19 Diseases of the Placenta Deborah J. Gersell . Frederick T. Kraus Normal Anatomy and Development .............. 1000 Insertion . 1054 Umbilical Vessels . 1056 Abnormal Placentation and Villous Development . 1003 Anomalous Shapes . 1003 Clinical Syndromes and Their Pathologic Extrachorial Placenta . 1004 Correlates in the Placenta ......................... 1059 Placenta Accreta, Increta, and Percreta . 1005 Preeclampsia . 1059 Mesenchymal Dysplasia . 1007 Essential Hypertension . 1060 Diabetes Mellitus . 1060 Multiple Pregnancy ................................ 1007 Preterm Birth, Preterm Labor, and Preterm Twin Gestation . 1007 Rupture of Membranes . 1060 Complications of Multiple Pregnancy . 1013 Post-Term Pregnancy . 1060 Higher Multiple Births . 1021 Fetal Growth Restriction, Intrauterine Growth Restriction (IUGR) . 1060 Placental Inflammation and Intrauterine Neonatal Encephalopathy (NE), Cerebral Infection ........................................... 1022 Palsy (CP), and ‘‘Birth Asphyxia’’ . 1061 Ascending Infection and Acute Fetal and Placental Hydrops . 1061 Chorioamnionitis . 1022 Nucleated Red Blood Cells in the Fetal Subacute Chorioamnionitis . 1027 Circulation . 1062 Villitis and Hematogenous Infection . 1027 Thrombophilias . 1063 Other Patterns of Placental Inflammation . 1032 Acute Fatty Liver of Pregnancy and HELLP Syndrome . 1063 Circulatory Disorders .............................. 1033 Sickle-Cell Trait/Disease and Other Maternal Circulation . 1034 Hemoglobinopathies . 1063 Fetal Circulation . 1042 Storage Disorders . 1064 Fetal Membranes .................................. 1045 Abortion, Stillbirth, and Intrauterine Fetal Death . 1064 Squamous Metaplasia . 1045 Early Abortion . 1064 Amnion Nodosum . 1046 Late Abortion, Stillbirth, and Intrauterine Amnionic Bands . 1046 Fetal Death . 1065 Meconium Stain . 1048 Gastroschisis . 1049 Nontrophoblastic and Metastatic Tumors . 1065 Extramembranous Pregnancy . 1050 Hemangioma (Chorangioma) . 1065 Hepatocellular Adenoma and Adrenocortical Umbilical Cord .................................... 1050 Nodules . 1066 Normal Anatomy and Embryonic Other Placental ‘‘Tumors’’ . 1067 Development . 1050 Placental Metastases . 1067 Vestigial Remnants . 1050 Stasis Problems and ‘‘Cord Accidents’’ . 1051 Examination of the Placenta ...................... 1067 Cord Length . 1051 Fetal membranes . 1068 Knots . 1052 Umbilical cord . 1068 Torsion . 1053 Placenta . 1068 Stricture . 1053 Sections . 1068 Cord Diameter . 1054 Special aspects of Multiple Pregnancy . 1069 Rupture . 1054 Special Techniques . 1069 R. J. Kurman, L. Hedrick Ellenson, B. M. Ronnett (eds.), Blaustein’s Pathology of the Female Genital Tract (6th ed.), DOI 10.1007/978-1-4419-0489-8_19, # Springer Science+Business Media LLC 2011 1000 19 Diseases of the Placenta 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 (espe- cially neurologic) disabilities can be traced to injury occur- ring before birth. The purpose of this chapter is to describe clinically important placental lesions and to emphasize the context in which these lesions are directly or indirectly important to the fetus, the mother, or both. Normal Anatomy and Development The monograph by Boyd and Hamilton [23] provides a detailed description and exquisite illustrations of the various stages of human implantation. The ovum is fertil- ized in the fallopian tube and develops rapidly, reaching the endometrial cavity as a blastocyst. At this stage, the outer cell layer of the blastocyst has differentiated into trophoblast, and there are only a few cells in the inner cell mass from which the embryo will develop. The tro- phoblast attaches to and penetrates the endometrium on the 6th to 7th postovulatory day, and by the 10th to 11th postovulatory day, the blastocyst is totally embedded in endometrial stroma that has reestablished continuity over the penetration defect. The trophoblast grows rapidly . Fig. 19.1 and circumferentially, invading maternal blood vessels. Implantation at 13 days. Trophoblast has differentiated into Blood-filled spaces (lacunae) separate the trophoblast into inner (cytotrophoblast) and outer (syncytiotrophoblast) > trabecular columns ( Fig. 19.1), with an outer syncytio- layers. Focally, the cytotrophoblast has proliferated to form trophoblastic layer oriented radially around central solid projections, the forerunners of the primary villi. The germ cores of cytotrophoblast. As the extraembryonic mesen- disk is located near the center (Reprinted courtesy of chyme penetrates the cytotrophoblastic cores, small blood Department of Embryology, Davis Division, Carnegie vessels form within it, and these eventually connect with Institute of Washington) each other and with those forming independently in the allantois of the body stalk (chorioallantoic placentation), establishing the fetoplacental circulation by the 5th–6th single, round–oval nuclei, clear cytoplasm, and distinct week. A shell of solid trophoblast remains at the periphery cell borders directly overlying the stromal core of the of the stem villi, anchoring them to the basal plate and villus. The syncytiotrophoblast (ST) overlies the CT continuing to grow and expand the intervillous space and is the terminally differentiated component of tropho- (> Fig. 19.2). blast responsible for transport functions, protection, and Successful implantation requires a series of complex, pregnancy-specific protein and hormone production. Its coordinated interactions between maternal tissue and abundant, often vacuolated cytoplasm is amphophilic trophoblast. The trophoblast consists of several morpho- with multiple small dark nuclei and a distinct brush bor- logically and functionally distinct cell types, each with der. Intermediate trophoblast (IT) is a constituent of vil- characteristic anatomic distribution. The great majority lous trophoblast, primarily in the anchoring cell columns, of cytotrophoblastic and syncytiotrophoblastic cells are but is most prevalent in extravillous sites. IT developing located on the villi (villous trophoblast). Cytotrophoblast from the trophoblastic shell invades the endometrium (CT), the germinative, mitotically active component of and myometrium at the implantation site. Subpopula- trophoblast, is present as a layer of uniform cells with tions of IT in the villi (villous IT), implantation site, Diseases of the Placenta 19 1001 and membranes (chorionic IT) are morphologically and keratin help distinguish IT (keratin positive) from decidua immunohistochemically distinct [172]. IT nuclei are irreg- (keratin negative). ular and hyperchromatic with coarsely granular chromatin. The IT that infiltrates the decidua and myometrium at Most cells are mononucleate, although multinucleate forms the implantation site is responsible for remarkable physio- occur. IT may be round, polyhedral, or spindle shaped logic structural modifications in the spiral arteries. In the depending on location with abundant eosinophilic, early weeks of pregnancy, IT invades the decidual segments amphophilic, or clear cytoplasm. The cytologic features of the spiral arteries, forming intraluminal plugs. Later, are generally sufficiently distinctive to identify IT, but between the 12th and 20th weeks of pregnancy, their intermingling with decidua at the implantation endovascular IT extends from the decidual into the site is so intimate that it may be difficult to characterize myometrial segments of the spiral arteries. Eventually, IT any particular cell as maternal or fetal by conventional and fibrinoid completely replace the endothelium and the light microscopy. When findings are equivocal (as in some muscular and elastic tissue of the media (> Fig. 19.3). abortion specimens), immunohistochemical stains for Altered by this process, the spiral arteries undergo progres- sive distension, eventuating in large funnel-shaped channels that augment blood flow to the implantation site. Dissolu- tion of the muscular media results in fixed vascular dilatation unresponsive to vasculospastic influences. As it grows and enlarges, the chorion undergoes gross structural modifications. Initially, villi surround the entire chorionic cavity, but as the chorion prolapses into the endometrial cavity, the villi oriented toward the uterine cavity undergo progressive atrophy to form the smooth chorion (chorion laeve) or fetal membranes (> Fig. 19.4). These atrophic villi are still apparent in sections of mem- branes in the mature placenta (> Fig. 19.5). The villi on the embryonic aspect of the chorion continue to prolifer- ate, forming the definitive placenta (chorion frondosum). Differential villous atrophy and proliferation reflect maternal blood flow. Departure from the usual pattern of villous growth and atrophy is thought to result in some . Fig. 19.2 of the aberrant placental shapes described below. Contin- Secondary villi. Mesenchyme has penetrated the ued growth and enlargement of the chorion results in trophoblastic cores. The trophoblastic shell is peripheral eventual obliteration of the uterine cavity through fusion . Fig. 19.3 Normal spiral artery remodeling. Intraluminal IT (left) later invades and replaces the vascular media along with fibrinoid matrix (right) 1002 19 Diseases of the Placenta . Fig. 19.4 . Fig. 19.6 Formation of chorion laeve.