Bloody amniotic fluid during labor – Prevalence, and association with placental abruption, neonatal morbidity, and adverse pregnancy outcomes

Author(s):  
Ohad Gluck ◽  
Michal Kovo ◽  
Daniel Tairy ◽  
Giulia Barda ◽  
Jacob Bar ◽  
...  
2022 ◽  
Vol 226 (1) ◽  
pp. S314-S315
Author(s):  
Alexandria Kraus ◽  
Lauren Kucirka ◽  
Hina Shah ◽  
Juan Prieto ◽  
Nancy Chescheir ◽  
...  

2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Samprikta Manna ◽  
Cathal McCarthy ◽  
Fergus P. McCarthy

Preeclampsia is a multisystemic pregnancy disorder and a major cause of maternal and neonatal morbidity and mortality worldwide. The exact pathophysiology of preeclampsia remains unclear; however, it is speculated that the various pathologies can be attributed to impaired vascular remodelling and elevated oxidative stress within the placenta. Oxidative stress plays a key role in cell ageing, and the persistent presence of elevated oxidative stress precipitates cellular senescence and mitochondrial dysfunction, resulting in premature ageing of the placenta. Premature ageing of the placenta is associated with placental insufficiency, which reduces the functional capacity of this critical organ and leads to abnormal pregnancy outcomes. The changes brought about by oxidative insults are irreversible and often lead to deleterious modifications in macromolecules such as lipids and proteins, DNA mutations, and alteration of mitochondrial functioning and dynamics. In this review, we have summarized the current knowledge of placental ageing in the aetiology of adverse pregnancy outcomes and discussed the hallmarks of ageing which could be potential markers for preeclampsia and fetal growth restriction.


2017 ◽  
Vol 217 (4) ◽  
pp. 478.e1-478.e8 ◽  
Author(s):  
Torri D. Metz ◽  
Amanda A. Allshouse ◽  
Carol J. Hogue ◽  
Robert L. Goldenberg ◽  
Donald J. Dudley ◽  
...  

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 1819-1819
Author(s):  
Karim Abou-Nassar ◽  
Marc Carrier ◽  
Marc Rodger

Abstract BACKGROUND: The Sapporo criteria for the diagnosis of the antiphospholipid syndrome (APS) are based on the presence of antiphospholipid antibodies (APLA) and clinical criteria. Although pre-eclampsia, intra-uterine growth restriction (IUGR), late fetal loss and placental abruption, collectively termed “placenta mediated complications”, are recognized as clinical criteria for the APS, their association with APLA remains controversial. OBJECTIVE: This review was conducted to evaluate the association between APLA (anticardiolipin antibodies, lupus anticoagulant, anti B2 glycoprotein 1 antibodies) and placenta mediated complications in untreated women without autoimmune diseases. METHODS: We performed a systematic review of published case-control, cohort and cross sectional studies using MEDLINE (1975 to October week 2 2007), EMBASE 16 (1980 to 2007 week 42) and all EBM Reviews (3rd quarter of 2007). For eligible studies, the rates of adverse pregnancy outcomes were compared between patients with and without specific APLA. Pooled odds ratios with 95% CI were generated using random-effects models. RESULTS: Our search strategy identified 1204 potentially relevant studies. Twenty five were included in the final analysis. Results are outlined in table 1. CONCLUSION: The association between various APLA and pregnancy complications is for the most part weak and inconsistent. There is currently insufficient data to support a significant link between anti-B2 glycoprotein 1 antibodies and pregnancy morbidity. Caution should be used when establishing a diagnosis of APS based on the presence of any APLA, particularly anti-B2 glycoprotein 1 antibodies, in the setting of late pregnancy complications. Table 1 Association Between APLA and Adverse Pregnancy Outcomes Pre-eclampsia OR (95%CI) # studies / participants IUGR OR (95%CI) # studies / participants Placental abruption OR (95%CI) # studies / participants Late fetal loss OR (95%CI) # studies / participants LA: Lupus anticoagulant; aCL: Anticardiolipin antibodies; Anti-B2 GP1 antibodies: Anti-B2 glycoprotein 1 antibodies italic characters indicate statistically significant associations LA 2.88 (1.42, 5.87)
 11 / 6085 3.51 (1.38, 8.93)
 4 / 3232 0.78 (0.13, 4.80)
 2 / 226 3.56 (0.12, 106.05)
 3 / 3870 aCL (IgG/IgM) 1.71 (1.09, 2.70)
 21 / 9722 2.31 (0.74, 7.17)
 6 / 5753 1.35 (0.45, 4.02)
 4 / 1274 3.86 (1.14, 13.07)
 7 / 5963 aCL IgG 1.65 (0.84, 3.22)
 15 / 3627 6.16 (2.50, 15.18)
 2 / 1006 1.87 (0.21, 16.83)
 2 / 500 10.06 (0.88, 114.96)
 2 / 1006 aCL IgM 1.36 (0.93, 1.97)
 13 / 5397 0.75 (0.19, 2.93)
 2 / 3002 0.96 (0.24, 3.85)
 2 / 500 1.37 (0.42, 4.46)
 3 / 3212 anti- B2GP1 (IgG/IgM) 2.97 (0.47, 18.69)
 4 / 2225 20.03 (4.59, 87.43)
 1 / 1108 2.64 (0.14, 50.63)
 1 / 510 6.74 (0.24, 191.23)
 3 / 1828 anti- B2GP1 IgG 0.87 (0.38, 2.01)
 2 / 607 N/A
 0 / 0 N/A
 0 / 0 0.52 (0.02, 11.02)
 1 / 212 anti- B2GP1 IgM 0.37 (0.16, 0.85)
 1 / 400 N/A
 0 / 0 N/A
 0 / 0 1.32 (0.24, 7.42)
 1 / 210


Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 4003-4003 ◽  
Author(s):  
Karim Abou-Nassar ◽  
Mark Walker ◽  
Shi-Wu Wen ◽  
Marisa Freedman ◽  
Steve Doucette ◽  
...  

Abstract Abstract 4003 Poster Board III-939 BACKGROUND The Sapporo criteria include anti-β2 glycoprotein1 (anti-B2GP1) antibodies among antiphospholipid antibodies used to diagnose the antiphospholipid syndrome (APS). Although pre-eclampsia, intra-uterine growth restriction (IUGR), late fetal loss and placental abruption, collectively termed “placenta mediated complications”, are recognized as clinical criteria for the APS, strong evidence to support their association with anti-B2GP1 antibodies is lacking. OBJECTIVE This study aims to assess the association between anti-B2GP1 antibodies and placenta mediated complications. METHODS We performed a nested case-control study from a prospective cohort of 7000 mother baby pairs whereby women and their fetuses were recruited between 12-20 weeks gestation. Five hundred cases were randomly selected amongst women who experienced one of the following adjudicated adverse pregnancy outcomes: pre-eclampsia (BP ≥140/90 with proteinuria), placental abruption (antepartum bleeding with objective evidence of placental thrombus), late pregnancy loss (≥ 12 weeks gestation) and IUGR (birth weight less than the 10th percentile of normal population). Random selection of 500 controls was performed amongst women who did not experience the above mentioned adverse pregnancy outcomes. Stored blood samples were analyzed for the presence of anti-B2GP1 IgG and IgM antibodies by enzyme-linked immunosorbent assay. Titers ≥ than 20 G or M units were considered positive. This study has an 80% power to detect an odds ratio of 2.25 at the 5% level of significance based on an estimated 4 % prevalence of anti-B2GP1 IgG and/or IgM antibodies in titers ≥ 20 G/M units in our cohort of pregnant women. RESULTS Anti-B2GP1 IgG and/or IgM antibodies in titers ≥ 20 G/M units were present in 24/497 (4.8%) controls and 33/503 (6.6%) cases. The presence of anti-B2GP1 IgG and/or IgM in titers ' 20 G/M units was not significantly associated with a composite outcome of pre-eclampsia, IUGR, late fetal loss and placental abruption (OR 1.38; 95%CI 0.8-2.37 p=0.18). This combination of antibodies and titers only demonstrated a weak association with IUGR (OR 1.86; 95%CI 1.09-3.18 p=0.02). The presence of anti-B2GP1 IgG and/or IgM antibodies in titers ≥ 40 G/M units also failed to show an association with a composite outcome of pre-eclampsia, IUGR, late fetal loss and placental abruption (OR 2.65; 95%CI 0.7-10.04 p=0.15). However, stronger associations were observed with placental abruption (OR 4.87; 95%CI 1.02-23.25 p=0.047) and IUGR (OR 3.53; 95%CI 1.03-12.15 p=0.045). CONCLUSION The presence of anti-B2GP1 IgG and/or IgM antibodies in titers 20 ≥ G/M units during pregnancy is only associated with an increased risk of IUGR. Anti-B2GP1 antibodies in titers ' 40 G/M units, as suggested in the Sapporo diagnostic criteria for the APS, are associated with IUGR and placental abruption and possibly other placenta mediated complications. Larger adequately powered studies will be required to provide definitive answers. Disclosures: No relevant conflicts of interest to declare.


2017 ◽  
Vol 4 (12) ◽  
pp. 1832 ◽  
Author(s):  
Nasibeh Roozbeh ◽  
Farzaneh Banihashemi ◽  
Mitra Mehraban ◽  
Fatemeh Abdi

Background: Thrombophilia is an inherited or acquired predisposition for development of thrombosis. One of the common thrombophilia polymorphisms is Factor V Leiden (FVL) mutation, which may contribute to negative pregnancy outcomes. This systematic review study seeks to describe the potential effects of factor V Leiden mutation on adverse pregnancy outcomes. Methods: Pubmed, Embase, ISI Web of Sciences, Scopus, ScienceDirect, Proquest and Google Scholar, for articles published during 1996-2017. Articles were evaluated by the Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) checklist for standard reporting. As well, the quality of studies was assessed by the Newcastle-Ottawa Scale (NOS). Results: A total of 14 studies were eligible based on the inclusion criteria. The papers were scored by the STROBE checklist. The range of STROBE score was 15-20. Only 37.5% of the studies confirmed the relationship between fetal loss and FVL. The effect of FVL mutation on spontaneous abortions and In Vitro Fertilization (IVF) failures was demonstrated in all the studies. In the reviewed studies, there was no observed relationship between FVL mutation with intrauterine growth restriction (IUGR), preeclampsia, placental abruption or small for gestational age (SGA). Conclusion: The reviewed studies showed an unclear association between FVL mutation and stillbirth, IUGR, preeclampsia, or placental abruption. The exact effects of hereditary thrombophilia on pregnancy outcome is also still controversial. However, FVL mutation appeared to have an effect on spontaneous abortions and IVF failures. Therefore, screening patients for thrombophilic polymorphisms might be helpful.


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