[Paleopsych] SW: Racial/Ethnic Disparities in Neonatal Mortality
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Racial/Ethnic Disparities in Neonatal Mortality
http://scienceweek.com/2004/sb041224-6.htm
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
available).
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,
2003
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.
2002;51(RR-13):9-11
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:
MEDICAL BIOLOGY: ON FETAL ALCOHOL SPECTRUM DISORDER
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.
1998;22:979-984
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.
1999;23:1070-1076
J. Am. Med. Assoc. http://www.jama.com
--------------------------------
ON FETAL ALCOHOL SYNDROME
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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