrane rupture and preterm birth.

Slide 56 · Fetal inflammatory response

Inflammation may extend to umbilical vessels or fetal chorionic plate vessels.

This vascular involvement as a fetal inflammatory response.

Intense responses correlate with perinatal morbidity and increased cerebral palsy risk.

Slide 57 · Hematogenous placental infection

Maternal bacteremia / viremia / parasitemia

Hematogenous passage to placenta

Villous inflammatory involvement

Potential fetal infection or growth restriction

Sequential mechanism (schematic)

Slide 58 · Acute versus chronic villous inflammation

Acute villitis

Chronic villitis

May arise in bacterial hematogenous infection

Chronic inflammatory infiltrate of the villi

Robbins documents acute infectious villitis

TORCH-associated placental involvement may be chronic

Assess accompanying necrosis / organisms

Relate to infection and FGR where supported

Slide 59 · TORCH infections and the villous compartment

Hematogenous spread permits several TORCH pathogens to infect the placenta.

These infections with chronic villitis and fetal growth restriction.

Specific pathogens require independent microbiologic / clinical correlation.

Slide 60 · Chronic villitis of unknown etiology

Robbins separately names chronic villitis of unknown etiology as a placental contributor to FGR.

Unknown etiology should not be labeled as a confirmed infectious process.

Morphology and clinical context are necessary before assigning a cause.

Slide 61 · Recognize infection by involved compartment

Predominant site

Most pertinent pathway

Chorion–amnion membranes with neutrophils

Usually ascending infection

Umbilical / chorionic-plate fetal vessels

Fetal inflammatory response to an ascending process

Chronically inflamed chorionic villi

Consider hematogenous infection or other villitis

Slide 62 · Case: Membrane neutrophils and funisitis

CLINICAL SCENARIO

Membranes contain a neutrophil-rich infiltrate; Fetal umbilical vessels are also inflamed.

What two inflammatory components are present?

Interpretation: Maternal acute chorioamnionitis plus a fetal inflammatory vascular response.

Slide 63 · Placental lesions and possible fetal outcome

Placental abnormality

Functional link

Placental hypoplasia, infarction

Reduced exchange capacity / maternal supply

Cord obstruction or vascular thrombosis

Reduced fetal-side placental perfusion

Chronic villitis or infection

Inflammatory injury with possible growth restriction

Monochorionic vascular shunts

Unequal distribution of circulation between twins

Slide 64 · Placental lesions can act at different gestational stages

Earlier severe placental disease may produce fetal loss when reserve is limited.

The third trimester amplifies the consequences of inadequate placental perfusion.

An acute cord event may leave fewer histologic clues than prolonged compromise.

Slide 65 · Why a small infant needs etiologic interpretation

Size alone cannot distinguish maternal, fetal or placental growth restriction.

Symmetry of growth and associated malformations help direct the differential.

Placental gross and microscopic abnormalities add independent mechanistic information.

Slide 66 · Placental FGR: Beyond the perinatal period

Morbidity extending into childhood and adult life.

Possible consequences include cerebral dysfunction and learning disability.

Hearing and visual impairment are also among the documented risks.

Slide 67 · Clinical implications depend on the mechanism

Placental growth impairment primarily concerns chronic nutrient / oxygen limitation.

Cord interruption may produce severe acute fetal compromise.

Ascending infection relates to preterm delivery and inflammatory complications.

Abnormal placental implantation can threaten maternal hemostasis.

Slide 68 · Approach to a suspected placental cause of FGR

Question

Look for / interpret

Is maternal inflow compromised?

Hypoplasia, infarcts, villous ischemia, decidual arteriopathy

Is fetal-side flow obstructed?

Cord lesion, fetal thrombi, avascular villi

Is there inflammatory injury?

Membrane neutrophils, fetal vascular response, villitis

Is placentation abnormal?

Previa, accreta, chorionicity and vascular shunts

Slide 69 · Case: Disproportionate fetal growth restriction

CLINICAL SCENARIO

A fetus has disproportionate late-gestation growth restriction with relative preservation of head growth.

Which etiologic category is most characteristic of this pattern?

Interpretation: Placental insufficiency is favored, although the growth pattern is not pathognomonic.

Slide 70 · Key clinicopathologic distinctions

Maternal malperfusion: Impaired inflow, villous ischemia and placental infarction.

Fetal malperfusion: Fetal vascular obstruction, thrombi and avascular villi.

Infection: Identify membrane, fetal vascular or villous involvement.

Implantation and monochorionic disorders have distinct hemorrhagic or shunting risks.

Slide 71 · Final synthesis: Anatomy explains the pathology

Adequate maternal inflow, exchange villi and fetal vascular flow are all essential.

Structural and inflammatory lesions can reduce effective placental performance.

Placental FGR is often asymmetric, with relative brain sparing.

Interpret placental findings with fetal growth, maternal disease and gestational timing.

Slide 72 · Primary textbook reference

Robbins, Cotran & Kumar. Pathologic Basis of Disease. 11th edition. 2026.

Relevant sections: Prematurity and Fetal Growth Restriction; Placental anatomy and disorders.

All diagrams are original conceptual PowerPoint schematics. No histopathology images are represented as diagnostic specimens.