Placenta

reporting placental pathology

1. Sampling and definitions of placental lesions Presenter- Dr. Pannaga P Kumar Moderator- Dr. Anisha T S AMSTERDAM PLACENTAL WORKSHOP GROUP CONSENSUS STATEMENT Khong et al Arch Pathol Lab Med- Vol 140, July 2016

2. INTRODUCTION The placenta is crucial for fetal growth and survival, performing the most important functions of many somatic organs before birth. Thus, pathologic processes interfering with placental function may result in abnormalities of fetal growth or development, malformation, or stillbirth, and There is increasing recognition that some long-term (especially neurologic) disabilities can be traced to injury occurring before birth.

3. PLACENTA This is a fetomaternal organ. It has two components: Fetal part – develops from the chorionic frondosum Maternal part – derived from the decidua The placenta and the umbilical cord are a transport system for substances between the mother and the fetus.

4. PLACENTA AT TERM Fleshy Weight-500gm Diameter- 15-20 cm Thickness-2.5 cm Spongy to feel Occupies 30% of the uterine wall Two surfaces- Maternal and fetal 4/5 th of the placenta is of fetal origin and 1/5 is of maternal origin

5. MATERNAL SURFACE Irregular, divided into convex areas (cotyledons) FETAL SURFACE Smooth, transparent, covered by amnion with umbilical cord attached near its center & umbilical vessels radiating from it

6. MATERNAL SURFACE Cotyledons –about 15 to 20 slightly bulging villous areas. Their surface is covered by shreds of decidua basalis from the uterine wall. After birth, the placenta is always carefully inspected for missing cotyledons . Cotyledons remaining attached to the uterine wall after birth may cause severe bleeding .

7. FETAL SURFACE This side is smooth and shiny. It is covered by amnion . The umbilical cord is attached close to the center of the placenta. The umbilical vessels radiate from the umbilical cord. They branch on the fetal surface to form chorionic vessels. They enter the chorionic villi to form arteriocapillary-venous system.

8. PLACENTA Margins of the placenta are formed by fused chorionic and the basal plate Placenta is attached to the upper part of the uterine body either at the posterior or anterior wall After delivery ,placenta separates with the line of separation being through decidua spongiosum (intermediate spongy layer of the decidua basalis

9. PLACENTA- GROSS ABNORMALITIES

10. PLACENTA- GROSS ABNORMALITIES BATTLEDORE PLACENTA VELAMENTOUS INSERTION OF CORD

11. ABNORMALITIES OF PLACENTA

12. ABNORMALITIES OF PLACENTA

13. STRUCTURE OF PLACENTA Placenta is limited by the amniotic membrane on the fetal side and by the basal plate on the maternal Between these two lies the intervillous space filled with maternal blood and stem villi with their branches

14. STRUCTURE OF PLACENTA Amniotic membrane- single layer of cuboidal epithelium loosely attached to adjacent chorionic plate and does not take part in placental formation. Chorionic plate- forms the roof of the placenta From outside inwards consists of Syncitotrophoblast Cytotrophoblast Extraembryonic mesoderm with branches of umbilical vessels

15. STRUCTURE OF PLACENTA Basal Plate- forms the floor From outside inwards it consist of Compact and spongy layer of decidua basalis Layer of Nitabuch Cytotrophoblastic shell Syncytiotrophoblast Basal plate is perforated by the spiral arteries allowing entry of maternal blood into intervillous space

16. DECIDUA DEFINITION: It is the functional layer of endometrium of the gravid (pregnant) uterus . It includes the endometrium of fundus & body of uterus The endometrium of the cervix does not form a part of decidua. STEPS OF FORMATION (DECIDUAL REACTION): The endometrium becomes thicker & more vascular The endometrial glands become full of secretion The connective tissue cells enlarge due to accumulation of lipid & glycogen. They are called “decidual cells”

17. DECIDUA Decidua basalis : It lies at the site of implantation ,it forms the maternal part of the placenta Decidua capsularis : it covers the conceptus Decidua parietalis: the rest of the endometrium that lines the body & the fundus.

18. DECIDUA- HISTOLOGY The hypersecretory glandular epithelium of the endometrium, which is progestationally induced, affords the proper environment for implantation Decidual cells of the endometrium are characterized as epithelioid and polygonal. Their small rounded nuclei are generally situated centrally in abundant pale eosinophilic, often vacuolated, cytoplasm. The cytoplasm is rich in glycogen and glycoproteins. In regions of decidual tissue, where trophoblastic derivatives are not present, nuclear content is diploid.

19. STRUCTURE OF PLACENTA Layer of Nitabuch - is a fibrinous layer formed at the junction of cytotrohoblastic shell with decidua due to fibrinoid degeneration of syncitotrohoblast It prevents excessive penetration of the decidua by the trophoblast Nitabuch membrane is absent in placenta accreta and other morbidly adherent placentas

20. STRUCTURE OF PLACENTA Stem (Anchoring villi ) Arise from the chorionic plate and extend to the basal plate Fetal cotyledon (60-100 ) – derived from one major primary stem villus and is the structural unit of placenta Maternal cotyledon (15-20 ) contains 3-5 fetal cotyledons Villus is the functional unit of placenta Total surface of the villi for exchange varies between 4-14 sq meters Intervillous space : Numerous branch villi arising from the stem villi project into this space It is lined internally on all sides by the syncytiotrophoblast and is filled with maternal blood

21. VILLI- GROSS The villous parenchyma is discoid and occupies the space beneath the chorionic plate. The substance of the parenchyma is red and “beefy.” On sectioning, it appears relatively homogeneous in contour and texture, such that significant irregularities denote abnormalities within the villous parenchyma. Many abnormalities, however, are common and when focal or minimal in quantity, can be considered as normal variants. Examples include small infarcts and perivillous fibrin deposition.

22. VILLI- GROSS On occasion, the placental parenchyma has spherical defects (usually 1 to 2 cm in greatest dimension), which represent the so-called jet lesions. These cleared areas within the villous parenchyma represent pressure heads from maternal decidual vascular flow. It is not uncommon to histologically identify a small zone of acute infarction peripheral to these lesions. Calcification is a common phenomenon in the mature placenta. Calcification has been used to diagnose placental maturity by ultrasonographic evaluation during pregnancy.

23. CHORIONIC VILLUS

24. VILLI- HISTOLOGY The histologic variations in placental architecture are largely dependent on the developmental state at which observations are made. The syncytiotrophoblast, the outer cell layer surrounding villi, possesses a brush border. Microvilli that constitute this border are felt to be involved in pinocytotic activity Vacuoles within the cytoplasm of these cells are indicative of the absorptive and secretory activities of the syncytiotrophoblast. Syncytiotrophoblasts are composed of pyknotic (often multiple) nuclei that are hyperchromatic.

25. VILLI- HISTOLOGY The cytotrophoblastic nuclei are more round and open. On occasion, cytotrophoblasts may possess mitotic figures. Ultrastructurally, the cytotrophoblast has fewer organelles than does the syncytiotrophoblast. Most prominent are large mitochondria, which may be numerous. Extravillus trophoblasts are major constituents of the cell columns that form the deepest structural components of the implantation site.

26. Placental Development

27. CORD- EMBRYOLOGY The open region on the ventral surface of the developing embryo diminishes in size and then forms the early umbilicus. Through this structure extend both the yolk stalk and the body stalk, as well as the allantois. This cylindrical structure elongates, and its surface becomes covered by the expanding amnion. This is a single-layered epithelium on a layer of connective tissue. Therefore, the developing umbilical cord contains the yolk stalk, a pair of vitelline blood vessels, the allantois, and the allantoic blood vessels (two arteries and one vein) and is covered by amnionic epithelium.

28. CORD- GROSS The gross anatomic features of the umbilical cord that are of importance are the location of its insertion in the placental disk, its length, and the number of vessels. The presence of true knots may be considered normal when there is no adverse outcome, yet this occurrence may lead to fetal demise when the knot is tight. The presence of vascular tortuosities (false knots) is common and rarely of clinical significance. The finding of meconium staining and the presence of surface plaques are definitely abnormal

29. CORD- GROSS The normal umbilical cord is pearly white and somewhat translucent. The length of the umbilical cord has great significance, principally when it is excessively long or excessively short. Cord length has been shown to vary with gestational age, and measurements indicate that the cord elongates as gestation proceeds. At approximately 20 weeks’ gestational age, the average cord length is 32 cm. The normal length of the umbilical cord at term has been determined to be, on average, between 55 and 65 cm

30. CORD

31. CORD- HISTOLOGY Histologic examination of the umbilical cord shows several distinct layers. On the surface is a well-defined single layer of amnionic epithelium. The epithelium is squamoid and, in the region of fetal cord insertion, often becomes multilayered and closely resembles its epidermal contiguity. Deep to the amnionic epithelium that comprises the surface of the cord is the substance of Wharton’s jelly. This material largely is composed of mucopolysaccharides (hyaluronic acid and chondroitin sulfate). Embedded within the substance of Wharton’s jelly are the umbilical vessels.

32. CORD- HISTOLOGY The vasculature of the umbilical cord is composed of two arteries and one vein. The arteries possess no internal elastic lamina and have a double-layered muscular wall. Each of these muscular layers is composed of a network of interlacing smooth muscle bundles. The vein does have an inner elastic lamina. The umbilical vein, which generally has a larger diameter, possesses a thinner muscular coat consisting of a single layer of circular smooth muscle.

33. PLACENTAL BARRIER This is a composite structure that separating the fetal blood from the maternal blood. It has four layers: Syncytiotrophoblast Cytotrophoblast Connective tissue of villus Endothelium of fetal capillaries After the 20 th week, the cytotrophoblastic cells disappear and the placental membrane consists only of three layers .

34. PLACENTAL BARRIER It separates fetal from maternal blood. It prevents mixing of them. It is an incomplete barrier as it only prevents large molecules to pass ( heparin & bacteria) But cannot prevents passage of viruses(e.g. rubella), micro-organisms(toxoplasma, treponema pallidum) drugs and hormones.

35. MEMBRANES The placental membranes consist of the amnion and the chorion. AMNION The amnion, which constitutes the innermost aspect of the embryonic cavity, develops from the margin of the embryonic disk. As the embryonic disk begins to take the form of a tube, the amnionic periphery also folds inward and its attachment to the ventral body is defined. The amnionic cavity subsequently develops by the process of cavitation The amnionic cavity remains filled with amniotic fluid, which by the end of gestation amounts to approximately 1 L.

36. CHORION The chorion forms the base for the peripherally radiating villi and serves to encapsulate the embryo and the developing amnion. As the early implantation embryo develops, the embryonic tissues (the trophoblast and its mesodermal investments) continue to expand in a spherical fashion. The inner aspect of the condensation of mesoderm, which forms the inner capsular structure deep to the peripheral trophoblast, is also termed chorion. In the region that becomes the placental disk proper, chorionic villi continue to develop beneath these structures, and the placenta proper or the chorion frondosum is defined.

37. CHORION The region of the chorion that covers the expanded amnionic cavity forms what has been termed chorionic laeve. This constitutes the reflected membranes and is discerned from the membranous covering of the chorionic plate. Chorionic villi in the region of the laeve (which delimits the sac containing amnionic fluid) atrophy by pressure, although remnants of villous tissue may be found in association with this structure. In the region of the chorion frondosum, the fetal blood vessels invest the chorionic plate. Such vessels only occur in the chorion; the amnion is an avascular structure

38. GROSS ANATOMY- MEMBRANES The fetal membranes have a particular and characteristic appearance in normal deliveries. The sac, when viewed from the fetal surface, is clear and often has a bluish hue, and the amnion is devoid of vasculature. Remnants of atrophied vasculature may be seen in the overlying chorion and appear as filamentous streaks. The chorionic plate also has a characteristic blue sheen and, as described previously, the distribution of chorionic vessels has a characteristic appearance. It is not infrequent to find a peripheral nodule on the surface of the disk membranes. This normal nodule is the remnant of the fetal yolk sac

39. MEMBRANES- HISTOLOGY

40. INTRODUCTION A systematic review concluded that pathology of the placenta, cord, or membranes is attributed as a cause or contributory to stillbirth in 11% to 65% of cases in various classifications, depending on the classification used. Following protocols and definitions can be applied by general practice pathologists and improve the value of placental pathology and perinatal autopsy reports.

41. PLACENTAL WEIGHT Description of the placenta should include the placental weight trimmed of extraplacental membranes and umbilical cord, and notation of whether the placenta was fresh or fixed when measured. Any prior sampling of the placental parenchyma should also be documented. Any disruption of the basal plate should be noted. The placental weight is a surrogate for placental function, and fetoplacental weight ratio has been suggested as a possible indicator of adequacy of placental reserve capacity in fetal growth restriction (FGR)

42. PLACENTAL DISK DIMENSIONS Description of the placenta should include the measurement of the placenta in three dimensions: maximal linear dimension (length), greatest dimension of the axis perpendicular to this linear measurement (width), mural minimal and maximal thickness.

43. DESCRIPTION OF UMBILICAL CORD Description of the umbilical cord should include average diameter of the cord; length; site of insertion in relation to the center/margin of the placenta, determined by measuring the distance between the insertion site and the nearest placental margin; presence of strictures; and whether the cord appears to be hypocoiled or hyper coiled. segmental or localized areas of hyper coiling should be recorded. direction of coiling (handedness) should be noted if possible.

44. Thin umbilical cords are associated with FGR, whereas thick cords are associated with maternal diabetes and with fetal hydrops. Excessively long and short cords can be associated with adverse outcomes. Marginal (<1 cm from the nearest margin) and velamentous insertions, but not peripheral (<3 cm from the nearest margin) insertions, are associated with an increased risk of adverse pregnancy outcomes, including preterm delivery.

45. Hypocoiling (<1 coil per 10 cm) and hypercoiling (>3 coils per 10 cm) may be associated with adverse outcomes in some cases. Opinion was divided about the best way to assess coiling, especially because cords are often incompletely submitted Fixation of the cord will affect the length and therefore the coiling index, underscoring the importance of stating whether the placenta was fresh or fixed when pathologic examination was performed.

46. DESCRIPTION OF MEMBRANES Description of the membranes should include the color/opacity and completeness. Recording the shortest distance between the site of rupture to the placental edge may be useful in some cases of placenta previa if the rupture was at the edge, but the group was divided on this recommendation. If circumvallate or circummarginate, the percentage of the circumference involved should be noted.

47. Sampling of Cord, Membranes, and Placental Disk Submit 4 blocks as a minimum: 1 block to include a roll of the extraplacental membranes from the rupture edge to the placental margin, including part of the marginal parenchyma; 2 cross sections of the umbilical cord, one from the fetal end and another approximately 5 cm from the placental insertion end. Three other blocks each containing a full thickness section of normal-appearing placenta parenchyma should be submitted .

48. Full-thickness samples should be taken from within the central two-thirds of the disc and include one adjacent to the insertion site itself. If the transmural thickness is greater than the length of the cassette, two options are available: the upper third (chorionic plate and subjacent tissue) and lower third (basal aspect) of the parenchyma can be submitted in one cassette, or the gross slice can be divided into two and submitted in two cassettes A full-thickness sample should be taken from close to the umbilical cord insertion site to document fetal vascular ectasia and fetal and/or maternal inflammatory response.

49. DESCRIPTION OF LESIONS Grossly identified lesions should be described with either an estimate of the percentage of the total parenchymal volume they affect or a measurement of the two maximal dimensions of each lesion. The number of lesions of the same gross appearance should be counted and stated as being single or multiple. The location(s) of the lesions should be stated: central/ paracentral or peripheral. Lesions that are microscopically different may appear similar grossly. A block of the lesion (one of each type of lesion) should be sampled, with adjacent normal parenchyma if possible, in up to 3 additional blocks

50. Figure 5. Chronologic dating of infarcts is easier in the fixed placenta because the lesions are better demarcated: the older infarcts appear tan colored, whereas the fresher ones appear red and congested. Figure 6. Fresh placental abruption resulting in marked congestion of the overlying placental parenchyma.

51. MATERNAL VASCULAR MALPERFUSION OF THE PLACENTAL BED Effects of inadequate spiral artery remodeling or spiral artery pathology manifest as a spectrum that includes FGR and preeclampsia, high-velocity malperfusion may be detrimental to placentation in early pregnancy and placental function in later pregnancy. Gross findings include placental hypoplasia, infarction, and retroplacental hemorrhage Microscopic findings include abnormalities of villous development, which can be separated into distal villous hypoplasia, and accelerated villous maturation

52. INFARCTION Whether they are recent or remote. When histology confirms that the hemorrhage is encased by infarction, the proposed term infarction hematoma should be used. Infarcts can be suspected by their generally pyramidal shape and usual involvement of the basal parenchyma or maternal floor of the placenta. Gross chronologic dating of infarcts is easier in the fixed placenta because the lesions are better demarcated

53. CHRONICITY OF INFARCTION Early infarcts are seen as crowding and congestion of villi, which may be hemorrhagic, accompanied by early loss of nuclear staining of the stroma. There may also be migration of neutrophils into the intervillous space, which may be compressed or obliterated. Later changes include necrotic changes (pyknosis and karyorrhexis of trophoblast), loss of trophoblast nuclear staining, and eventually ghost villi.

54. RETROPLACENTAL HEMORRHAGE When a retroplacental hemorrhage is associated with indentation of the placental parenchyma, the indentation should be described, and two dimensions (length and width) or the percentage of maternal surface area involved should be recorded. Any clot that is separate from the placenta but submitted in the specimen container should be weighed and, if possible, measured in three dimensions. At least one sample of the area of retroplacental hemorrhage should be submitted for histology, which should include part of the basal plate.

55. RETROPLACENTAL HEMORRHAGE Grossly, there is blood accumulation on the maternal surface, with congestion and/or hemorrhage within or compression of the overlying parenchyma. Microscopically, there is blood accumulation beneath and dissecting the decidua and compression of the overlying intervillous space, with villous crowding, congestion, and/or intravillous hemorrhage with touching villi; there is also a smudged appearance, as evidence of early coagulation necrosis of the syncytiotrophoblast nuclei, and pale appearance of syncytiotrophoblast nuclei

56. RETROPLACENTAL HEMORRHAGE

57. DISTAL VILLOUS HYPOPLASIA (DVH) Defined as the paucity of villi in relation to the surrounding stem villi. The villi are thin and relatively elongated-appearing, and syncytial knots are increased. The diagnosis should be made when the features are seen in the lower two-thirds and involve at least 30% of 1 full-thickness parenchymal slide. It may be further graded as focal— finding of lesion in 1 full-thickness slide only—or diffuse— present in 2 or more full-thickness slides sampled. Diffuse distal villous hypoplasia is associated with early-onset FGR.

58. Distal villous hypoplasia: there is a paucity of villi, many of which are thin and elongated (hematoxylin-eosin, original magnification)

59. ACCELERATED VILLOUS MATURATION Presence of small or short hypermature villi for gestational period, usually accompanied by an increase in syncytial knots. It is diagnosed by identifying a diffuse pattern of term-appearing villi with increased syncytial knots and intervillous fibrin, usually alternating with areas of villous paucity. Accelerated villous maturation is a common pattern that may be found in mild, moderate, or severe forms of placental insufficiency, which includes FGR, preeclampsia, and preterm labor.

60. DECIDUAL ARTERIOPATHY The elements include acute atherosis, fibrinoid necrosis with or without foam cells, mural hypertrophy, chronic perivasculitis , absence of spiral artery remodeling, arterial thrombosis, and persistence of intramural endovascular trophoblast in the third trimester.

61. FETAL VASCULAR MALPERFUSION The lesions described under this umbrella of FVM are likely to be due to obstruction in fetal blood flow that could result from a number of conditions (eg, umbilical cord lesions, hypercoagulability, complications of fetal cardiac dysfunction, such as hypoxia, etc.) Findings consistent with FVM are thrombosis, segmental avascular villi, and villous stromalvascular karyorrhexis. Other possible markers, such as vascular intramural fibrin deposition, stem vessel obliteration/fibromuscular sclerosis, and vascular ectasia, should also be sought.

62. Two patterns of FVM are recognized, and either may be low grade or high grade. The first is segmental FVM, indicating thrombotic occlusion of chorionic or stem villous vessels, or stem vessel obliteration—although the distribution of the lesions is segmental, the thrombus or obstruction would be expected to result in complete obstruction to the villi downstream. The second is global FVM, indicating partially obstructed umbilical blood flow with venous ectasia, intramural fibrin deposition in large vessels, and/ or small foci (,5 villi per focus) of avascular or karyorrhectic villi—the obstruction is partial or intermittent, but the lesions can be distributed over much of the placenta.

63. High-grade FVM is manifest by the finding of more than one focus of avascular villi (a cumulative assessment of >45 avascular villi over 3 sections examined or an average of >15 villi per section) with or without thrombus, or 2 or more occlusive or nonocclusive thrombi in chorionic plate or major stem villi, or multiple nonocclusive thrombi.

64. THROMBOSIS Arterial or venous. The location(s) of the thrombosis should be specified as to whether it is at the umbilical, chorionic plate, or stem vessel vascular level, or any combination thereof.

65. Avascular villi Distribution and extent. The criteria for avascular villi that have been published previously are amended slightly. Small foci are the finding of 3 or more foci of 2 to 4 terminal villi showing total loss of villous capillaries and bland hyaline fibrosis of the villous stroma. Intermediate foci are 5 to 10 villi, and large foci are more than 10 villi.

66. Intramural fibrin deposition Isolated -if there is no more than one such lesion per slide. Whether the lesion is recent or remote should be noted. The location of the fibrin deposition is subendothelial or intramuscular, and thus intramural. It is also noted that the depositions are, by definition, nonocclusive. The criteria for intramural fibrin deposition have been published previously: fibrin or fibrinoid deposition (subendothelial or intramuscular) within the wall of large fetal vessels (indicates recent), with calcification (indicates remote)

67. VILLOUS STROMAL-VASCULAR KARYORRHEXIS 3 or more foci of 2 to 4 terminal villi showing karyorrhexis of fetal cells (nucleated erythrocytes, leukocytes, endothelial cells, and/or stromal cells) with preservation of surrounding trophoblast

68. STEM VESSEL OBLITERATION In stem vessel obliteration there is marked thickening of the vessel wall and resultant obliteration of the vascular lumen. VASCULAR ECTASIA The cause of vascular ectasia is not clear at this stage and may be nonspecific or related to umbilical cord compromise in combination with FVM. Vascular ectasia is characterized by the finding of vessels that are four times the luminal diameter of the surrounding corresponding vessel.

69. DELAYED VILLOUS MATURATION The lesion is defined by a monotonous villous population (defined as at least 10 such villi) with centrally placed capillaries and decreased vasculosyncytial membranes, recapitulating the histology in early pregnancy. The diagnosis should be made when it is present in at least 30% of 1 full-thickness parenchymal slide. Grading: focal, which is a finding of the lesion in 1 full-thickness parenchymal slide only, and diffuse, which is a presence in 2 or more full-thickness slides sampled.

70. Ascending Intrauterine Infection Describing the topography of the inflammation will allow separation of the maternal from the fetal inflammatory response. This is thought to be important because there is evidence that poor fetal outcomes are more often associated with a fetal inflammatory response. Chronicity of inflammation may have clinical implications different from those of a purely acute response, and should therefore be documented

71. SUBCHORIAL INFLAMMATION The presence of neutrophils in the subchorial intervillous space or beneath the chorion laeve layer in the absence of inflammation elsewhere, should be reported as subchorionitis. Involvement of artery or vein or both should be specified.

72. REPORTING FORMAT Histologic acute inflammation in the placenta, extraplacental membranes, and umbilical cord be reported as: acute chorioamnionitis (or acute chorionitis) with/without fetal inflammatory response in (specify) chorionic vessels, umbilical vein, and/or umbilical artery (or arteries).

73. VILLITIS OF UNKNOWN ETIOLOGY Histologic diagnosis and, although it may have a variable distribution, evidence indicates that 3 parenchymal blocks will identify 62% of villitis. It is usually lymphohistiocytic: although the presence of rare plasma cells does not exclude the diagnosis.

74. VILLITIS OF UNKNOWN ETIOLOGY Grading Schema Low grade is defined as the presence of inflammation affecting fewer than 10 contiguous villi in any one focus, with more than one focus required for the diagnosis. High grade is defined as the presence of multiple foci, on more than one section, at least one of which shows inflammation affecting more than 10 contiguous villi

75. Low-grade lesions should be further classified as focal when they are seen in one slide, all foci affecting fewer than 10 villi, with more than one focus required for diagnosis; or as multifocal when they are present in more than one slide, all foci affecting fewer than 10 contiguous villi. High-grade lesions should be further classified as patchy when there are multiple foci, with at least one focus with 10 or more contiguous villi, and seen in one or more slides; or as diffuse when more than 30% of all distal villi are involved

76. Vascular Damage When inflammatory cells damage vessels that have a muscular wall, the term villitis with stem vessel obliteration should be used. When avascular villi are seen in a placenta with villitis, the report should designate the finding as chronic villitis with associated avascular villi. Villitis may cause impairment of the fetoplacental circulation. Such damage is associated with adverse effects, such as neurologic impairment

77. When possible, the distribution of the foci of villitis should be reported as being located parabasal/ paraseptal, randomly in the midparenchyma or subchorionic zone, or combinations thereof.

78. Entities reported to be associated with villitis, such as eosinophilic/T-cell vasculitis, chronic intervillositis, and chronic deciduitis, should be noted.

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