Corangiosis placentaria como causa de mortalidad perinatal / Placental chorangiosis can be a fetalnewborn death cause

La corangiosis placentaria (hipervascularidad vellosa capilar placentaria) ocurre raramente en las gestaciones normales; es un cambio placentario a nivel del capilar velloso y se relaciona con hipoxia fetal. La corangiosis placentaria se ha asociado con diabetes gestacional, maduración vellosa retrasada, preeclampsia, infección placentaria y con importantes formas de trisomías (21, 18 y 13). También se ha asociado con nudos de cordón y abruptio placentae, de modo que la asociación de estas condiciones obstétricas aparentemente agudas con corangiosis placentaria puede ser la causa de muertes de recién nacidos (RN) que previamente fueron asumidas como resultado de una deficiente dirección del parto. Por ecografía se aprecia un aumento en el grosor placentario o hiperplacentosis que traduce el edema del órgano. Se hará el diagnóstico diferencial con el corioangioma, la corangiomatosis y con la trombosis subcorial masiva. Dado que la corangiosis es un importante signo de morbimortalidad perinatal, se enfatiza la importancia de un examen completo de la placenta en los casos en que se detecte alguna anomalía por ecografía y en todos los casos de mortalidad perinatal. Se presenta aquí un caso de corangiosis placentaria con mal resultado perinatal (muerte fetal anteparto extraclínica en la semana 36 de gestación)

The placental chorangiosis (placental villous capillary hipervascularity) happens rarely in normal gestations. It is a placental change at nevel of the villous capillary and it is related to fetal hypoxia. The placental chorangiosis has been associated with maternal diabetes, delayed villous maturation and chronic villitis, toxemia of pregnancy, placental infection and with important form to trisomies (21,18 y 13). It has also been associated with nuchal cord and placental abruption, so that the association of apparent acute obstetrical conditions with placental chorangiosis may be the cause of fetal-newborn deaths that were previously assumed to be issues of labor management. The chorangiosis is associated to an increase in the placental thickness, or hyperplacentosis, detectable by echography. The increase in the placental thickness translates the edema of the organ. The diagnosis differential of the chorangiosis will be necessary to do it with chorioangioma, chorangiomatosis and massive subcorial thrombosis. The chorangiosis would be an important sign of neonatal morbidity and mortality; by this, it has great importance the histological study of the placenta in the cases that present some anomaly and in all the cases of perinatal mortality. A case of chorangiosis with badly perinatal result appears here (extraclinical fetal death antepartum, in week 36 of gestation)

Chronic villitis in untreated neonatal alloimmune thrombocytopenia: an etiology for severe early intrauterine growth restriction and the effect of intravenous immunoglobulin therapy.

OBJECTIVE: The objective of the study was to examine placental histopathology in intravenous immunoglobulin-treated and untreated neonatal alloimmune thrombocytopenia and correlate pathological findings with clinical outcomes. STUDY DESIGN: Placentas from 14 neonatal alloimmune thrombocytopenia-affected pregnancies were identified. Maternal antepartum treatment with intravenous immunoglobulin and pregnancy outcomes were abstracted from medical records. Placental histopathology and clinical outcomes were compared between intravenous immunoglobulin and no intravenous immunoglobulin treatment groups using Fisher's exact test. One subject, treated only after an intracranial hemorrhage (ICH) was diagnosed, was excluded from the analysis. P < .05 was considered significant. RESULTS: Untreated pregnancies demonstrated a lymphoplasmacytic chronic villitis not seen in the intravenous immunoglobulin-treated pregnancies (P = .005). Intrauterine growth restriction and intrauterine fetal demise occurred as frequently as ICH in the untreated group. No ICH, intrauterine growth restriction, or intrauterine fetal demises occurred in the treated group, although the P value was not significant. CONCLUSION: Chronic villitis is frequently manifest in neonatal alloimmune thrombocytopenia, with intravenous immunoglobulin alleviating this inflammatory immunologic response. We suspect a more universal role for the maternal antibody, such as fetal endothelial cell damage, in the sequelae of neonatal alloimmune thrombocytopenia.

Fatal placental subinvolution in a captive capybara (Hydrochaeris hydrochaeris, Order Rodentia).

An adult, captive-born female capybara died of systemic thrombosis and hemoperitoneum associated with placental subinvolution. Grossly, the uterus was enlarged, segmentally thickened, and associated with a large blood clot in the abdominal cavity. There was hemometra and a large ovoid mass in each uterine horn weakly adhered to the endometrium, and the right uterine horn wall had a small perforation over the mass. The mesometrial veins were markedly dilated due to thrombosis and occasionally perforated. Histologically, the uterine masses consisted of partly necrotic placental and subplacental tissue. The uterine wall surrounding the masses had full-thickness coagulative necrosis of the myometrium and diffuse endometrial ulceration with abundant syncytiotrophoblast-like cells within capillaries. Vascular lesions in the uterus and mesometrium consisted of mural invasion by cytotrophoblast and syncytiotrophoblast-like cells, thrombosis, fibrinoid necrosis, and/or heterophilic vasculitis. This is the first report of placental subinvolution in capybaras or any rodent species, to the authors' knowledge.

Predictors of vaginal bleeding during the first two trimesters of pregnancy.

This study evaluates maternal age, race, cigarette smoking, prior spontaneous abortion, prior induced abortion, and prior preterm birth in relation to vaginal bleeding during the first two trimesters of pregnancy. Information on vaginal bleeding and predictors came from the Pregnancy, Infection, and Nutrition Study, which enrolled 2806 pregnant women at 24-29 weeks' gestation during 1995-2000 in central North Carolina, USA. Generalised estimating equations were applied to take into account repeated episodes of vaginal bleeding during pregnancy. Women with advanced maternal age and passive smoking exposure were more likely to experience more intense vaginal bleeding during pregnancy, as were women with prior preterm birth. More intense bleeding was also more likely to be reported among women with multiple prior spontaneous abortions or multiple prior induced abortions, but not among women with a single prior spontaneous or induced abortion. The combination of prior spontaneous and induced abortion showed a dose-response association with the occurrence of vaginal bleeding during pregnancy.

Histologic placental lesions in women with recurrent preterm delivery.

BACKGROUND: The aim of this study was to evaluate whether particular placental histopathology lesions are associated with recurrent preterm birth. METHODS: We analyzed a database of 413 consecutive singleton pregnancies delivered at <32 weeks with past reproductive history available. After the exclusion of nulliparous women, the pregnancies were divided according to the obstetrical history into group 1 (n = 328), women without prior preterm delivery (PTD); group 2 (n = 49), women with one prior preterm childbirth; and group 3 (n = 36), women with > or =2 prior preterm deliveries. Demographic and clinical variables were compared among the three groups by using Kruskal-Wallis test and chi-square test for trend. Finally, the individual placental lesions (i.e. 42 lesions of acute or chronic inflammation, uteroplacental vascular pathology, and intraplacental villous lesions) were correlated with the number of prior preterm deliveries by using regression analysis. A two-tailed P < 0.05 was considered significant. RESULTS: No differences were found among the three groups in demographic or clinical variables. Regression analysis of scored placental lesions corrected for gestational age at delivery showed that the number of prior preterm deliveries was correlated only with chronic marginating choriodeciduitis (correlation coefficient = 0.13; P = 0.01) and acute choriodeciduitis (correlation coefficient = 0.14; P = 0.008). CONCLUSIONS: Among women delivered at <32 weeks, those with prior preterm birth have histologic findings compatible with acute or chronic inflammatory involvement of the uterine cavity, suggesting that a prepregnancy endometrial infection rather than an ascending intrapregnancy pathway may be responsible for some recurrences of PTD.

Pontosubicular apoptosis ("necrosis") in human neonates with intrauterine growth retardation and placental infarction.

In a previous study of 37 autopsied stillbirths with non-dysmorphic intrauterine growth retardation (IUGR), 26 cases were associated with placental infarction, a morphologic marker of uteroplacental insufficiency. Nine of the 26 cases with both IUGR and placental infarction, where archival tissue was available, had grey matter ischaemic lesions that were subsequently identified as "pontosubicular necrosis". This lesion is now regarded as a localized form of apoptosis. A further eight third trimester stillbirth cases with both IUGR and placental infarction were ascertained prospectively. Sixteen of these 17 cases showed pontosubicular apoptosis, identified morphologically and verified using activated caspase-3 and TUNEL. Five of the 17 cases showed apoptosis in the frontal or temporal cortex as well. In this current study, pontosubicular apoptosis was strongly associated with IUGR and placental infarction in third trimester stillborns, suggesting that uteroplacental insufficiency leading to chronic fetal hypoxaemia may cause cerebral apoptosis.

Stillbirths with placental hemorrhagic endovasculitis: a morphologic assessment with clinical implications.

CONTEXT: Hemorrhagic endovasculitis (HEV) is a vasodisruptive alteration affecting fetal-placental blood vessels of all calibers. Hemorrhagic endovasculitis is found in association with stillbirth and abnormalities of growth and development in livebirths. The role of HEV in the pathogenesis of these conditions is not known. OBJECTIVE: To further understand these events, we compare clinicopathologic features of HEV-affected placentas from stillbirths with those from livebirth pregnancies. Additionally, we assess the relationship of morphologic forms of HEV to clinical events and time of fetal death in utero and evaluate the significance of extensive versus localized HEV lesions in placentas of stillbirths. DESIGN: We reviewed the clinical records and slides from 119 stillbirths with placentas affected by HEV classified above a specified severity level (cases) and 119 matched stillbirths with placentas not affected by HEV (controls). A subset of 21 stillbirth placentas exhibiting focal HEV lesions was similarly evaluated. Slides were graded for HEV, villitis of unknown etiology, chorionic thrombi, villous fibrosis, erythroblastosis, and lesions indicative of maternal hypertension. Hemorrhagic endovasculitis was subcategorized into active, bland, and healed forms and clustered capillary lesions (hemorrhagic villitis). Focal, segmental, and diffuse patterns of villous fibrosis were delineated. Interlesional relationships were established by matching HEV severity indices with severity indices of co-existing lesions. Timing of fetal death was determined by published criteria. Data were analyzed for significance using chi2 and t tests. Results were compared with published analyses of livebirths with placental HEV. RESULTS: Lesions occurring with significant frequency in HEV-affected (case) placentas include villitis of unknown etiology, chorionic thrombi, villous fibrosis, erythroblastosis, and meconium staining. Interlesional relationships were evident between HEV and villous fibrosis, villitis of unknown etiology, and chorionic thrombi. Growth restriction was more common in case versus control infants (P = .02). A segmental pattern of villous fibrosis predominated in cases versus controls and within the case group (P < .001). Time to delivery after fetal death was longer in cases than controls. Active-vasodestructive forms of HEV correlate with shorter intervals of intrauterine retention, whereas bland forms correlate with longer intervals (P = .04). Placentas with focal HEV were associated with coexisting chorionic thrombi and villous fibrosis but not with fetal growth restriction. CONCLUSIONS: Patterns of interlesional interplay are similar in HEV-affected placentas of livebirths and stillbirths. This suggests that the pathogenesis of infant morbidity and mortality is similar in both groups. Active-vasodestructive forms of HEV may precede whereas bland forms may follow intrauterine demise. The segmental pattern of villous fibrosis and high incidences of growth restriction, erythroblastosis, and meconium in cases suggests a chronicity of adverse intrauterine events that may precede fetal loss. Stillbirths with focal HEV lesions are probably not at risk.

The antiphospholipid syndrome in pregnant rabbits and their offspring. Neuropathological aspects.

OBJECTIVE: Although the obstetric consequences of antiphospholipid syndrome (APS) in pregnant rabbits have been described, there are no data on the serological and neuropathological aspects of the syndrome in their offspring. It would also be interesting to recognize whether the CNS abnormalities in rabbit fetuses relate to placental damage or depend on the antiphospholipid antibodies, transmitted from the pregnant animal through the placenta to the fetal serum. MATERIAL AND METHODS: A post-mortem neuropathological examination was done on 36 adult female New Zealand rabbits, and their offspring (100 fetuses). The material was divided into 4 groups: Group I--26 pregnant rabbits with experimental APS, Group IC 10--pregnant rabbits without APS (control group I), Group II--64 fetuses derived from animals included in Group I, and Group IIC--36 fetuses derived from individuals included in Group IC (control group II). The platelet count, activated partial thromboplastin time (APTT), antiplatelet antibodies in serum and coated on the platelets were evaluated to identify the APS in adult rabbits and their offspring. RESULTS: A significantly higher number of fetuses demonstrating weaker vitality and shorter survival time was observed in Group II. The percentage of dead and reabsorbed fetuses was also considerably higher in Group II. The serum markers of APS occurred both in Group I and II while the neuropathological evidences of APS: the thrombo-necrotic and inflammatory changes were found exclusively in APS pregnant animals. Moreover, cytoarchitecture of the fetal brains was intact. There were no disturbances in neuronal migration and abnormalities of cytodifferentiation. CONCLUSIONS: 1. The antiphospholipid syndrome in pregnant rabbits results in serological markers of the syndrome in their offspring. 2. The central nervous system of fetuses delivered from pregnant rabbits with the antiphospholipid syndrome remains intact despite the serological markers of the syndrome in fetus circulation. 3. The miscarriages in pregnant rabbits with the antiphospholipid syndrome depend rather on placental pathology related to the syndrome than on the syndrome per se transmitted from adult females to fetal circulation.

Placental mesenchymal dysplasia associated with fetal aneuploidy.

OBJECTIVES: To describe three cases of placental mesenchymal dysplasia (PMD) associated with abnormal karyotype and review the cases reported in the literature. METHODS: The cases were retrieved from the files of three different institutions. A search of the English language literature was performed using Medline database. RESULTS: Placental abnormalities suggestive of molar changes were seen on the prenatal ultrasound scans. Histologically, the cases had large, hydropic stem villi with myxomatous stroma, cistern formation and 'chorangiomatoid' changes. The placental and fetal karyotypes identified were trisomy 13 (47,XX,t(1:13)(q32;q32)+ 13); Klinefelter syndrome (47,XXY) and triploidy (69,XXX). Including these 3 cases, of 66 reported cases, 51 (78%) were female and 14 (22%) male (ratio 3.6:1); the karyotype was normal in 32/36 (89%) and abnormal in 4/36 (11%); Beckwith-Wiedemann syndrome was confirmed or suspected in 15/66 (23%). Excluding termination of pregnancies, intrauterine death occurred in 18/54 (33%) cases. CONCLUSION: Molar ultrasonographic appearances associated with increased maternal serum alpha-fetoprotein but normal, or slightly elevated, levels of ss human Chorionic Gonadotrophin should raise the clinical suspicion of PMD. The diagnosis of this condition should not be disregarded when an abnormal fetus and/or an abnormal karyotype are demonstrated.

Severe fetal placental vascular lesions in term infants with neurologic impairment.

OBJECTIVE: This study tests the hypothesis that placental disease can identify antepartum processes that either progress into the intrapartum period or predispose to intrapartum brain injury. STUDY DESIGN: Lesions that affect large fetal vessels were compared in the placentas of 125 neurologically impaired term infants who were the focus of clinical negligence litigation and 250 consecutive singleton deliveries of >/=36 weeks of gestation. RESULTS: One or more of 4 severe placental fetal vascular lesions (fetal thrombotic vasculopathy, chronic villitis with obliterative fetal vasculopathy, chorioamnionitis with severe fetal vasculitis, and meconium-associated fetal vascular necrosis) were found in 51% of index cases versus 10% of the comparison group ( P <.0001). Prevalence of these lesions in the 64 infants with cerebral palsy was 52% ( P <.0001). CONCLUSION: Severe fetal placental vascular lesions are correlated highly with neurologic impairment and cerebral palsy. Their nature, duration, and anatomic location make them strong candidates for the antepartum processes that place fetuses at risk for brain injury during the intrapartum period.

[Thrombophilias and vascular placental pathology. A survey of the literature]. / Thrombophilies et pathologies vasculaires placentaires. Revue de la littérature.

PURPOSE: Hereditary thrombophilia as antiphospholipid syndrome (APS) may represent a new risk factor for placental vascular diseases. CURRENT KNOWLEDGE AND KEY POINTS: General screening for biological abnormalities related to thrombophilia is poorly associated with placental vascular diseases and therefore, may be unwarranted. Women with an history of thrombotic diseases may be at risk for late fetal loss or preeclampsia. Adverse obstetric outcomes are particularly high despite anticoagulation regimens in patients with APS. A high frequency for biological abnormalities related to thrombophilia was detected in pregnancies complicated by late fetal loss in comparison with controls. However, no beneficial strategy prevention was clearly reported and therefore, a selective testing was actually debated for these patients. FUTURE PROSPECTS AND PROJECTS: Searching for acceptable treatment alternatives in patients with APS in order to reduce the high rate for pregnancy complications which may be persistent despite anticoagulation regimens. To determine by controlled studies the role for a prophylactic low molecular weight heparin regimens in patients with haemostatic abnormalities and previous pregnancy complications.

Spontaneous reversal of mirror syndrome in a twin pregnancy after a single fetal death.

The case report illustrates that pre-eclampsia like symptoms can arise as a consequence of pathological changes in a single feto-placental unit of a twin pregnancy and may resolve spontaneously when the cause is removed.

The protein C system in placental massive perivillous fibrin deposition.

Massive perivillous fibrin deposition (MPFD) is associated with intrauterine growth retardation and first-trimester and second-trimester spontaneous abortion. Histologically, villi near the maternal interface are completely surrounded by fibrinoid material. This work compared the expression of thrombomodulin (TM) and endothelial protein C receptor (EPCR) in early miscarriage specimens with and without MPFD. Ten specimens with a gestational age of 7-12 weeks (mean 10 weeks) and 10 age-matched miscarriage specimens lacking MPFD were sampled. Formalin-fixed paraffin-embedded sections were stained with monoclonal antibodies against TM and EPCR using an immunoperoxidase method. The slides were independently reviewed by two pathologists using a semiquantitative grading system. Among unaffected villi, there was no difference in staining for TM or EPCR in cases of massive perivillous fibrin deposition compared with the control group. In the MPFD cases, loss of membrane positivity was noted for both TM and EPCR at the junction between normal villous epithelium and villous epithelium with deposition of fibrin. This could imply an underlying defect of trophoblastic protein C activation. Alternatively, it may represent a degenerative change secondary to impedence of oxygen and nutrient supply to the trophoblastic epithelium.

Placenta percreta, rotura uterina e histerectomía obstétrica / Placenta percreta. Uterine perforation and obstetric hysterectomy

La placenta percreta es aquella cuya inserción alcanza la serosa o incluso penetra en la cavidad abdominal. Es una entidad poco frecuente, aunque su incidencia aumenta en los casos que se asocian a placenta previa y con el antecedente de cesárea. En nuestro caso clínico, presentamos a una paciente diagnosticada de placenta previa, con antecedentes de cesárea y útero bicorne a la que indicamos una cesárea urgente por riesgo de pérdida de bienestar fetal y en la cual se objetivó hemoperitoneo, placenta percreta y rotura uterina, por lo que se realizó una histerectomía abdominal total simple. La evolución materna y fetal fue satisfactoria (AU)

Placenta percreta causing acute abdomen in the second trimester of pregnancy.

Two cases of acute abdomen due to haemoperitoneum caused by placenta percreta in the second trimester are presented. Both had a history of previous lower segment caesarean section, a factor well-known to predispose the condition. However, the rarity of the condition, presenting in mid pregnancy makes diagnosis and management difficult. Optimum ways of management are discussed.

Placental infarcts, intervillous fibrin plaques, and intervillous thrombi: incidences, cooccurrences, and epidemiological associations.

The incidences, cooccurrences and epidemiological associations at term of the three common focal macroscopic placental lesions, infarcts, intervillous fibrin plaques (IVFP), and intervillous thrombi (IVT) were investigated as part of a population-based case-control study of small-for-gestational age (SGA) infants. Five hundred and nine placentas from women delivering SGA infants (10th percentile or less for gestational age) and 529 placentas from women delivering infants with birthweights appropriate for gestational age were examined using fixed protocols for identification of macroscopic lesions and microscopic diagnoses. One or more of these lesions were found in 280 placentas (28%), including infarcts in 150 (15%), IVFP in 132 (13%), and IVT in 64 (6%). Macroscopic misidentifications, particularly of IVFP as infarcts, emphasize the need for microscopic diagnoses. There were strong associations between the occurrence of any one type of lesion and cooccurrence of either of the other two, and these associations were site-dependent: between central (nonmarginal) infarcts and central IVFP (P = 0.0023); marginal infarcts and marginal IVFP (P < 0.0001); and between IVT (all central) and marginal infarcts (P < 0.0001) and marginal IVFP (P = 0.012). However, a study of associations between the incidences of placentas bearing each of the three lesions and 31 socio-demographic and pregnancy-related factors showed no associations in common. IVFP, an IVFP variant termed "labyrinthine," and IVT did not show any of the independent associations demonstrated between infarcts and SGA, pregnancy-induced hypertension, nonsmoking, age at first pregnancy, and ethnicity. IVFP had no significant associations, and IVT were associated only with male gender. The study has shown that IVFP and IVT do not share the important clinical associations demonstrated for infarcts, but has not identified the pathogenetic factor or factors responsible for the frequent cooccurrence of these lesions. The maternal thrombophilias may have such a role.

Placental fetal thrombotic vasculopathy is associated with neonatal encephalopathy.

Neonatal encephalopathy (NE) remains an important cause of morbidity and mortality in the term infant, and many cases have an antepartum, rather than an intrapartum, etiology. Chronic processes such as thrombosis result in changes in the placenta. We sought to determine whether histopathological examination of the placenta in cases of NE, focusing on these changes, could identify significant antenatal processes that are not recognized by clinical assessment alone. Infants born at term with NE were identified retrospectively over a 12-year period. Placental tissue from deliveries during the study period was available for reexamination. Controls were selected from a cohort of 1000 consecutive deliveries on which clinical and pathological data were collected as part of an earlier study. Bivariate and multivariate analyses of clinical and pathological factors for cases and controls were used to test for an independent association with NE. Clinical and placental data was collected on 93 cases of NE and 387 controls. The placental features of fetal thrombotic vasculopathy (FTV), funisitis (signifying a fetal response to infection), and accelerated villous maturation were independently associated with NE. Of the clinical factors studied, meconium-stained liquor and abnormal cardiotocograph were independently associated. There were no independently associated clinical antenatal factors. Placental features of infection, thrombosis, and disturbed uteroplacental flow are significant independent factors in the etiology of NE in this study. Acute and chronic features suggest that NE may result from acute stress in an already compromised infant. The absence of significant clinical antenatal factors supports the value of placental examination in the investigation of infants with NE.

Fetal death: comparative aspects in large domestic animals.

Although the majority of pregnancy failures occur during the embryonic period, reports indicate that approximately 5% of detected pregnancies are lost during the fetal period, underlining the fact that fetal death is a substantial cause of economic loss. However, examination for fetal development or death during pregnancy is not performed routinely in domestic animals, and reference curves for normal fetal growth are, therefore, scarce. In this paper, the numerous possible causes of fetal death are reviewed briefly, with emphasis on the role of placental problems in fetal death and impaired fetal viability. In this respect, the role of placental insufficiency as a cause of pregnancy loss in twin pregnancies in monotocous species is well known, whereas the abnormal placental development leading to retarded fetal growth during pregnancies in recipients of in vitro produced (IVP) or nuclear transfer (NT) embryos has been less extensively documented. Fetal viability or death can be evaluated using hormonal, chemical and ultrasonographic parameters. For example, the viability of the feto-placental unit can be examined by measuring maternal plasma concentrations of oestrone sulphate or the placental proteins, including pregnancy-associated glycoprotein (PAG) and pregnancy-specific protein B-60 (PSPB-60). Low concentrations of any of these three indicate either no pregnancy, or if pregnancy was confirmed earlier, fetal death and abnormally high or low levels can indicate fetal abnormality. Ultrasound can be used to examine the fetal heart rate (FHR), the incidence of fetal movements (FM), the appearance of fetal fluids and the development of the fetus and placenta. However, although abnormal FHRs have been correlated to subsequent fetal death, it is important to remember that there is a large physiological variation in FHR at the end of gestation, due to different behavioural states and differences in FM patterns. Although monitoring fetal viability and death using hormonal and ultrasonographic evaluations is possible during pregnancy in domestic animals, there is considerable physiological variations in the 'normal' values. Therefore, suitable combinations of tests need to be identified and more accurate reference values generated before such approaches can be considered reliable for monitoring the status of individual fetuses.