Understanding three approaches to reporting sudden unexpected infant death in the USA.

INTRODUCTION: In the USA each year, there are approximately 3400 sudden unexpected infant (<1 year of age) deaths (SUID) which occur without an obvious cause before an investigation. SUID includes the causes of death (COD) undetermined/unknown, sleep-related suffocation/asphyxia and sudden infant death syndrome (SIDS); these are often called SUID subtypes. Three common ways SUID subtypes are grouped (SUID subtype groups) include International Classification of Diseases (ICD) Codes, SUID Case Registry Categories or Child Death Review (CDR)-Assigned Causes. These groups are often used to monitor SUID trends and characteristics at the local, state and national levels. We describe and compare the characteristics of these three SUID subtype groups. DISCUSSION: SUID subtype groups are distinct and not directly interchangeable. They vary in purpose, strengths, limitations, uses, history, data years available, population coverage, assigning entity, guidance documentation and information available to assign subtypes. CONCLUSION: Making informed decisions about which SUID subtype group to use is important for reporting statistics, increasing knowledge of SUID epidemiology and informing prevention strategies.

Medicaid healthcare expenditures for infants with birth defects potentially related to Zika virus infection in North Carolina, 2011-2016.

BACKGROUND: In 2016, Zika virus (ZIKV) was recognized as a human teratogen. North Carolina (NC) had no local transmission of ZIKV but infants with relevant birth defects, including severe brain anomalies, microcephaly, and eye abnormalities, require specialized care and services, the costs of which have not yet been quantified. The objective of this study is to examine NC Medicaid healthcare expenditures for infants with defects potentially related to ZIKV compared to infants with no reported defects. METHODS: Data sources for this retrospective cohort study include NC birth certificates, Birth Defects Monitoring Program data, and Medicaid enrollment and paid claims files. Infants with relevant defects were identified and expenditure ratios were calculated to compare distributions of estimated expenditures during the first year of life for infants with relevant defects and infants with no reported defects. RESULTS: This analysis included 551 infants with relevant defects and 365,318 infants with no reported defects born 2011-2016. Mean total expenditure per infant with defects was $69,244 (median $30,544) for the first year. The ratio of these expenditures relative to infants with no reported defects was 14.5. Expenditures for infants with select brain anomalies were greater than those for infants with select eye abnormalities only. CONCLUSIONS: Infants with defects potentially related to ZIKV had substantially higher Medicaid expenditures than infants with no reported defects. These results may be informative in the event of a future outbreak and are a resource for program planning related to care for infants in NC.

Population-Based Surveillance for Birth Defects Potentially Related to Zika Virus Infection - 22 States and Territories, January 2016-June 2017.

Zika virus infection during pregnancy can cause congenital brain and eye abnormalities and is associated with neurodevelopmental abnormalities (1-3). In areas of the United States that experienced local Zika virus transmission, the prevalence of birth defects potentially related to Zika virus infection during pregnancy increased in the second half of 2016 compared with the first half (4). To update the previous report, CDC analyzed population-based surveillance data from 22 states and territories to estimate the prevalence of birth defects potentially related to Zika virus infection, regardless of laboratory evidence of or exposure to Zika virus, among pregnancies completed during January 1, 2016-June 30, 2017. Jurisdictions were categorized as those 1) with widespread local transmission of Zika virus; 2) with limited local transmission of Zika virus; and 3) without local transmission of Zika virus. Among 2,004,630 live births, 3,359 infants and fetuses with birth defects potentially related to Zika virus infection during pregnancy were identified (1.7 per 1,000 live births, 95% confidence interval [CI] = 1.6-1.7). In areas with widespread local Zika virus transmission, the prevalence of birth defects potentially related to Zika virus infection during pregnancy was significantly higher during the quarters comprising July 2016-March 2017 (July-September 2016 = 3.0; October-December 2016 = 4.0; and January-March 2017 = 5.6 per 1,000 live births) compared with the reference period (January-March 2016) (1.3 per 1,000). These findings suggest a fourfold increase (prevalence ratio [PR] = 4.1, 95% CI = 2.1-8.4) in birth defects potentially related to Zika virus in widespread local transmission areas during January-March 2017 compared with that during January-March 2016, with the highest prevalence (7.0 per 1,000 live births) in February 2017. Population-based birth defects surveillance is critical for identifying infants and fetuses with birth defects potentially related to Zika virus regardless of whether Zika virus testing was conducted, especially given the high prevalence of asymptomatic disease. These data can be used to inform follow-up care and services as well as strengthen surveillance.

Prenatal cortisol exposure predicts infant cortisol response to acute stress.

Experimental animal findings suggest that early stress and glucocorticoid exposure may program the function of the hypothalamic-pituitary-adrenal (HPA) axis in the offspring. The extension of these findings to human development is not yet clear. A prospective longitudinal study was conducted on 125 mothers and their normally developing children. Amniotic fluid was obtained at, on average, 17.2 weeks gestation; infant behavior and cortisol response to a separation-reunion stress was assessed at 17 months. Amniotic fluid cortisol predicted infant cortisol response to separation-reunion stress: infants who were exposed to higher levels of cortisol in utero showed higher pre-stress cortisol values and blunted response to stress exposure. The association was independent of prenatal, obstetric, and socioeconomic factors and child-parent attachment. The findings provide some of the strongest data in humans that HPA axis functioning in the child may be predicted from prenatal cortisol exposure.

Maternal prenatal cortisol and infant cognitive development: moderation by infant-mother attachment.

BACKGROUND: Experimental animal studies suggest that early glucocorticoid exposure may have lasting effects on the neurodevelopment of the offspring; animal studies also suggest that this effect may be eliminated by positive postnatal rearing. The relevance of these findings to humans is not known. METHODS: We prospectively followed 125 mothers and their normally developing children from pregnancy through 17 months postnatal. Amniotic fluid was obtained at, on average, 17.2 weeks gestation; infants were assessed at an average age of 17 months with the Bayley Scales of Infant Development, and ratings of infant-mother attachment classification were made from the standard Ainsworth Strange Situation assessment. RESULTS: Prenatal cortisol exposure, indexed by amniotic fluid levels, negatively predicted cognitive ability in the infant, independent of prenatal, obstetric, and socioeconomic factors. This association was moderated by child-mother attachment: in children with an insecure attachment, the correlation was [r(54) = -.47, p < .001]; in contrast, the association was nonexistent in children who had a secure attachment [r(70) = -.05, ns]. CONCLUSIONS: These findings mimic experimental animal findings and provide the first direct human evidence that increased cortisol in utero is associated with impaired cognitive development, and that its impact is dependent on the quality of the mother-infant relationship.

In utero cortisol and testosterone exposure and fear reactivity in infancy.

Fetal programming is emerging as a major conceptual model for understanding developmental origins of health and disease, including behavioral outcomes. As part of a larger study of prenatal stress and child development, we examined the association between prenatal hormone exposure and fear reactivity, a temperament dimension that is a predictor of long-term behavioral adjustment. Amniotic fluid was collected from a sample of women undergoing clinically indicated amniocentesis for later analysis of cortisol and testosterone. Children with normal birth outcomes were recalled for follow-up assessment at 17 months, at which time we administered an observational assessment of temperament (lab-TAB; n=108). Information on pregnancy and obstetric outcome was included as covariates. Results indicated that there was a significant association between prenatal testosterone and observed fear reactivity in boys (r(53)=0.34, p=0.01); no significant effect was found in girls (r(54)=-0.07, ns); the effect remained when obstetric, psychosocial, and parental anxiety were controlled for. There was not a significant association between fetal cortisol exposure and fear reactivity. The prediction from in utero testosterone exposure to fear reactivity in boys extends prior research on prenatal testosterone and may represent an association with a general predisposition to greater arousal and reactivity.

Association between maternal and amniotic fluid cortisol is moderated by maternal anxiety.

Maternal stress or anxiety during pregnancy can lead to neurodevelopmental and other problems in the child, and cortisol is one possible mediator. Animal models show that maternal prenatal stress can affect placental function, including regulation of placental 11beta-HSD2, the main barrier to the placental passage of cortisol. It is not known whether a parallel process exists in humans. The aim of the current study was to determine whether maternal anxiety increases the association between maternal plasma cortisol and amniotic fluid cortisol. The sample consisted of 262 women having amniocentesis, with normal pregnancies, who completed Spielberger State and Trait anxiety scales, from whom a plasma sample and an aliquot of amniotic fluid was obtained. The correlation between maternal and amniotic fluid cortisol was strongly dependent on both State and Trait maternal anxiety; in the most anxious State quartile r(62)=.59, p<.001 and in the least r(60)=.05, ns, a significant difference (p<.0015). The moderating effect of maternal anxiety on the association between maternal plasma and amniotic fluid cortisol remained when gestational age, maternal age, fetal sex, medication and time of collection were controlled for. There was no difference in amniotic fluid cortisol levels between the most and least anxious groups of mothers. However, the finding that there is a stronger correlation between maternal and fetal cortisol among more anxious pregnant women does suggests that the maternal emotional state can affect the function of the placenta.

Maternal stress during pregnancy predicts cognitive ability and fearfulness in infancy.

OBJECTIVE: To examine the effects of prenatal stress on cognition and behavioral fearfulness in infants. METHOD: Mothers were recruited at amniocentesis at Queen Charlotte's and Chelsea Hospital, London, between 2001 and 2005, and recalled when their children were 14 to 19 months to assess cognitive development using the Bayley Scales and fearfulness using the Lab-TAB. Measures of prenatal and postnatal life events and current psychological state were collected at the postnatal visit. RESULTS: Prenatal stress predicted both mental development (rs = -0.39, n = 123 p < .0001) and observed fearfulness (rs = 0.33, n = 106, p < .001); the magnitude of effect was essentially unchanged after covarying postnatal stressors, maternal education and psychological state, exposures to medications and substances during pregnancy, and birth outcomes. Prenatal stress accounted for 17% of the variance in cognitive ability and 10% of the variance in observed fearfulness. The correlation between mental development and fearfulness was minimal (r = -0.06, not significant). Prenatal partner relationship strain accounted for 73.5% and 75.0% of the prenatal stress related variance on infant cognitive and fearfulness scores, respectively. CONCLUSIONS: These findings strengthen previous research that suggests that fetal programming can be important for neurodevelopmental and psychiatric outcomes. They imply that the mechanisms by which mental development and fearfulness are affected are different and that prenatal stress due to relationship strain may warrant particular attention.