ABSTRACT
Pre-eclampsia (Table 12) is defined as pregnancy-induced hypertension with proteinuria. Hypertension in pregnancy is defined as a systolic pressure of ≥140 mmHg, and/or a diastolic pressure of ≥90 mmHg in pregnancies over 20 weeks in previously normotensive women. Proteinuria is defined as 0.3 g or more of protein in a 24-h urine collection. Severe pre-eclampsia is classified when at least one of the following is present: a blood pressure of ≥160 mmHg systolic and/or ≥110 mmHg diastolic on two separate occasions 6h or more apart on bedrest; ≥5 g of protein in a 24-h collection (or two separate spot readings of 3+ over 4 h apart); oliguria (<500 ml in 24 h); cerebral or visual disturbances; pulmonary edema or cyanosis; epigastric or right upper quadrant pain; impaired hepatic function; thrombocytopenia; or fetal growth restriction574. Edema is often associated with pre-eclampsia. A variety of terms may be applied to this condition, including pre-eclampsia, toxemia, and pregnancy-induced hypertension (PIH). If new-onset grand mal seizures have occurred, the diagnosis is eclampsia. The HELLP syndrome (hemolysis, elevated liver enzymes, low platelets) is a severe form of preeclampsia. Proteinuria may be absent in HELLP syndrome. Gross features Placentas from pre-eclamptic pregnancies may be of reduced weight, or may be within normal limits. Infarcts involving more than 5% of the placenta are commonly seen, and in severe preeclampsia, more than 50% of the placenta may be infarcted. Retroplacental hematoma (with or without a clinical history of abruption) may be present. Histologic features Increased syncytial knots (see Figure 39a-1), stromal fibrosis, prominent and cytotrophoblastic hyperplasia (cytotrophoblast present in >20-40% of villi at term), and excessive fibrinoid necrosis may also be seen in the villi (see Chapter 9). PAS stain and thin sections of plastic embedded material may enhance detection of cytotrophoblastic hyperplasia, but these special steps are not generally taken in routine practice. Hypoplasia of the distal villous tree with reduced vascularity with increased knots (see Figure 45), and/or fibromuscular hyperplasia and obliterative endarteritis of the fetal stem arteries, may be present. Increased apoptosis has been reported in placentas, and in their respective sites of implantation in the uterus, from gestations complicated by pre-eclampsia111,575, but this feature cannot be readily assessed in practice. The basic and most consistently seen (although not pathognomonic) lesion is acute atherosis in the basal arteries of the decidua basalis and the spiral arteries of the decidua parietalis, characterized by fibrinoid necrosis and lipid-laden macrophages in the
vessel wall, with perivascular lymphocytic infiltration (Figure 98). Occlusive thrombosis may also occur in these maternal arteries, particularly associated with
infarcts. Careful examination of the arteries in the decidua of the membrane roll and along the maternal surface is essential to recognize the lesion, and extra sections to ensure adequate sampling of the maternal arteries may be considered. The membrane roll is particularly useful. In cases of mild pre-eclampsia, and if sampling is inadequate, there may be no abnormalities appreciated in placental sections. It is also possible that the clinical diagnosis of pre-eclampsia may have been incorrect. If insufficient arteries are present to assess, a comment can be made on the report. A shave section of the basal plate is helpful if the other sections do not demonstrate the lesion.
