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246 Appendices 2020 | NMH Annual Rep t Placental pathology A triage system is in place for placental examination. The entire placenta is submitted to the laboratory: a) from cases of Caesarean section b) from cases born in the delivery ward, where there is an abnormality of pregnancy, labour, delivery or the neonatal period. In other cases, the placenta is kept refrigerated for seven days and retrieved if an indication for analysis becomes apparent. Data from analysis of cases of Perinatal morbidity or mortality is returned in an anonymised fashion to the National Perinatal Epidemiology Centre, UCC, where it is pooled with data from other maternity units and national trends and benchmarks are published. The terminology used is the same consensus terminology as that used by NPEC (Khong TY et al). Some of these terms are expanded on below. Maternal vascular malperfusion (MVM) This is a spectrum: at the less severe end is mild accelerated villous maturation, then ischemic villous crowding and latterly infarction, also referred to as uteroplacental insufficiency (UPI). Increasingly, terms such as "shallow implantation" are being used to explain the pathogenesis. Expected findings in a case of severe PET would be a small placenta with recent and old infarcts, located centrally and peripherally in the parenchyma. Atherosis is fibrinoid change in vessels, seen in about half of cases of PET and occasionally in other conditions eg connective tissue disease. Hypoxic membrane lesions Laminar decidual necrosis may be regarded as an acute hypoxic lesion, and microcystic change in the chorion as a chronic hypoxic lesion. Meconium When present in large quantities, meconium may cause necrosis of muscle cells in the walls of chorionic vessels and possibly lead to vasospasm and ischaemia. Chorangiosis More vessels than normal are seen in terminal villi. It may be present as a primary finding or as a reaction where adjacent villi have been destroyed by villitis, and is suggested to be a marker of chronic hypoxia. PATTERNS OF INFLAMMATION Chorioamnionitis The terms "maternal inflammatory response" and "fetal inflammatory response are used with each being staged and graded according to consensus guidelines. There is an association between a severe fetal inflammatory response and brain damage in both term and pre-term infants. Maternal-fetal immune interaction. This may be manifest as any or all of villitis, intervillositis, chronic chorioamnionitis and deciduitis. Villitis Rare cases of villitis are due to infection eg CMV, but most are of unknown aetiology and are immunologically mediated. Villitis is graded as low- grade or high-grade. Overall, villitis is seen in 10% of placentas; high-grade villitis occurs in < 2% and is associated with an adverse perinatal outcome. Villitis may cause damage to fetal vessels in the placenta and this is associated with neurologic damage in term infants. It may recur in subsequent pregnancies. Intervillositis Chronic histiocytic intervillositis is relatively rare, but is over-represented in the cases in this report. It is associated with growth restriction and perinatal loss, with a mean gestation of loss of 25/40. It is more common in patients with immune dysregulation, and is likely to recur in subsequent pregnancies. THROMBOSIS AND HAEMORRHAGE Fetal vascular malperfusion (FVM) Occlusions of the fetoplacental circulation are manifest by: extensive avascular villi, obliterated stem arteries, haemorrhagic villitis, and occlusive thrombi. The term fetal thrombotic vasculopathy is also used. High- grade FVM, in particular, is associated with neonatal encephalopathy. Non-occlusive mural fibrin thrombi These are found in large fetal vessels in approx 10% of placentas. They are more common in cases with FTV and abnormal coiling; they reflect impaired fetoplacental flow, but the significance of isolated ones in smaller stem vessels is at present unclear.