Perinatal placental pathology.

Examination of the placenta may be viewed as a diary of the pregnancy. Apart from its immediate diagnostic value, it can also broadly serve two purposes: 1) it provides a method of auditing antenatal clinical judgment by clinicopathologic correlation, and 2) it makes an important contribution in the context of unsolved clinical problems. The placenta's strategic location at the fetomaternal interphase mirrors disorders of both mother and fetus; however, "merged images" still cause some confusion, eg, villitis. This review summarizes recent areas of clinicopathologic correlation that have enhanced our understanding of placental function and the fetoplacental unit.     

HELLP syndrome and placental inflammatory pathology

HELLP syndrome, acronym for hemolysis (H), elevated liver enzymes (EL), and low platelet count (LP), is a multisystemic disease that complicates pregnancy and is considered a severe variant of hypertensive disorders in pregnancy, that causes maternal and perinatal mortality and morbidity. The pathogenesis of HELLP syndrome is not completely understood and the obstetric approach with the induction of delivery is still the only specific therapy in HELLP syndrome. It is well known that the placenta and the incomplete trophoblast invasion of spiral arteries have a central role, but especially in severe pre-eclampsia and in the HELLP syndrome there is a systemic endothelial activation and damage. In this review we emphasize the inflammatory hypothesis and the role of inflammatory cytokines deriving from placenta in pre-eclampsia and HELLP syndrome, also in the light of our recent studies on cytokines pattern.     

Umbilical blood flow and placental pathology.

The aim of the study was to establish whether or not placental morphostructural damage correlates with umbilical artery Doppler waveform and neonatal condition. To this end, seriated ultrasonographic monitoring, flowmeter tests on the cord artery and computerized cardiotocography were carried out in a population of 93 pregnant women in the second half of pregnancy. After birth placentas were subjected to macroscopic and microscopic examination. The Resistance Index showed a good correlation with placental vascular lesions, characterized by a distinct reduction in terminal villi and muscular wall arterioles. Two types of intrauterine growth retardation were discernible, the first of genetic origin with a low-profile growth curve and therefore not amenable to treatment, but with a positive fet l-neonatal prognosis, and the second with a pathologic placental component, presenting a late flattening growth curve with evolution towards fetal distress and a negative fetal-neonatal prognosis.     

Risk of recurrent preterm birth and placental pathology

OBJECTIVE: To estimate whether placental pathological lesions from an index preterm birth are associated with an increased risk of recurrent preterm birth and to estimate whether certain pathologic lesions recur in a woman's next delivery. METHODS: We performed a retrospective cohort study of all women who delivered at less than 37 weeks and had their next delivery at our institution during a 5-year period. Women were included in the cohort if placental pathology was available from their preterm birth. Placental pathology from their subsequent birth was also collected. Placental pathology was classified into presence or absence of two classes of lesions-inflammatory and thrombotic. Variables considered as possible confounders included race, gestational age of preterm birth, interpregnancy interval, tobacco use, payor status, years of education, and maternal medical problems. RESULTS: Inflammatory lesions (n=173) were associated with recurrent preterm birth overall as well as recurrent spontaneous preterm birth (P<.001). Thrombotic lesions (n=158) were not associated with recurrent preterm birth or any subtypes of preterm birth. The association between inflammatory lesions and recurrent spontaneous preterm birth remained significant when controlling for gestational age of preterm birth, race, and tobacco use, with an adjusted odds ratio of 2.4 (95% confidence interval 1.2-4.7). Inflammatory placental lesions (n=194) were associated with inflammatory lesions in the subsequent delivery P=.001). CONCLUSION: Recurrent preterm birth is more likely among women with inflammatory lesions on placental pathology from a prior preterm birth. Additionally, these women are more likely to have placental inflammatory lesions with their next delivery. LEVEL OF EVIDENCE: II.     

Preterm labor: placental pathology and clinical correlation.

OBJECTIVE: To determine the relevance of ischemia in the incidence of preterm labor. A second objective was to document perinatal outcomes for patients with preterm labor classified according to its clinical, functional, and pathologic characteristics (infectious, ischemic, mixed, or idiopathic). METHODS: Perinatal outcomes were evaluated for 145 consecutive patients with preterm labor, subdivided into etiologic categories according to clinical, functional (Doppler), and morphologic (placental pathology) characteristics. A group of 44 normal pregnancies delivered at term served as controls. RESULTS: Of the preterm labor group, 28.3% were classified as ischemic, compared with 4.5% of the control group (odds ratio and 95% confidence interval = 8.28 [1.8, 51.8]; P < .05). Compared with the control group, the preterm labor patients who delivered preterm had higher rates of ischemia (31.4% compared with 4.5%; P < .05) and infection (16.1% compared with 2.3%; P < .05). Among the preterm labor group, patients classified in the infectious or ischemic subgroups had a higher rate of preterm delivery (95.0% and 90.2% compared with 73.2%; P < .05), admission to the neonatal intensive care unit (75.0% and 61.0% compared with 40.0%; P < .05), and newborn weight under 1500 g (35.0% and 19.5% compared with 3.7%; P < .05) than the idiopathic subgroup. CONCLUSION: Preterm labor resulting from infection or ischemia is associated with a higher perinatal complication rate than idiopathic preterm labor.     

Thrombophilia and pregnancy

The incidence of venous thromboembolism is increased five to six times in pregnancy; and it is estimated that thromboembolic episodes- superficial and deep venous thromboembolism and pulmonary embolism occur in 1:1000 to 1:1500 pregnancies. These complications during pregnancy and puerperium, are not common but serious and leading cause of maternal morbidity and mortality. Thrombophilias--acquired or inherited, result of anticoagulant regulatory proteins deficiency, could compromise normal pregnancy by increasing the risk of developing first or recurrent thromboembolic incidents and adverse obstetric events.     

Comparison of placental pathology between severe preeclampsia and HELLP syndrome

Objective  

This study was performed to evaluate and compare the placental pathology in patients with severe pre-eclampsia (PE) and HELLP syndrome. Moreover, neonatal birth weight was compared between the two groups.     

Intrapartum fever at term: clinical characteristics and placental pathology

Objectives: To investigate the association between clinical characteristics and placental histopathology in women with intrapartum fever (IPF) at term. Methods: Maternal characteristics, intrapartum parameters, neonatal outcome and placental pathology were compared between 120 patients with IPF (≥380C) and a control group matched for mode of delivery. Placental lesions were classified as consistent with maternal circulation abnormalities or fetal thrombo-occlusive disease or inflammatory responses of maternal (MIR) or fetal (FIR) origin. Results: Compared to controls the study group was characterized by significantly higher rates of nulliparity, extra-amniotic balloon induction of labor, and epidural anesthesia, higher gestational age, higher white blood cell count, and more vaginal examinations. On multivariate logistic regression analysis, multiple vaginal examinations were independently associated with IPF. MIR was detected in 71% of the study group compared to 21% of controls (p < 0.001), and FIR, in 32.5% and 7.5%, respectively (p < 0.001). IPF was independently associated with inflammation of maternal origin (adjusted odds ratio (OR) 8.0, 95% CI 4.2–15.2, p < 0.001) and fetal origin (adjusted OR 5.2, 95% CI 2.07–13.4, p < 0.001). Neonatal outcome was similar in the two groups. Conclusions: Multiple vaginal examinations are a significant risk factor for the development of IPF. IPF at term is independently associated with placental inflammatory lesions.     

Thrombophilia is not associated with an increase in placental abnormalities in women with intra-uterine fetal death

BACKGROUND: The aim of this study was to investigate whether women with thrombophilia and intrauterine fetal death have a higher incidence of placental lesions as compared with those without thrombophilia. METHOD: In a case-control study comprising 50 women with an obstetrical history of intrauterine fetal death, placental histology comparison was made between those with thrombophilia and those without thrombophilia. RESULTS: Of the women who had an intrauterine fetal death, eight (16%) had a thrombophilia factor. There were no differences in birth weight, gestational age and parity or in placental volume and weight between the eight women with and the 42 women without thrombophilia. There was no statistically significant difference between placentas of the women with and those without thrombophilia. CONCLUSION: In a group of women who had an obstetrical history of intrauterine fetal death, those with thrombophilia do not have a difference in placental histological lesions compared with the women without a thrombophilia factor. Future thrombophilia research should be focused on placental bed specimens.     

Thrombophilia and pregnancy complications

OBJECTIVE: This systematic review examines the strength of the association between thrombophilia and recurrent pregnancy loss and other serious obstetric complications.Study design Electronic databases and manual bibliography searches were used to identify studies evaluating the association between thrombophilia and pregnancy loss, preeclampsia, fetal growth retardation, and placental abruption. RESULTS: Thrombophilic disorders are associated with an increased risk of fetal loss in the majority of case control and cohort studies. The risk is increased throughout pregnancy, but may be higher in the second and third trimester. The common pathologic finding of placental infarction suggests unexplained fetal loss may result from uteroplacental insufficiency and thrombosis. Thrombophilic disorders are not consistently associated with preeclampsia, fetal growth retardation, or placental abruption. Preliminary data suggest prophylactic anticoagulation may improve outcome in thrombophilic women with unexplained recurrent fetal loss. CONCLUSION: Women with thrombophilia have an increased risk of pregnancy loss and possibly other serious obstetric complications, although definition of the magnitude of risk will require prospective longitudinal studies. Preliminary data suggesting prophylactic anticoagulation may improve gestational outcome provide a rationale for prospective randomized trials in thrombophilic women with unexplained recurrent fetal loss.     

Thrombophilia and pregnancy loss

Thrombophilia is defined as a tendency to thrombosis. The association between specific thrombophilic defects--both inherited and acquired--and pregnancy loss is a rapidly developing field. However, apart from antiphospholipid antibodies (aPL), an acquired thrombophilic defect, the role of other defects in the haemostatic pathways remains to be established. In this invited review we discuss the recent advances in our understanding of aPL related pregnancy loss, the association between genetic thrombophilic mutations and pregnancy outcome and the role of whole blood haemostasis testing in the investigation of women with recurrent miscarriage.     

Preterm delivery: correlations of fetal growth and placental pathology.

The present study of 466 consecutive liveborn preterm singleton deliveries included 238 cases of spontaneous preterm labor and delivery, 175 cases with premature rupture of membranes, 13 cases of nonhypertensive abruption, 18 cases of preeclampsia, and 22 cases of placenta previa. Placental infarction, chronic villitis, and decidual pathologic processes showed different associations with fetal growth, depending on the clinical circumstances. Placental infarction was associated with decreased growth in all groups except placenta previa; in cases of placenta previa, placental infarction was associated with heavier infants. Chronic villitis was related to decreased growth in spontaneous rupture of membranes and preterm labor cases but was related to increased growth in cases of preeclampsia.