Placental Pathology

MONOAMNIOTIC-MONOCHORIONIC

shows no cleavage plane

MONOZYGOTIC PLACENTA

●● Division of a single fertilized ovum resulting in identical twins

●● Can be any type (diamniotic-dichorionic, diamniotic-monochorionic, monoamnioticmonochorionic)

DIZYGOTIC PLACENTA

●● Fertilization of two separate ova, twins are genetically different

●● Mostly diamniotic-dichorionic (two separate discs or single fused disc)

MONOCHORIONIC PLACENTAS

●● Vascular communications; surface arterialarterial combined with deep parenchymal artery-artery, vein-vein, and artery-vein

●● Twin-to-twin transfusion (TTT) syndrome: Large deep artery-vein anastomoses and paucity of counterbalancing surface arteryartery anastomoses

●● Insertion of membranes into the disc away from disc edge

Circumvallate

●● Membrane folded back upon itself (partial or complete)

●● Associated with antepartum/postpartum hemorrhage, premature rupture of membranes (PROM), second trimester abortions

Circummarginate

●● Thinning of placental membranes on fetal surface

VARIATION IN LOBATION

●● Accessory lobe/bilobed, lobes of unequal size

●● Clinically insignificant, though sometimes may cause postpartum hemorrhage

PLACENTA ACCRETA

●● Abnormal attachment of entire/part of placenta to uterine wall after delivery

section scars, prior dilation and curettage

Accreta

●● Villi attached to endometrium without decidua; most common

Increta

Percreta

●● Full thickness penetration of chorionic villi in uterine wall

PLACENTA PREVIA

●● Abnormally implanted placenta in lower uterine segment/cervix

●● Associated with antepartum bleeding, PROM, premature labor

PLACENTOMEGALY

●● Large for gestational age placenta (weight >650 gm)

ders, infections, maternal diabetes mellitus [DM], Beckwith-Wiedemann syndrome)

AMNION NODOSUM

●● Nodules (tiny pinpoint) on amniotic surface of placenta

●● Composed of squamous cell aggregates derived from fetal skin and vernix caseosa

MECONIUM STAINED PLACENTA

●● Green-stained umbilical cord and placental membranes

●● Vacuolated pigment-laden macrophages in chorionic vessels/umbilical vessels with apoptosis of peripheral vascular smooth muscle (vascular necrosis)

●● Indicative of fetal distress, hypoxicischemic injury

PLACENTAL DYSMATURITY

illaries, increased villous stroma, diminished syncytiotrophoblastic knots, paucity of vasculosyncytial membranes

●● Associated with maternal uncontrolled DM, maternal obesity, hypercoiled umbilical cord, chromosomal abnormalities

●● May lead to intrauterine fetal demise (IUFD)

Decidual arteriopathies

Acute atherosis

●● Prevalent in severe pre-eclampsia, maternal DM, anti-phospholipid antibody syndrome

●● Prominent intimal macrophage proliferation

●● Fibrinoid degeneration/medial necrosis of uterine arteries/arterioles

Mural hypertrophy

sion, DM, or pre-eclampsia ●● Defective non-trophoblast related remodel-

ing of spiral arteries during early pregnancy ●● Thickness of arteriolar smooth muscle

exceeds two-third of the total diameter ●● May be associated with acute atherosis

Villous changes associated with maternal perfusion

●● Leads to fetal growth retardation/pre-term delivery

●● Increased villous syncytial knots (due to increased trophoblast turnover), intervillous fibrin deposits (due to circulatory stasis), and villous agglutination (due to foci of trophoblast necrosis)

Villous infarction

●● Ischemic necrosis of villous parenchyma due to cessation of maternal vascular flow

●● Multiple infarcts at term/any infarct in premature infant = indicative of underlying maternal vascular disease

●● Fetal growth retardation, pre-eclampsia, pre-term labor, maternal anti-phospholipid antibodies, chronic hypertension

●● Infarts are wedge shaped, dark red (fresh less than 1 day old), or pale yellow (remote)

●● Collapse of intervillous space, villous agglutination, ischemic necrosis of trophoblastic cell layer

Perivillous fibrin deposition

lous agglutination) ●● Massive perivillous fibrin deposition

(maternal floor infarction) = leads to IUGR, stillbirth, preterm delivery

●● Prevalent in maternal hypertension, antiphospholipid antibody syndrome

Abruptio placentae

●● Rupture of spiral arteries leading to central retroplacental hemorrhage

●● Indentation/rupture of basal plate, irregular intraplacental hemorrhage, villous stromal hemorrhage

●● Risk factors: Maternal hypertension, trauma, vasoactive drugs

Marginal abruption

tion/vaginal bleeding ●● Association with circumvallate placenta

FETAL VESSELS

Fetal thrombotic vasculopathy (FTV)

●● Thrombotic occlusion of chorionic plate or major stem villous vessels

●● Prevalent in umbilical cord entanglement/ abnormalities, maternal DM, thrombophilic conditions (anti-phospholipid antibody syndrome, clotting disorders)

●● Adverse fetal outcomes; neonatal encephalopathy, cerebral palsy, disseminated intravascular coagulation (DIC)

●● More than 15 affected villi per section of villous parenchyma

●● Hyalinized avascular villi, stromal vascular karyorrhexis (hemorrhagic endovasculitis), organized thrombi in major fetal vessels, fibromuscular sclerosis of the vessels

Partial/chronic/intermittent umbilical cord obstruction

●● Scattered small foci of avascular villi (near basal plate and distal villi)

Intervillous thrombi

villi ●● Significant in ABO incompatibility

CHORANGIOSIS

●● More than 10 capillaries in at least 10 terminal villi in at least three low power fields of placenta

●● Indicative of chronic placental hypoperfusion/low-grade tissue hypoxia

CHORANGIOMA

congestive heart failure ●● Well-circumscribed mass of small capillar-

ies lined by benign endothelium

CHORANGIOMATOSIS

●● Non-expansile vascular proliferation in normal stem villi

●● Proliferation of capillaries and the surrounding pericytes

non-contiguous areas of placenta ●● Associated neonatal morbidity/mortality

MESENCHYMAL DYSPLASIA

●● Placental vascular anomaly involving varying combinations of small and large fetal vessels

●● Increased villous stroma, cavitated edematous cisterns

●● Associated with Beckwith-Wiedemann syndrome

COMPLETE MOLE (CM)

●● Large for gestational age uterus, vaginal bleeding, spontaneous abortion with passage of molar tissue

●● Elevated HCG levels, bilateral ovaries may show theca-lutein cysts

●● Diploid karyotype (46XX) = both chromosomes are androgenic

●● Diffuse circumferential trophoblastic proliferation, uniform dilation of avascular villi, central cisterns (grape-like clusters), absent fetal parts/cord/membranes

●● Spontaneous regression in most, after evacuation

●● A few develop either invasive mole or choriocarcinoma (2%)

tor) is negative

PARTIAL MOLE (PM)

tions; dilated villi mixed with normal villi ●● Polarized trophoblastic proliferation, less

villous edema, no cistern formation, fetal tissue may be present

●● Triploid karyotype (mostly 69 XXY or 69 XXX)

●● HCG (weakly +ve), p53 +ve and p57kip2 is +ve (paternally imprinted and expressed from maternal alleles)

INVASIVE MOLE (CHORIOADENOMA DESTRUENS)

●● Uterine bleeding and persistently elevated HCG after evacuation of mole

lize to other organs with hemorrhagic complications

●● Abnormal proliferation of intermediate trophoblasts

deeply invade the myometrium ●● Absence of villi/cytotrophoblasts ●● Mostly benign, risk of uterine rupture ●● 10%–15% are malignant, may metastasize

to distant organs

CHORIOCARCINOMA

tory of complete mole ●● Other cases associated with spontaneous

abortion, normal pregnancy, or ectopic pregnancy

cytotrophoblasts ●● Absent chorionic villi ●● Markedly elevated serum HCG

INFECTIOUS CAUSES

Amniotic fluid infection (chorioamnionitis)

●● Ascending infection from organisms in genital tract or bloodborne infection

or Staphylococcus aureus ●● Pre-term labor, maternal fever, fetal/mater-

nal tachycardia, foul-smelling discharge ●● Grade I (neutrophils in subchorionic fibrin),

Grade II (neutrophils in both amnion and chorion), Grade III (necrotizing chorioamnionitis)

Funisitis

abscesses on surface of umbilical cord

Chronic deciduitis

TORCH infections, villitis of unknown etiology (VUE), maternal vascular disease

Placental malaria

●● Diffuse infiltration of intervillous space by histiocytes, fibrin, malarial pigment, and parasitized red cells

Congenital infections and TORCH group

●● TORCHS is an acronym for feto-placental infections caused by Toxoplasma gondii, Others (Epstein-Barr virus, varicella-zoster virus, Treponema pallidum), rubella virus, cytomegalovirus, herpes simplex viruses, and syphilis

splenomegaly, IUGR, petechiae, central nervous system damage and placental villitis (infectious)

●● Syphilis: Histiocytic villitis with villous edema

●● CMV: Plasma cell villitis with villous fibrosis

●● Lymphoplasmacytic inflammatory infiltrate noted in umbilical cord, membranes, all villi

●● Screening tests: “TORCH titer” test, IgG, IgM antibodies, polymerase chain reaction on fetal blood or amniotic fluid from amniocentesis

Toxoplasmosis

●● Microcephaly, periventricular calcification, myocarditis, and chorioretinitis

Rubella

●● Fetal rubella syndrome-cataracts, deafness, patent ductus arteriosus

●● Worse prognosis if infection occurs before 8 weeks of gestation

Herpes

●● Prematurity/stillbirth, pneumonitis, hepatosplenomegaly

Congenital syphilis

●● Hydrops fetalis with IUGR, pneumonia alba, Hutchinson’s incisors, saddle nose, saber shin

Listeria

Parvovirus

NON-INFECTIOUS CAUSES

Villitis of unknown etiology (VUE)

in villous stroma (less than 25% villous affected)

●● Maternal T lymphocytes react to fetal macrophages in the villous stroma

●● Focal/patchy nature of villous infiltrate (d/d infectious villitis)

●● Adverse outcomes include IUGR, cerebral palsy, fetal neurological impairments, recurrence of VUE

Obliterative fetal vasculopathy

tion involving stem villi leading to vascular occlusion/avascular villi

●● Hypercoiling (more than two to three coils per 10 cm)

false) ●● Membranous/furcated umbilical cord

insertion (Battledore placenta) ●● Decreased Wharton jelly ●● Encirclement of UC by amniotic bands

●● Morphological changes similar to FTV but seen diffusely throughout placenta

●● Early demise (24-48 h) shows nuclear karyorrhectic debris in blood vessels and villous capillaries

●● Later morphological changes include vascular septation, avascular villi, villous fibrosis, calcification