[Paleopsych] SW: Racial/Ethnic Disparities in Neonatal Mortality

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Racial/Ethnic Disparities in Neonatal Mortality

    The following points are made by S.L Lukacs and K.C. Schoendorf (Morb.
    Mort. Wkly. Rep. 2004 53:655):
    1) Neonatal mortality (i.e., death at age less than 28 days) accounts
    for approximately two-thirds of infant deaths in the US. During
    1989-2001, neonatal mortality rates (NMRs) declined. However, 2002
    preliminary data indicated an increase. To characterize trends in
    neonatal mortality by gestational age and race/ethnicity, the Centers
    for Disease Control and Prevention (CDC) analyzed linked birth/infant
    death data sets for 1989-1991 and 1995-2001 (2002 linked data were not
    2) Results indicated that (a) extremely preterm infants (i.e., born at
    less than 28 weeks gestation) accounted for 49%-58% of neonatal deaths
    during 1989-2001 and (b) racial/ethnic disparities persisted despite
    NMR declines among infants of all gestational ages.(1,2)
    3) The findings document a considerable decline in neonatal mortality
    among infants of all gestational ages and racial/ethnic populations
    during the 1990s; despite this decline, racial/ethnic disparities
    persisted. Implementation of new therapies and recommendations likely
    contributed to the decline; however, the effects of these advances
    might differ within racial/ethnic populations. The medical advances
    include (a) surfactant therapy, which improves infant lung maturity,
    resulting in a decreased risk for death for high-risk preterm
    infants(3); (b) folic acid consumption by women of childbearing age to
    reduce the risk for neural tube defects(4); and (c) intrapartum
    antimicrobial prophylaxis for women colonized with or at high risk for
    maternal-infant transmission of group B streptococcal infection.(5)
    4) In 2001, blacks continued to have the highest overall NMR, more
    than twice that of any other racial/ethnic population. The high rate
    among this population is likely attributable to a combination of high
    mortality among black infants born at 37 weeksÆ gestation (full-term
    infants account for approximately 90% of all births) and a high
    proportion of preterm births (17.6% black preterm births versus 10.8%
    white preterm births).
    5) Preterm white infants had higher NMRs in 2001, compared with other
    racial/ethnic populations, despite a greater rate of decline in
    mortality. Although black preterm infants had lower NMRs in 2001, the
    annual rate of decline was lower than among other racial/ethnic
    populations. The narrowing gap in mortality between preterm white
    infants and preterm black infants might reflect the widened
    distribution of neonatal intensive care in the 1990s beyond urban
    tertiary-care centers and a possible difference in benefit from
    surfactant therapy between black and white infants.
    6) Differences in neonatal mortality trends among racial/ethnic
    populations also might be explained by changing patterns in the
    occurrence of multiple births. The rate of multiple births has
    increased substantially over the preceding decade, and trends vary
    among infants of different races/ethnicities.
    References (abridged):
    1. National Center for Health Statistics. National Center for Health
    Statistics linked birth/infant death data set: 1989-91 cohort data,
    1995-2001 period data. Hyattsville, Maryland: U.S. Department of
    Health and Human Services, CDC, National Center for Health Statistics,
    2. Alexander GR, Himes JH, Kaufman RB, Mor J, Kogan M. A United States
    national reference for fetal growth. Obstet Gynecol. 1996;87:163-168
    3. Horbar JD, Wright EC, Onstad L, National Institute of Child Health
    and Human Development Neonatal Research Network. Decreasing mortality
    associated with the introduction of surfactant therapy: an
    observational study of neonates weighing 601 to 1,300 grams at birth.
    Pediatrics. 1993;92:191-196
    4. Mathews TJ, Honein MA, Erickson JD. Spina bifida and anencephaly
    prevalence--United States, 1991-2001. MMWR Recomm Rep.
    5. CDC. Prevention of perinatal group B streptococcal disease: a
    public health perspective. MMWR Recomm Rep. 1996;45(RR-7):1-24
    Centers for Disease Control and Prevention http://www.cdc.gov
    Related Material:
    The following points are made by R.J. Sokol et al (J. Am. Med. Assoc.
    2003 290:2996):
    1) "Fetal alcohol syndrome" (FAS), currently considered part of "fetal
    alcohol spectrum disorder" (FASD), was first described in 1973.(1)
    Although much has been learned in 30 years, substantial challenges
    remain in diagnosing and preventing this disorder. Individuals with
    FAS have characteristic facial dysmorphology (midfacial hypoplasia,
    long smooth philtrum, thin upper lip, small eyes that appear widely
    spaced, and inner epicanthal folds); growth restriction, including
    relative microcephaly; and central nervous system and
    neurodevelopmental abnormalities, including ophthalmic involvement. As
    children, they typically struggle in school because of decreased
    cognitive functioning and social problems.
    2) Fetal alcohol syndrome is diagnosed when characteristic facial
    dysmorphology, growth restriction, and central nervous
    system/neurodevelopmental abnormalities are present, with or without
    confirmed prenatal alcohol exposure.(2) Although it has long been
    recognized that affected individuals may have some but not all of the
    FAS characteristics, research has not identified a reliable way of
    defining those individuals who are less affected. Fetal alcohol
    effects (FAE), prenatal alcohol effects (PAE), alcohol-related birth
    defects (ARBD), and alcohol-related neurodevelopmental disorder (ARND)
    have all previously been suggested as terms to identify those children
    with a spectrum of problems but not with classic FAS.
    3) Although much available research still uses the older
    nomenclatures, the term FASD has recently been used by advocates,
    educators, and federal agencies (National Institute on Alcohol Abuse
    and Alcoholism and Centers for Disease Control and Prevention) as an
    umbrella term to cover the range of outcomes associated with all
    levels of prenatal alcohol exposure. Adoption of a common and
    overarching term, such as FASD, will allow researchers and physicians
    who work with affected individuals to better understand and describe
    the current state of knowledge.
    4) How much drinking during pregnancy is too much? For nonpregnant
    women, physicians and many researchers define light drinking as 1.2
    drinks per day, moderate drinking as 2.2 drinks per day, and heavy
    drinking as 3.5 or more drinks per day.(3) However, risk-drinking
    during pregnancy (enough to potentially damage offspring) has been
    defined as an average of more than 1 drink (0.5 oz) per day,(4) or
    less if massed (binges of >5 drinks per episode). Although many
    reports of adverse effects related to prenatal exposure involve
    heavier drinking,(5) recent research documenting deleterious outcomes
    for children prenatally exposed to small amounts of alcohol (0.5 drink
    per day) has led to recognition that a threshold has not been
    adequately identified. This, along with varying susceptibility
    (vulnerability), leads to the conclusion and recommendations by both
    the American Academy of Pediatrics and the American College of
    Obstetricians and Gynecologists that abstinence during pregnancy
    should be recommended to preconceptional and pregnant women.
    5) Detection of maternal alcohol exposure is a particular challenge;
    no reliable biological marker is available. Although analysis of both
    meconium and hair samples for fatty acid ethyl esters has been
    proposed, there are no large population-based validation studies for
    these methods. Similarly, other biochemical markers, including
    gamma-glutamyl transferase, hemoglobin-associated acetaldehyde, and
    carbohydrate-deficit transferrin, have not yet been validated or have
    not been shown to have adequate diagnostic sensitivity and specificity
    in identifying drinking in pregnant women. Most researchers and
    physicians rely on self-report of maternal alcohol use during
    pregnancy, with underreporting common because of stigmatization of
    drinking during pregnancy. Alcohol use histories must be sensitively
    elicited to yield complete information. Studies indicate that
    obstetricians often obtain inaccurate consumption information. For
    example, in a prospective study that included high-risk women, almost
    twice as many admitted to drinking during a research assessment
    compared with indications from maternal medical records.
    References (abridged):
    1. Jones KL, Smith DW. Recognition of the fetal alcohol syndrome in
    early infancy. Lancet. 1973;2:999-1001
    2. Stratton K, ed, Howe C, ed, Battaglia F, ed. Fetal Alcohol
    Syndrome: Diagnosis, Epidemiology, Prevention, and Treatment.
    Washington, DC: National Academy Press; 1996
    3. Abel EL, Kruger ML, Driedl J. How do physicians define "light,"
    "moderate," and "heavy" drinking? Alcohol Clin Exp Res.
    4. Hankin JR, Sokol RJ. Identification and care of problems associated
    with alcohol ingestion in pregnancy. Semin Perinatol. 1995;19:286-292
    5. Roebuck TM, Mattson SN, Riley EP. Behavioral and psychological
    profiles of alcohol-exposed children. Alcohol Clin Exp Res.
    J. Am. Med. Assoc. http://www.jama.com
    The following points are made by L. Miller et al (J. Am. Med. Assoc.
    2002 288:38):
    1) Fetal alcohol syndrome is caused by maternal alcohol use during
    pregnancy and is one of the leading causes of preventable birth
    defects and developmental disabilities in the US. Fetal alcohol
    syndrome is diagnosed on the basis of a combination of growth
    deficiency (pre- or postnatal), central nervous system dysfunction,
    facial dysmorphology, and maternal alcohol use during pregnancy.
    Estimates of the prevalence vary from 0.2 to 1.0 per 1,000 live-born
    infants. This variation is due, in part, to the small size of the
    populations studied, varying case definitions, and different
    surveillance methods. In addition, differences have been noted among
    racial/ethnic populations. To monitor the occurrence of fetal alcohol
    syndrome, the Centers for Disease Control (CDC) collaborated with five
    states (Alaska, Arizona, Colorado, New York, and Wisconsin) to develop
    the Fetal Alcohol Syndrome Surveillance Network (FASSNet). The authors
    report a summary of the results of an analysis of FASSNet data on
    children born during 1995-1997, which indicate that FAS rates in
    Alaska, Arizona, Colorado, and New York ranged from 0.3 to 1.5 per
    1,000 live-born infants and were highest for black and American
    Indian/Alaska Native populations.
    2) The CDC suggests this report demonstrates that maternal alcohol use
    during pregnancy continues to affect children. Recent data indicate
    that the prevalence of binge (i.e., >5 drinks on any one occasion) and
    frequent drinking (i.e., >7 drinks per week or >5 drinks on any one
    occasion) during pregnancy reached a high point in 1995 and has not
    declined. FASSNet prevalence rates are similar to rates published
    previously from population-based prevalence studies, despite different
    case definitions and surveillance methods. These data indicate that
    children born to mothers in certain racial/ethnic populations have
    consistently higher prevalence rates of fetal alcohol syndrome. For
    example, prevalence was 3.0 per 1,000 live-born infants for American
    Indians/Alaska Natives during 1977-1992 compared with 0.2 for other
    Alaska residents during the same period. FASSNet findings confirm
    higher prevalence rates among black and American Indian/Alaska Native
    populations. Alaska health authorities have increased efforts to
    address this health problem. Increased awareness of maternal alcohol
    use and more complete documentation by Alaska Native health
    organizations might result in more vigilant reporting of potential
    cases of FAS, which could contribute to high reported FAS prevalence
    in this population.
    3) The number of children affected adversely by in-utero exposure to
    alcohol is probably underestimated for at least four reasons. First,
    some fetal alcohol syndrome cases might not be diagnosed because of
    the syndromic nature of the condition, the lack of pathognomonic
    features, and the negative perceptions of fetal alcohol syndrome
    diagnosis. Second, medical records of children with fetal alcohol
    syndrome often lack sufficient documentation to determine case status.
    For example, 10 children diagnosed with fetal alcohol syndrome by a
    clinical geneticist, dysmorphologist, or developmental pediatrician
    did not meet the surveillance case definition for confirmed or
    probable fetal alcohol syndrome because documentation in the
    abstracted medical records was insufficient or the child did not meet
    FASSNet surveillance case definition criteria. However, adding these
    10 children to the total case count would change the overall
    prevalence only slightly, from 0.43 to 0.45 per 1,000 live-born
    infants. Third, some children might not be identified as having fetal
    alcohol syndrome until they reach school age, at which point central
    nervous system abnormalities and learning disabilities are recognized
    more easily. Because only part of the cohort under surveillance was of
    school age and education records were not used in this surveillance
    system, the actual number of cases might have been underestimated.
    Finally, an unknown number of persons with fetal alcohol syndrome left
    the surveillance area before being identified by the surveillance
    system. Because of the small numbers and differences in sources and
    awareness among clinicians, prevalence rates across racial/ethnic
    populations and across states should be compared with caution.
    4) The CDC suggests that ongoing, consistent, population-based
    surveillance systems are necessary to measure the occurrence of fetal
    alcohol syndrome and the impact of fetal alcohol syndrome prevention
    activities. These systems also are useful in evaluating the need for
    early intervention and special education services for children with
    birth defects such as fetal alcohol syndrome.
    Centers for Disease Control and Prevention http://www.cdc.gov

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