placenta pathology

Placenta pathology

2. PLACENTAL PATHOLOGY
Part 2
FereshtehAmeli

3. Acknowledgements
Some of the information including images and slides are reproduced
from :
•Categories ofplacental pathology-Dr. Roberts;
https://www.youtube.com/watch?v=V7WoSRq_jzI

4. •Placental vascular processes
-Maternal stromal-vascular lesions
-Fetal stromal-vascular lesions
•Placental inflammatory-immune processes
-Infectious: Acute/chronic
-Immune/idiopathic
•Other placental processes
-Massive perivillousfibrin(oid) deposition
-Morbidly adherent placentas (accretaspectrum)
Categories of Placental Pathology

5. Placental inflammatory-immune processes
Can be divided into two major categories:
1. Acute chorioamnionitis(ACA):
-invariably infectious due to microorganisms
-usually bacteria that ascend from the vagina or cervix (ascendinginfection)
2. Villitis–inflammation
-usually chronic( inflammation of the villous parenchyma)
-usually idiopathic
-but rarely infectiousfrom viruses, some bacteria, or protozoa that reach the placenta
homogeneously.

6. Infectious lesions
Acute
Maternal inflammatory response: subchorionitis, chorioamnionitis
Fetal inflammatory response: chorionic/umbilical vasculitis
Chronic
TORCH, malaria, others

7. •There is a maternaland fetalacute inflammatory response to
infectious agents that have gained access to the gestational sac.
•Histologically there is a maternaland then later a fetalinflammatory
response to amniotic infection that progress sequentially.
Placental inflammatory-immune processes

8. •The acute inflammatory infiltrate in chorioamnionitisis
characteristically confined to the fetal membranes
and umbilical cord.
•The villous parenchyma is not involved unless fetal or maternal
septicemia results secondarily in villitis.
•Acute villitisand intervillousabscesses are most commonly due to
Listeria monocytogenes.
Placental inflammatory-immune processes

9. Maternal inflammatory response
Stage
1 –early –acute subchorionitisand/or acute chorionitis
2 –intermediate –acute chorioamnionitis
3 –late –necrotizing chorioamnionitis
Grade
1 –mild (not severe)
2 –severe (>30 PMNs/hpf, confluent PMNs, microabscesses)

10. Early –acute subchorionitis

11. Intermediate –acute chorioamnionitis

12. Late –necrotizing chorioamnionitis

13. •The first manifestation of a fetal inflammatory reaction is the
migration of fetal neutrophils into the umbilical vein (umbilical
phlebitis) and/or chorionic plate vessels (chorionic vasculitis).
•In later stages, fetal neutrophils migrate from the umbilical arteries
(umbilical arteritis) and into Wharton’s jelly.
Fetal inflammatory response

14. •A fetal leukocyticresponse is often absent in gestations less than 19-
20 weeks and in fetuses less than 500 g.
•Umbilical cord inflammation is often segmental, sometimes identified
in only one of multiple sections, often from the fetal end.
Fetal inflammatory response

15. Fetal inflammatory response
Stage
1 –early –umbilical phlebitis and/or chorionic plate vasculitis
2 –intermediate –umbilical arteritis + umbilical phlebitis
3 –late –necrotizing funisitisand/or concentric umbilical perivasculitis
Grade
1 –mild (not severe)
2 –severe (near-confluent intramural PMNs with attenuation of
vascular smooth muscle); associated with CNS injury

16. Umbilical arteritis

17. •Placental inflammatory-immune processes
-Infectious: Acute/chronic
-Immune/idiopathic
-Villitisof unknown etiology
-Lymphoplasmacyticdeciduitis
-Chronic histiocyticintervillositis

18. •Mixed maternal and fetal inflammatory infiltration of the chorionic villi.
•Associated with perinatal and fetal morbidity and mortality.
Chronic Villitis

19. Chronic Villitis
•Chronic inflammationof the villous parenchyma, is of two different
etiologies:
1. The vast majority of villitsarevillitisof unknown etiology or VUE, which
is thought to be an immune-mediated response of the mother to fetal
antigens in the placenta (host vs. graft reaction;CD8-positive maternal T
lymphocytes).

20. 2. Very rarely, villitismay result from a hematogenousinfection in
which infectious agents, usually viruses but also some bacteria and
protozoa (TORCH infection), reach the placenta through the maternal
blood (hematogenousinfection)→ specific chronic villitis-identifiable
infectious etiology
Chronic Villitis

21. Chronic villitis of unknown etiology
•T-cell mediated disorder targeting distal villi
•Maternal graft-vs-host-type response
•High-grade VUE associated with growth restriction, CNS injury, fetal
demise
•5-10% of term placentas
•Increased incidence and severity in obese women
•Significant recurrence risk (25-50%)

22. •Villitisis almost always discovered incidentally on microscopic
examination. Typically, there is neither clinical suspicion of nor
gross pathologic clue to the underlying inflammatory process.
Chronic Villitis

23. •The essential feature common to all
villitisis an inflammatory infiltrate in
the villi, usually chronic, composed
of lymphocytes and histiocytes, in
variable proportion, but occasionally
it may be granulomatous, and rarely
neutrophils are prominent.
•If there are plasma cells→ search for
specific cause
Chronic Villitis

24. Chronic Villitis

25. Chronic Villitis-cellular

26. Amsterdam Placental Workshop Group Consensus Statement

27. Vascular Damage a/wVillitis
•Villitismay cause impairment of the fetoplacentalcirculation. Such
damage is associated with adverse effects, such as neurologic
impairment.
•When inflammatory cells damage vessels that have a muscular wall,
the term villitiswith stem vessel obliteration should be used.
•When avascular villi are seen in a placenta with villitis, the report
should designate the finding as chronic villitiswith associated
avascular villi.

28. large areas of contiguous, uniformly hyalinized, avascular villi may suggest upstream vascular
occlusion
Vascular Damage a/wVillitis

29. Vascular Damage a/wVillitis

30. Chronic Deciduitis
•Chronic deciduitishas been defined as
either the presence of plasma cells or
diffuse chronic inflammation (with or
without plasma cells) in the decidua
basalis.
•The chronic inflammatory response
may be directed against maternal or
fetal antigens or microorganisms.

32. Infectious Villitis
•In general, infectious villitidestend to be more severe and diffuse
with more villous necrosis and may be associated chronic
chorioamnionitis

33. CMV villitis
A plasmacyticvillous infiltrate and
stromal hemosiderin, often deposited
around the remnants of occluded vessels,
are characteristic
CMV is the commonest
identified infectious cause of villitis.

34. Listeria placentitis
Neutrophils aggregate in the intervillousspace. Entrapped
villi undergo necrosis forming abscesses.

35. Toxoplasma placentitis
-Granulomatous villitis
-Chronic avascular thrombosis
-Toxoplasma cysts often found just
under the amniotic epithelium

36. Granulomatous villitis

37. •Parvovirus B19 preferentially infects actively
replicating cells, especially erythroblasts,
which are then destroyed.
•Grossly, the placentas are large, pale, and
friable and may be hydropicparticularly when
the infection is associated with fetal hydrops.
•Uniform pattern of relative villous immaturity
and edema.
•Diagnostic intranucleareosinophilicinclusions
with peripheral chromatin condensation are
present in erythroblasts in the villous vessels
Parvovirus B19

44. Chronic
Histiocytic
Intervillositis

45. Chronic
Histiocytic
Intervillositis

47. CD68

50. Association of CHI
•Pregnancy losses at any gestational ages
•Autoimmune disease
•Hypertension
•Elevated AlkPhos
•IUGR
•IUFD

53. •Placental vascular processes
-Maternal stromal-vascular lesions
-Fetal stromal-vascular lesions
•Placental inflammatory-immune processes
-Infectious: Acute/chronic
-Immune/idiopathic
•Other placental processes
-Massive perivillousfibrin(oid) deposition
-Morbidly adherent placentas (accretaspectrum)
Categories of Placental Pathology

69. •Failure of normal decidua to form, at least focally, because
endometrium is deficient and cannot decidualize
•Trophoblastdoes not stop invading when it should, villi penetrate
myometrium
•Usually hxof C-section or curettage
•25-30% recurrence rate
Accreta spectrum