Classification of placental lesions
2015; Elsevier BV; Volume: 213; Issue: 4 Linguagem: Inglês
10.1016/j.ajog.2015.05.056
ISSN1097-6868
Autores Tópico(s)Reproductive System and Pregnancy
ResumoPlacental pathology can be useful in a variety of ways including immediate diagnosis of important conditions affecting the mother or infant, identifying conditions that are likely to recur in subsequent pregnancies, separating clinical syndromes into distinct pathological phenotypes for further investigation, and uncovering the underlying cause of unexpected adverse outcomes. Classification of placental lesions has evolved from being a purely descriptive exercise through a stage in which the major pathophysiological processes such as disorders of maternal implantation and the amniotic fluid infection syndrome were first described to a recently proposed comprehensive classification system that includes all of the major maternal and fetal vascular and infectious and idiopathic/immune inflammatory processes (Amsterdam Placental Workshop Group). Implementation of this unified system with reproducible grading and staging should help establish evidence-based recommendations for placental submission and facilitate progress in studying the pathogenesis, diagnosis, and treatment of obstetric disorders with an underlying placental etiology. Placental pathology can be useful in a variety of ways including immediate diagnosis of important conditions affecting the mother or infant, identifying conditions that are likely to recur in subsequent pregnancies, separating clinical syndromes into distinct pathological phenotypes for further investigation, and uncovering the underlying cause of unexpected adverse outcomes. Classification of placental lesions has evolved from being a purely descriptive exercise through a stage in which the major pathophysiological processes such as disorders of maternal implantation and the amniotic fluid infection syndrome were first described to a recently proposed comprehensive classification system that includes all of the major maternal and fetal vascular and infectious and idiopathic/immune inflammatory processes (Amsterdam Placental Workshop Group). Implementation of this unified system with reproducible grading and staging should help establish evidence-based recommendations for placental submission and facilitate progress in studying the pathogenesis, diagnosis, and treatment of obstetric disorders with an underlying placental etiology. The placenta is the perennial Holy Grail, a putative diary of intrauterine life promising to explain the mysteries underlying poor pregnancy outcome. Its practical counterpart, placental pathology, is finally emerging as a respectable specialty after many years of confusion related to experts with divergent views, pathologists with varying levels of interest and relevant training, and nomenclature having little relationship to either the underlying biology or clinical presentation. Recent progress has been realized through the gradual acceptance of a standardized, reproducible, and biologically based classification system. Much work remains to disseminate this new information to practicing pathologists and clinicians. In this review, I will summarize the utility of placental diagnoses, review early contributions to our understanding of placental pathology, go into more depth describing the new Amsterdam international consensus criteria for placental diagnosis (Table 1), and conclude by speculating on how further progress in this area could facilitate the goals of the Human Placental Project to develop biomarkers and imaging techniques that can identify placental disease processes in real time when targeted intervention may be of benefit.1Khong TY, Mooney EE, Gordijn SJ, et al. Sampling and definitions of placental lesions: a consensus from the Amsterdam Placental Workshop Group, submitted for publication.Google Scholar, 2Guttmacher A.E. Maddox Y.T. Spong C.Y. The Human Placenta Project: placental structure, development, and function in real time.Placenta. 2014; 35: 303-304Abstract Full Text Full Text PDF PubMed Scopus (165) Google ScholarTable 1Placental classification (incorporating the 2014 Amsterdam Placental Workshop Group criteria)1.Placental vascular processesa.Maternal stromal-vascular lesionsDevelopmentalSuperficial implantation/decidual arteriopathyIncreased immature extravillous trophoblastMalperfusionGlobal/partialEarly: distal villous hypoplasiaLate: accelerated villous maturationSegmental/completeVillous infarct(s)Loss of integrityAbruptio placenta (arterial)Marginal abruption (venous)AcuteChronicb.Fetal stromal-vascular lesionsDevelopmentalVillous capillary lesionsDelayed villous maturation (maturation defect)Dysmorphic villiMalperfusionGlobal/partialObstructive lesions of umbilical cordRecent intramural fibrin in large fetoplacental vesselsSmall foci of avascular or karyorhectic villiSegmental/completeChorionic plate or stem villous thrombiLarge foci of avascular or karyorhectic villiLoss of integrityLarge vessel rupture (fetal hemorrhage)Small vessel rupture (fetomaternal hemorrhage)Villous edema2.Placental inflammatory-immune processesa.Infectious inflammatory lesionsAcuteMaternal inflammatory response: chorioamnionitis, subchorionitisFetal inflammatory response: chorionic/umbilical vasculitisChronicVillitis (CMV, others)Intervillositis (malaria, others)b.Immune/idiopathic inflammatory lesionsVillitis of unknown etiology and related/associated lesionsChronic villitisChronic chorioamnionitisLymphoplasmacytic deciduitisEosinophil T-cell fetal vasculitisChronic histiocytic intervillositis3.Other placental processesMassive perivillous fibrin(oid) deposition (maternal floor infarction)Abnormal placental shape or umbilical insertion siteMorbidly adherent placentas (accreta)Meconium-associated changesIncreased circulating nucleated red blood cellsCMV, cytomegalovirus.Redline. Classification of placental lesions. Am J Obstet Gynecol 2015. Open table in a new tab CMV, cytomegalovirus. Redline. Classification of placental lesions. Am J Obstet Gynecol 2015. Submission of placentas for examination generally follows 1997 College of American Pathologists guidelines.3Langston C. Kaplan C. Macpherson T. et al.Practice guideline for examination of the placenta.Arch Pathol Lab Med. 1997; 121: 449-476PubMed Google Scholar Approximately 40-50% of all placentas delivered in a high-risk setting will be examined according to these criteria.4Curtin W.M. Krauss S. Metlay L.A. Katzman P.J. Pathologic examination of the placenta and observed practice.Obstet Gynecol. 2007; 109: 35-41Crossref PubMed Scopus (36) Google Scholar, 5Spencer M.K. Khong T.Y. Conformity to guidelines for pathologic examination of the placenta.Arch Pathol Lab Med. 2003; 127: 205-207PubMed Google Scholar Additional high-quality evidence is needed to decide whether these guidelines are optimal for patient care. Useful information from a competently performed placental evaluation falls into the following 4 categories: (1) identification of previously unsuspected disease processes in the mother or infant that require immediate attention (eg, fragmentation suggestive of retained placenta or placenta accreta, unusual infections such as cytomegalovirus or listeria, and findings suggestive of aneuploidy or metabolic storage diseases); (2) conditions associated with a high probability of recurrence in subsequent pregnancies (Table 2); (3) information that can guide the management of future pregnancies or influence the long-term care of mother and infant (Table 3); and (4) diagnoses that provide a specific explanation for an adverse outcome such as fetal death, fetal growth restriction (FGR), spontaneous preterm birth, or central nervous system (CNS) injury.Table 2Placental lesions with significant recurrence risk in subsequent pregnanciesRare Chronic histiocytic intervillositis (75–90%)53Boyd T.K. Redline R.W. Chronic histiocytic intervillositis: a placental lesion associated with recurrent reproductive loss.Hum Pathol. 2000; 31: 1389-1392Abstract Full Text PDF PubMed Scopus (143) Google Scholar Massive perivillous fibrin(oid) deposition (maternal floor infarction) (40–60%)64Redline R.W. Invited Commentary: maternal floor infarction and massive perivillous fibrin deposition: clinicopathologic entities in flux.Adv Anat Pathol. 2002; 9: 372-373Crossref Google ScholarMore common Villitis of unknown etiology (25–50%)46Redline R.W. Villitis of unknown etiology: noninfectious chronic villitis in the placenta.Hum Pathol. 2007; 38: 1439-1446Abstract Full Text Full Text PDF PubMed Scopus (265) Google Scholar Placenta accreta (25–30%)65Sentilhes L. Kayem G. Ambroselli C. et al.Fertility and pregnancy outcomes following conservative treatment for placenta accreta.Hum Reprod. 2010; 25: 2803-2810Crossref PubMed Scopus (131) Google Scholar Severe global/partial maternal malperfusion (10–25%)66Lausman A. McCarthy F.P. Walker M. Kingdom J. Screening, diagnosis, and management of intrauterine growth restriction.J Obstet Gynaecol Can. 2012; 34: 17-28Abstract Full Text PDF PubMed Scopus (71) Google Scholar Spontaneous preterm birth with histological chorioamnionitis (10–25%)67Himes K.P. Simhan H.N. Risk of recurrent preterm birth and placental pathology.Obstet Gynecol. 2008; 112: 121-126Crossref PubMed Scopus (38) Google ScholarRedline. Classification of placental lesions. Am J Obstet Gynecol 2015. Open table in a new tab Table 3Management implications of current placental diagnoses: selected examplesSevere global/partial maternal vascular malperfusion Evaluate maternal cardiovascular status, glucose tolerance, thrombophilia, and renal function; suggest weight loss; consider ASA therapy, uterine artery Doppler, early third-trimester placental ultrasound, early delivery in subsequent pregnanciesSpontaneous preterm delivery with histological chorioamnionitis Extend neonatal antibiotics, treat underlying periodontal disease or chronic endometritis, early second-trimester cervical ultrasound, cerclageIdiopathic/immune lesions (chronic villitis [VUE]), massive perivillous fibrin(oid) deposition ([maternal floor infarction] chronic histiocytic intervillositis) Genetic counseling; maternal autoimmune testing; weight loss; consider low-molecular-weight heparin, aspirin, and/or immunosuppressive therapy; intensive early pregnancy surveillance; elective early deliveryComplete/segmental fetal vascular malperfusion with neonatal sequelae Maternal/neonatal thrombophilia workup, diabetes screen, maternal platelet evaluationDelayed villous maturation Diabetes screen, suggest weight loss, perform third-trimester fetal movement counts, consider delivery prior to 40 weeksASA, aspirin; VUE, villitis of unknown etiology.Redline. Classification of placental lesions. Am J Obstet Gynecol 2015. Open table in a new tab Redline. Classification of placental lesions. Am J Obstet Gynecol 2015. ASA, aspirin; VUE, villitis of unknown etiology. Redline. Classification of placental lesions. Am J Obstet Gynecol 2015. These outcomes all have a wide differential diagnosis that placental pathology can sort through for the purposes of quality assurance, risk management, and patient education (Table 4). Although these benefits are important, a more thorough understanding of placental abnormalities could both expand and focus the utility of placental examination.Table 4Common underlying placental causes of specific adverse outcomesPreterm fetal death Global/partial maternal vascular malperfusion (accelerated maturation), global/partial fetal vascular malperfusion (UC accident), abruptio placentaSpontaneous preterm birth Acute chorioamnionitis, marginal abruption, mild global/partial maternal malperfusion (accelerated maturation)Fetal growth restriction/indicated preterm birth Global/partial maternal malperfusion (accelerated maturation), chronic villitis (VUE), complete/segmental fetal vascular malperfusion (fetal thrombotic vasculopathy), fetal stromal-vascular developmental lesionsTerm fetal death Abruptio placenta, global/partial fetal vascular malperfusion (UC accident), fetomaternal hemorrhage, delayed villous maturationCNS injury at term Complete/segmental fetal vascular malperfusion (fetal thrombotic vasculopathy), global/ partial fetal vascular malperfusion (UC accident), chronic villitis (VUE) with obliterative fetal vasculopathy, acute chorioamnionitis with severe fetal cellular inflammatory response, multiple placental lesionsUC, umbilical cord; VUE, villitis of unknown etiology.Redline. Classification of placental lesions. Am J Obstet Gynecol 2015. Open table in a new tab UC, umbilical cord; VUE, villitis of unknown etiology. Redline. Classification of placental lesions. Am J Obstet Gynecol 2015. Placental pathology in its earliest stages focused on macroscopic abnormalities such as battledore placentas, succenturiate lobes, and velamentous insertions of the umbilical cord (UC). Although distinctive, these conditions proved not to be closely related to adverse outcomes. A series of seminal studies published between 1970 and 1995 laid the groundwork for our present understanding of placental pathology. Pijnenborg et al6Pijnenborg R. Dixon G. Robertson W.B. Brosens I. Trophoblastic invasion of human decidua from 8 to 18 weeks of pregnancy.Placenta. 1980; 1: 3-19Abstract Full Text PDF PubMed Scopus (663) Google Scholar established the conceptual framework for disorders of placental implantation and their sequelae. Blanc7Blanc W. Pathology of the placenta and cord in ascending and hematogenous infections.in: Marshall W. Perinatal infections, CIBA Foundation Symposium 77. Excerpta Medica, London (UK)1980: 17-38Google Scholar first delineated the sequence of placental changes that characterize amniotic fluid infection. Harris8Harris B.A. Peripheral placental separation: a review.Obstet Gynecol Surv. 1988; 43: 577-581Crossref PubMed Scopus (42) Google Scholar distinguished marginal venous abruption from the much less common syndrome of arterial rupture and abruptio placenta. Benirschke and colleagues9Naftolin F. Khudr G. Benirschke K. Hutchinson D.L. The syndrome of chronic abruptio placentae, hydrorrhea, and circumallate placenta.Am J Obstet Gynecol. 1973; 116: 347-350Abstract Full Text PDF PubMed Scopus (34) Google Scholar, 10Vernof K.K. Benirschke K. Kephart G.M. Wasmoen T.L. Gleich G.J. Maternal floor infarction—relationship to X-cells, major basic protein, and adverse perinatal outcome.Am J Obstet Gynecol. 1992; 167: 1355-1363Abstract Full Text PDF PubMed Scopus (52) Google Scholar described how early marginal venous abruptions could progress to the chronic abruption-oligohydramnios sequence and was the first to describe the important lesion known as maternal floor infarction. Stallmach et al11Stallmach T. Hebisch G. Meier K. Dudenhausen J.W. Vogel M. Rescue by birth: defective placental maturation and late fetal mortality.Obstet Gynecol. 2001; 97: 505-509Crossref PubMed Scopus (115) Google Scholar demonstrated the association between delayed villous maturation (maturation defect) and fetal death. Altshuler and Russell12Altshuler G. Russell P. The human placental villitides: a review of chronic intrauterine infection.Curr Topics Pathol. 1975; 60: 63-112Google Scholar brought idiopathic chronic villitis to attention, and Altshuler13Altshuler G. Chorangiosis: an important placental sign of neonatal morbidity and mortality.Arch Pathol Lab Med. 1984; 108: 71-74PubMed Google Scholar was the first to describe villous chorangiosis. Finally, Sander14Sander C.H. Hemorrhagic endovasculitis and hemorrhagic villitis of the placenta.Arch Pathol Lab Med. 1980; 104: 371-373PubMed Google Scholar described the patterns that would later come to be known as fetal thrombotic vasculopathy (now segmental fetal vascular malperfusion). A more systematic approach to placental diagnosis was undertaken by the Perinatal Section of the Society of Pediatric Pathology beginning in 1998.15Redline R.W. Faye-Petersen O. Heller D. Qureshi F. Savell V. Vogler C. Amniotic infection syndrome: nosology and reproducibility of placental reaction patterns.Pediatr Dev Pathol. 2003; 6: 435-448Crossref PubMed Scopus (528) Google Scholar, 16Redline R.W. Boyd T. Campbell V. et al.Maternal vascular underperfusion: nosology and reproducibility of placental reaction patterns.Pediatr Dev Pathol. 2004; 7: 237-249Crossref PubMed Scopus (296) Google Scholar, 17Redline R.W. Ariel I. Baergen R.N. et al.Fetal vascular obstructive lesions: nosology and reproducibility of placental reaction patterns.Pediatr Dev Pathol. 2004; 7: 443-452Crossref PubMed Scopus (221) Google Scholar Ensuing publications proposed and validated the grading and staging of lesions related to amniotic fluid infection and the maternal and fetal vascular disorders. Building on this work, a schematic framework for all placental lesions was presented at the International Federation of Placenta Associations meeting in 2006.18Redline R.W. Placental pathology: a systematic approach with clinical correlations.Placenta. 2008; 29: S86-91Abstract Full Text Full Text PDF PubMed Scopus (293) Google Scholar These efforts provided the background for a comprehensive system proposed by 26 placental pathologists from around the world who met in Amsterdam in September 2014.1Khong TY, Mooney EE, Gordijn SJ, et al. Sampling and definitions of placental lesions: a consensus from the Amsterdam Placental Workshop Group, submitted for publication.Google Scholar The consensus recommendations agreed upon during this meeting and in subsequent online discussions are incorporated into the next section and have been submitted for publication. A secondary goal of the meeting was to establish sampling guidelines for placental evaluation. Although not the focus of this review, the following recommendations were made: submit 4 blocks as a minimum; one to include 2 cross-sections of the UC and a roll of the extraplacental membranes including part of the marginal parenchyma; 3 others containing full-thickness sections of normal-appearing placenta parenchyma taken from within the central two thirds of the disc including one adjacent to the UC insertion site. The proposed new framework for placental classification (Table 1) is discussed in the following text. The placenta is essentially an interhemal membrane mediating the exchange of nutrients and waste products between the maternal and fetal circulations. It is therefore not surprising that abnormalities in the structure and function of these circulatory beds are dominant patterns of placental injury. Developmental abnormalities of the maternal stromal-vascular compartment of the placenta have recently been reviewed and contribute to placental dysfunction via malperfusion and loss of integrity (discussed below).19Brosens I. Pijnenborg R. Vercruysse L. Romero R. The “Great Obstetrical Syndromes” are associated with disorders of deep placentation.Am J Obstet Gynecol. 2010; 204: 193-201Abstract Full Text Full Text PDF PubMed Scopus (946) Google Scholar For the purposes of this review, I will say only that developmental abnormalities all appear to involve defects in the appropriate differentiation and expansion of trophoblast, both extravillous (shallow implantation, lack of spiral artery remodeling, increased trophoblast islands and cysts in the intervillous space) and villous (persistent cytotrophoblast). Although some of these defects may be intrinsic to the trophoblast, most evidence suggests that they are caused by poorly understood maternal genetic or environmental factors that shape the early intrauterine environment. Maternal vascular malperfusion develops as a consequence of abnormal spiral artery flow and can be separated into 2 subgroups.16Redline R.W. Boyd T. Campbell V. et al.Maternal vascular underperfusion: nosology and reproducibility of placental reaction patterns.Pediatr Dev Pathol. 2004; 7: 237-249Crossref PubMed Scopus (296) Google Scholar The first, global/partial maternal vascular malperfusion, leads to accelerated villous maturation (Figure, A). Accelerated maturation is the term agreed upon to encompass all of the histological changes seen in portions of the villous tree deprived of the low-velocity, high-volume maternal blood flow that characterizes normal placentas. These findings include alternating areas of agglutinated villi with increased syncytial knots and intervillous fibrin and villous paucity due to decreased villous branching. When paucity affects more than 30% of all distal villi, the process is termed distal villous hypoplasia. The second pattern, segmental/complete maternal vascular malperfusion, is characterized by villous infarcts which represent areas of ischemic necrosis overlying occluded spiral arteries. Whereas single infarcts, especially at the placental margin, are not unusual in term placentas, any infarct in a preterm placenta should be considered abnormal. Loss of maternal vascular integrity encompasses 2 distinct processes. The first, abruptio placenta, frequently occurs secondary to arterial maldevelopment in preeclampsia and represents the rupture of incompletely remodeled spiral arteries due to ischemia-reperfusion or atherosis. Vasoactive drugs (cocaine or nicotine) and shear stress (trauma or uterine rupture) can also cause arterial hemorrhages. Abruptio placenta is characterized by central location and placental evidence of high pressure flow (large volume, indentaton of the basal plate, and extension into the intervillous space). Although most cases lead to immediate delivery, some arterial hemorrhages evolve gradually, leading to overlying recent villous infarction (subacute abruptio placenta). The second process, marginal abruption, represents the rupture of maternal veins, usually at the periphery of the placenta.8Harris B.A. Peripheral placental separation: a review.Obstet Gynecol Surv. 1988; 43: 577-581Crossref PubMed Scopus (42) Google Scholar Risk factors include sudden changes in uterine geometry (rupture of membranes, cervical insufficiency), poor support (lower uterine segment implantation, abnormal marginal anatomy), increased maternal venous pressure, and decidual inflammation (chorioamnionitis). Acute marginal abruption is an important cause of spontaneous preterm birth but only rarely causes fetal hypoxia. Chronic (marginal) abruption develops when acute marginal abruption does not progress to delivery. The hallmarks of chronic abruption include circumvallate membrane insertion, organizing marginal blood clots, and hemosiderin deposition. Severe cases show diffuse chorioamnionic hemosiderosis, reflecting hemorrhage into the amniotic fluid.20Redline R.W. Wilson-Costello D. Chronic peripheral separation of placenta: the significance of diffuse chorioamnionic hemosiderosis.Am J Clin Pathol. 1999; 111: 804-810PubMed Google Scholar Developmental abnormalities of the fetal stromal-vascular compartment of the placenta can be separated into 3 categories. Delayed villous maturation (also known as distal villous immaturity or maturation defect) is characterized by a decreased fetoplacental weight ratio, excessive villous stroma, and central capillaries lacking vasculosyncytial membranes (Figure, B).21Redline R. Distal villous immaturity.Diagn Histopathol. 2012; 18: 189-194Abstract Full Text Full Text PDF Scopus (41) Google Scholar This pattern is seen with diabetes, some cases of FGR, and chronic umbilical cord obstruction.22de Laat M.W. van der Meij J.J. Visser G.H. Franx A. Nikkels P.G. Hypercoiling of the umbilical cord and placental maturation defect: associated pathology?.Pediatr Dev Pathol. 2007; 10: 293-299Crossref PubMed Scopus (44) Google Scholar Lack of placental reserve in these placentas may increase the risk of fetal death.11Stallmach T. Hebisch G. Meier K. Dudenhausen J.W. Vogel M. Rescue by birth: defective placental maturation and late fetal mortality.Obstet Gynecol. 2001; 97: 505-509Crossref PubMed Scopus (115) Google Scholar Villous capillary lesions include chorangiosis (hypercapillarization of terminal villi), chorangioma (a benign placental vascular tumor arising in stem villi), and multifocal chorangiomatosis (a more pervasive developmental abnormality involving small vessels at the periphery of immature intermediate villi).23Ogino S. Redline R.W. Villous capillary lesions of the placenta: distinctions between chorangioma, chorangiomatosis, and chorangiosis.Hum Pathol. 2000; 31: 945-954Abstract Full Text PDF PubMed Scopus (146) Google Scholar, 24Bagby C. Redline R.W. Multifocal chorangiomatosis.Pediatr Dev Pathol. 2010; 14: 38-44Crossref PubMed Scopus (13) Google Scholar Although distinct, all share a relationship with maternal hypoxemia and/or excessive fetal growth factor expression. They sometimes occur together in conditions such as Beckwith Wiedemann syndrome.25McCowan L.M. Becroft D.M. Beckwith-Wiedemann syndrome, placental abnormalities, and gestational proteinuric hypertension.Obstet Gynecol. 1994; 83: 813-817PubMed Google Scholar Dysmorphic villi represent a more pervasive disorder encompassing abnormalities in villous architecture that resemble features seen in aneuploid gestations. These include irregular contour, trophoblast inclusions, cystic degeneration, stromal overgrowth, proximal-distal villous disproportion, and abnormal vascular patterning.26Redline R.W. Zaragoza M.V. Hassold T. Prevalence of developmental and inflammatory lesions in non-molar first trimester spontaneous abortions.Hum Pathol. 1999; 30: 93-100Abstract Full Text PDF PubMed Scopus (73) Google Scholar, 27Dicke J.M. Huettner P. Yan S. Odibo A. Kraus F.T. Umbilical artery Doppler indices in small for gestational age fetuses: correlation with adverse outcomes and placental abnormalities.J Ultrasound Med. 2009; 28: 1603-1610PubMed Google Scholar Mesenchymal dysplasia is the most dramatic example of this pattern.28Pham T. Steele J. Stayboldt C. Chan L. Benirschke K. Placental mesenchymal dysplasia is associated with high rates of intrauterine growth restriction and fetal demise: a report of 11 new cases and a review of the literature.Am J Clin Pathol. 2006; 126: 67-78Crossref PubMed Scopus (108) Google Scholar Some cases of dysmorphic villi may represent examples of confined placental mosaicism.29Hoffner L. Dunn J. Esposito N. Macpherson T. Surti U. P57KIP2 immunostaining and molecular cytogenetics: combined approach aids in diagnosis of morphologically challenging cases with molar phenotype and in detecting androgenetic cell lines in mosaic/chimeric conceptions.Hum Pathol. 2008; 39: 63-72Abstract Full Text Full Text PDF PubMed Scopus (84) Google Scholar Fetal vascular malperfusion can be separated into 2 subgroups.30Redline R.W. Correlation of placental pathology with perinatal brain injury.in: Placental pathology. Vol 6. Elsevier, Philadelphia2013: 153-180Google Scholar Global/partial, often associated with potentially obstructive umbilical cord lesions such as hypercoiling, stricture, abnormal placental insertion site, or long-standing fetal entanglements, is characterized by histological features suggestive of increased venous pressure (dilatation or mural fibrin deposition in large fetoplacental veins; Figure, C) and poor circulation in the most distal portions of the villous tree (scattered small foci of avascular villi; Figure, D). Its clinical correlate, chronic partial/ intermittent umbilical cord obstruction, has been associated with CNS injury.31Clapp 3rd, J.F. Lopez B. Simonean S. Nuchal cord and neurodevelopmental performance at 1 year.J Soc Gynecol Investig. 1999; 6: 268-272Crossref PubMed Scopus (49) Google Scholar, 32Myers R.E. Four patterns of perinatal brain damage and their conditions of occurrence in primates.Adv Neurol. 1975; 10: 223-234PubMed Google Scholar The second pattern, segmental/complete occlusion of large fetoplacental vessels by thrombi, leads to larger foci of degenerating downstream villi.33Redline R.W. Pappin A. Fetal thrombotic vasculopathy: the clinical significance of extensive avascular villi.Hum Pathol. 1995; 26: 80-85Abstract Full Text PDF PubMed Scopus (192) Google Scholar, 34Chisholm K.M. Heerema-McKenney A. Fetal thrombotic vasculopathy: significance in liveborn children using proposed society for pediatric pathology diagnostic criteria.Am J Surg Pathol. 2014; 39: 274-280Crossref Scopus (28) Google Scholar These villi initially show degenerative changes (stromal-vascular karyorrhexis) and eventually lose all vessels (avascular villi) (Figure, E). When extensive, this pattern has been called fetal thrombotic vasculopathy and has been associated with CNS injury and other adverse outcomes. Loss of fetal vascular integrity encompasses 2 processes: hemorrhage and edema. Fetal hemorrhages can involve large vessels (eg, ruptured vasa previa) or smaller vessels in the distal villi (fetomaternal hemorrhage). The latter can present as intervillous thrombi.35Devi B. Jennison R.F. Langley F.A. Significance of placental pathology in transplacental haemorrhage.J Clin Pathol. 1968; 21: 322-331Crossref PubMed Scopus (42) Google Scholar, 36Kaplan C. Blanc W.A. Elias J. Identification of erythrocytes in intervillous thrombi: a study using immunoperoxidase identification of hemoglobins.Hum Pathol. 1982; 13: 554-557Abstract Full Text PDF PubMed Scopus (40) Google Scholar Significant amounts of fetomaternal hemorrhage may be associated with increased fetal nucleated red blood cells (NRBC) in the placenta and a positive maternal Kleihauer Betke test. Edema of the placental villi accompanies hydrops fetalis, and placental pathology can contribute to differential diagnosis by highlighting coexisting fetal anemia (increased NRBC) or identifying a specific etiology (eg, parvovirus inclusions). A second pattern of edema seen in the immature intermediate villi of very premature placentas has been associated with perinat
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