Download Pathways To Pregnancy And Parturition 3rd Edition Zip Full
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Maternity care has emerged as a key issue in the current policy debates about the future of the Affordable Care Act (ACA) and Medicaid restructuring. While the inclusion of maternity care as an essential health benefit has been important to many women who gained private coverage because of the ACA coverage expansion, Medicaid has been the primary funding source for perinatal and maternal services for low-income women in the US for several decades. In 2010, Medicaid financed nearly 45% of all births in the United States.1 By federal law, all states provide Medicaid coverage for pregnancy-related services to pregnant women with incomes up to 133% of the federal poverty level (FPL) and cover them up to 60 days postpartum. All states must provide some level of maternity care free of cost-sharing to eligible pregnant women, although there are state level variations in the scope and type of services that states offer. In addition, many states extend eligibility to pregnant women with incomes considerably higher than this threshold. The ACA broadened Medicaid eligibility by allowing states to extend continuous Medicaid eligibility in 2014 to individuals with family income at or below 138% FPL and 31 states and the District of Columbia (DC) have adopted Medicaid expansion programs which extended coverage for new mothers beyond the postpartum period, where historically many women lost coverage. 2
Because there is no formal federal definition of what services states must cover for pregnant women beyond inpatient and outpatient hospital care, states have considerable discretion to determine the specific scope of maternity care benefits. While the ACA also does not define maternity benefits, states that have expanded Medicaid eligibility under the ACA must cover all preventive services recommended by the United States Preventive Services Task Force (USPSTF) for beneficiaries that qualify as a result of the ACA expansion. These now include many pregnancy-related services, such as prenatal screenings, folic acid supplements, and breastfeeding supports for those who qualify for Medicaid as a result of the expansion. This coverage requirement, however, does not apply to any of the Medicaid eligibility pathways that were available prior to the ACA (i.e., for parents or pregnant women). As a result, there is leeway for states to vary coverage standards for different Medicaid eligibility pathways (e.g. traditional Medicaid available prior to the ACA, ACA Medicaid expansion, or pregnancy-related eligibility).
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Prenatal care services monitor the progress of a pregnancy and identify and address potential problems before they become serious for either the mother or baby. Routine prenatal care encompasses a variety of services, including provider counseling, assessment of fetal development, genetic screening and testing, prenatal vitamins that contain folic acid and other nutrients, and ultrasounds, which provide important information about the progress of the pregnancy.
There are a variety of support services that can aid pregnant and postpartum women with pregnancy, delivery, and child rearing and improve birth outcomes. These include educational classes on childbirth and infant care, transportation to appointments, and home visits during or after pregnancy to assist with basic medical care, counseling on healthy behaviors, and in-person infant care assistance.
The analysis of state responses to this survey found that overall most states cover a broad range of perinatal services in their full scope traditional Medicaid program, under full scope ACA Medicaid expansion, and pregnancy-related eligibility pathways. Most, but not all, of the 41 surveyed states report that they cover basic prenatal services such as ultrasounds and vitamins, prenatal genetic testing, home visits, delivery in birth centers, postpartum visits, and breast pumps for nursing mothers. Many states recognize that these services are critical to improving birth outcomes. Coverage for services that help women and their families care for their children after delivery, such as childbirth and parenting classes, breastfeeding education and lactation consultation is less common (Table 1). Only half of reporting states cover home births, and very few states cover doula supports despite research suggesting that this assistance results in better health outcomes.3 While coverage requirements differ between eligibility pathways, in general, there is strong alignment within states across the various pathways.
The Medicaid program has a long history and excellent record of providing coverage for low-income pregnant women, with nearly half of all births nationwide provided through the program. Regardless of the outcome of current debates over the future of Medicaid or the ACA, the millions of low-income pregnant women that are served by Medicaid will continue to need to have access to coverage that includes the broad range of pregnancy-related services that help assure healthy maternal and infant outcomes.
Doulas educate mothers to be healthy and have healthy babies, and empower them to confidently make some of the most important decisions of their lives. A State-Certified Doula is a trained, community-based nonmedical professional who provides continuous physical, emotional, and informational support to a pregnant person. They will continue support throughout pregnancy, at labor and delivery and continue support after pregnancy period or during the period up to one year after pregnancy. A Virginia State-Certified Doula must be approved by the Virginia Certification Board (VCB) .
It is well documented that maternal exposure to second-hand smoke (SHS) during pregnancy causes low birth weight (LBW), but its mechanism remains unknown. This study explored the potential pathways. We enrolled 195 pregnant women who delivered full-term LBW newborns and 195 who delivered full-term normal birth weight newborns as the controls. After controlling for maternal age, education level, family income, pre-pregnant body mass index, newborn gender and gestational age, logistic regression analysis revealed that LBW was significantly and positively associated with maternal exposure to SHS during pregnancy, lower placental weight, TNF-α and IL-1β and that SHS exposure was significantly associated with lower placental weight, TNF-α and IL-1β. Structural equation modelling identified two plausible pathways by which maternal exposure to SHS during pregnancy might cause LBW. First, SHS exposure induced the elevation of TNF-α, which might directly increase the risk of LBW by transmission across the placenta. Second, SHS exposure first increased maternal secretion of IL-1β and TNF-α, which then triggered the secretion of VCAM-1; both TNF-α and VCAM-1 were significantly associated with lower placental weight, thus increasing the risk of LBW. In conclusion, maternal exposure to SHS during pregnancy may lead to LBW through the potential pathways of maternal inflammation and lower placental weight.
The aforementioned hypothesis is suggested by the following strands of evidence. First, SHS exposure leads to abnormal levels of inflammatory markers in different populations8,9. Second, the elevated maternal inflammatory markers are independently related to LBW10 and mediate the associations between periodontal disease11, maternal sleep disturbances during pregnancy12, maternal pre-pregnancy body mass index (BMI)13 and LBW. Third, the placenta is associated with birth weight and IUGR14,15,16. Fourth, maternal smoking during pregnancy impairs the structure and functioning of the placenta17. Fifth, placental weight partially mediates the effects of prenatal factors such as pre-pregnancy obesity, gestational diabetes mellitus and excessive gestational weight gain on foetal growth18. Sixth, abnormal inflammatory markers have been found in the placentas of LBW cases19.
To the best of our knowledge, there is no research that links the above evidence together to explore the plausible mechanisms. As such, this study aimed to explore the potential pathways that integrate maternal inflammation and the placenta, which might explain the mechanism by which maternal exposure to SHS during pregnancy leads to LBW.
This study tested the hypothesis that maternal SHS exposure during pregnancy leads to full-term LBW through maternal inflammation and lower placental weight. The SEM results showed that maternal exposure to SHS during pregnancy initially induced maternal inflammation by increasing the secretion of IL-1β and TNF-α, which then triggered the secretion of IL-6, CRP and VCAM-1; both TNF-α and VCAM-1 caused a decrease in placental weight; and eventually, TNF-α and the damaged placenta increased the risk of full-term LBW.
Previous studies have reported inconsistent associations between SHS exposure and the six measured inflammatory markers in our study. For example, two studies of male workers reported that SHS exposure was significantly associated with elevated serum CRP9,20, while two further studies in adults8,21 and one in adolescents22 found a non-significant relationship between SHS exposure and serum CRP. Our study showed an insignificant association between maternal SHS exposure during pregnancy and maternal serum CRP levels. Regarding the associations between SHS exposure and three pro-inflammatory markers, IL-1β, IL-6 and TNF-α, Wilson et al. found that healthy children exposed to SHS had lower serum concentrations of IL-1β than those without SHS exposure23, but an inverse association was observed in adults24 and an insignificant association in adolescents was reported by Matsunaga et al.22. Five studies found that SHS exposure had no significant effect on serum IL-6 in adolescents22,23 and adults9,21,24, while a study in the elderly reported a significant association between SHS and elevated serum IL-6 levels25. An insignificant association between SHS exposure and serum TNF-α was reported by four studies, two in adolescents22,23 and two in adults9,24 and a positive association was reported by another study in adults24. Our study found that maternal exposure to SHS during pregnancy was significantly associated with elevated serum levels of TNF-α and IL-1β but not IL-6. There is little information on the relationship between SHS exposure and serum VCAM-1. Only one study, by Matsunaga et al., has reported an insignificant association between them in adolescents22 and a similar result was observed in our study. To the best of our knowledge, there has been no report on the effect of SHS exposure on serum MCP-1 levels. Nevertheless, two studies in aged persons25 and healthy adults26 reported that active smokers had higher serum MCP-1 concentrations than never smokers and Garliches et al. found that young healthy male smokers had slightly decreased serum MCP-1 levels27. However, there was no significant difference between the serum MCP-1 levels of pregnant women with and without SHS exposure in our study. Taken as a whole, the previous discrepant results on inflammatory markers may be explained by differences in the duration and extent of SHS exposure and the age, gender, biological status and ethnicity of the subjects in different studies22. Therefore, further studies are needed to clarify the effects of SHS exposure on inflammatory markers in pregnant women.
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