Preterm Delivery and Age of SIDS Death

doi:10.1016/j.annepidem.2005.11.007

Annals of Epidemiology

Volume 16, Issue 8, August 2006, Pages 600-606

https://doi.org/10.1016/j.annepidem.2005.11.007 Get rights and content

Purpose

The aim of the study is to (i) reexamine risk factors for sudden infant death syndrome (SIDS) and (ii) describe the relationship between length of gestation and age at death from SIDS.

Methods

To evaluate risk factors for SIDS, we used multivariable logistic regression and included maternal demographic characteristics, maternal health and behavioral factors, and infant characteristics, including fetal growth, using US national linked birth and death files from 1996 to 1998. We used multivariable linear regression with mean postnatal age of death as the outcome of interest, controlling for the factors listed (referent length of gestation, 40 to 41 weeks).

Results

The crude SIDS rate was 0.7 deaths/1000 live births (8199 deaths). Length of gestation was a strong risk factor for SIDS, with the adjusted odds ratio (OR) greatest at shorter gestations: 28 to 32 weeks (OR, 2.9; 95% confidence interval, 2.6–3.2). Infants with gestations of 22 to 27 and 28 to 32 weeks died at mean ages of 20.9 (SD = 0.8) and 15.3 (SD = 0.5) weeks, respectively (p ≤ 0.002). Term infants (40 to 41 weeks) died of SIDS at an adjusted mean age of 14.5 (SD = 0.4) weeks.

Conclusions

Preterm birth continues to be a strong risk factor for SIDS after controlling for fetal growth. With increasing gestational age, mean age of SIDS death decreases considerably, with the postnatal age of death of very preterm infants 6 weeks later than that of term infants.

Introduction

Sudden infant death syndrome (SIDS) remains the leading cause of postneonatal death in the United States, accounting for more than 2000 infant deaths each year (1). It is defined as the sudden death of an infant younger than 1 year that remains unexplained after a thorough case investigation, including performance of a complete autopsy, examination of the death scene, and review of the clinical history (2).

A dramatic decline in SIDS occurred in the United States during the 1990s after such national interventions as the Back-to-Sleep Campaign. The SIDS rate decreased from 1.2 deaths/1000 live births in 1991 to 0.7 deaths/1000 in 1996 (3, 4). Simultaneously, prone sleep position declined from 70% in 1992 to 18% in 1996 (5, 6). Although there has been a decrease in this risk factor, the rate of preterm births, another important risk factor, has increased. In 1990, a total of 10.6% of infants were preterm (1, 7). By 2002, a total of 12.1% of all infants were preterm, corresponding to almost a half million infants. There has been little decrease in the rate of SIDS since 1996, with the rate of SIDS in 2002 at 0.6 deaths/1000 live births (1).

Using data from before SIDS rates decreased, several investigators observed an inverse relationship between gestational length and mean age of death from SIDS. When Grether and Schulman (8) examined birth weight, a proxy for preterm birth, as a risk factor for SIDS, they found a later age of SIDS death in infants with very low birth weight compared with normal birth weight. Furthermore, Malloy and Hoffman (9) identified preterm birth as a risk factor for SIDS and noted a later postnatal age of death in preterm infants. Finally, Adams et al. (10) also observed that length of gestation was related inversely to age at death from SIDS, with the median age of death in white infants decreasing sharply from preterm to term birth. In light of the changing epidemiologic characteristics of SIDS and preterm births, reexamining the relationship between preterm birth and SIDS and identifying the impact of length of gestation on age of death may extend our understanding of SIDS.

National linked infant birth and death files provide an opportunity to assess risk factors for SIDS after the epidemiologic transition of the mid-1990s. Using these national data sets, we sought to: (i) reexamine risk factors for SIDS deaths and (ii) describe the relationship between length of gestation and age at death from SIDS. We anticipate that this information will be useful to clinicians who counsel patients regarding SIDS prevention and researchers seeking insights into the cause of SIDS.

Section snippets

Study Population

The study population consisted of all singleton infants born in the United States from 1996 through 1998 to women who were US residents. Given the known elevated risk for SIDS in multiple-gestation births, we excluded these children from the analyses (11). We excluded infants born to nonresidents because of the poor reliability of death certificates if mothers subsequently left the United States. Infants with gestation less than 22 weeks or more than 44 weeks also were excluded from the

Results

Of 11,378,083 infants born from 1996 through 1998, a total of 8199 infants died of SIDS, equal to a rate of 0.72 deaths/1000 live births. SIDS rates were greatest among infants of women who had ethnicity of non-Hispanic black or Native American, had a low level of education, were younger than 20 years, were unmarried, smoked, drank alcohol, or had five or more previous births (Table 1). SIDS rates also were elevated for infants who were male, SGA, or preterm.

Adjusted analyses showed that

Discussion

In the years after the Back-to-Sleep Campaign, as the rate of preterm birth increased and SIDS rates decreased, preterm birth has remained a significant predictor of SIDS. Although the rate of SIDS decreased dramatically during the early years of the campaign, there has been little decrease in the rate of SIDS since 1996. This may be caused in part by the ongoing increase in rate of preterm birth and increasing rate of preterm survival, as well as the associated high risk for SIDS in these

References (51)

H.R. Bigger et al.
Influence of increased survival of very low birth weight, low birth weight, and normal birth weight infants on the incidence of sudden infant death syndrome in the United States: 1985–1991
J Pediatr
(1998)
J.K. Grether et al.
Sudden infant death syndrome and birth weight
J Pediatr
(1989)
J.A. Taylor et al.
A reexamination of the risk factors for the sudden infant death syndrome
J Pediatr
(1995)
H.J. Hoffman et al.
Epidemiology of the sudden infant death syndrome: Maternal, neonatal, and postneonatal risk factors
Clin Perinatol
(1992)
L. Black et al.
Effects of birth weight and ethnicity on incidence of sudden infant death syndrome
J Pediatr
(1986)
T.C. Hulsey et al.
Hyaline membrane disease: The role of ethnicity and maternal characteristics
Am J Obstet Gynecol
(1993)
W.M. Gilbert et al.
The cost of prematurity: Quantification by gestational age and birth weight
Obstet Gynecol
(2003)
G.R. Alexander et al.
A United States national reference for fetal growth
Obstet Gynecol
(1996)
K.D. Kochanek et al.
Deaths: Preliminary data for 2002
Natl Vital Stat Rep
(2004)
M. Willinger et al.
Defining the sudden infant death syndrome: Deliberations of an expert panel convened by the National Institute of Child Health and Human Development
Pediatr Pathol
(1991)

T.J. Mathews et al.

Infant mortality statistics from the 1998 period linked birth/infant death data set

Natl Vital Stat Rep

(2000)

K.D. Peters et al.

Deaths: Final data for 1996

Natl Vital Stat Rep

(1998)

M. Willinger et al.

Factors associated with caregivers' choice of infant sleep position, 1994–1998: The National Infant Sleep Position Study

JAMA

(2000)

M.J. Corwin et al.

Secular changes in sleep position during infancy: 1995–1998

Pediatrics

(2003)

M.H. Malloy et al.

Prematurity, sudden infant death syndrome, and age of death

Pediatrics

(1995)

M.M. Adams et al.

Are race and length of gestation related to age at death in the sudden infant death syndrome

Paediatr Perinatal Epidemiol

(1990)

US Department of Health and Human Services, Centers for Disease Control and Prevention. 1995–1998 Birth Cohort Linked Birth/Infant Death Data Set

(1998)

D.J. Peterson et al.

Seasonal variation in adolescent conceptions, induced abortions, and late initiation of prenatal care

Public Health Rep

(1992)

G.R. Alexander et al.

1994-6 U.S. singleton birth weight percentiles for gestational age by race, Hispanic origin, and gender

Matern Child Health J

(1999)

M. Hollander et al.

Nonparametric Statistical Methods

(1999)

D.R. Peterson

Sudden, unexpected death in infants: An epidemiologic study

Am J Epidemiol

(1966)

J.F. Kraus et al.

Postneonatal sudden unexplained death in California: A cohort study

Am J Epidemiol

(1972)

A.B. Bergman et al.

Studies of the sudden infant death syndrome in King County, Washington. III. Epidemiology

Pediatrics

(1972)

J.E. Yount et al.

Evidence for an exponentially increasing incidence of sudden infant death syndrome with decreasing birth weight

Pediatr Res

(1979)

J. Goldberg et al.

Age at death and risk factors in sudden infant death syndrome

Aust Paediatr J

(1986)

Cited by (35)

Infant mortality at term in Canada: Impact of week of gestation
2016, Early Human Development
Citation Excerpt :
In Norway, Apgar scores at 1 and 5 min were more favourable among infants born at 39 weeks than 40 or 41 weeks [29], a finding corroborated by US data suggesting generally lower neonatal morbidity in at 39 weeks [28]. Studies of sudden infant death syndrome and cerebral palsy in contrast suggest that risks were lowest at 40 or 41 weeks [30–32], and asthma in infancy lowest at 41 weeks [33], aligning more with our results. Reasons for these differences are unclear.
Infants born at term have low mortality, but risk may vary from week to week. We determined the risk of infant mortality at term by gestational week and cause.
We analyzed 4.1 million infants born at ≥ 37 weeks of gestation in Canada from 1991 to 2010, followed for mortality the first year of life. We estimated hazard ratios (HR) and 95% CIs for early, late and post neonatal mortality from 37 through 41 weeks of gestation, adjusting for individual characteristics. The main outcomes were mortality due to congenital anomaly, asphyxia, immaturity, infection, sudden infant death, and injury.
Infant mortality decreased progressively from 4.55 per 1000 at 37 weeks to 1.62 per 1000 at 41 weeks. Early neonatal mortality varied little between 39 and 41 weeks, but post neonatal mortality was lowest at 40–41 weeks. Relative to 41 weeks of gestation, mortality at 39 weeks was higher for congenital anomaly (HR 1.30, 95% CI 1.05–1.60) and sudden infant death (HR 1.58, 95% CI 1.18–2.11).
In Canada, mortality at term is lowest for infants born at 40 or 41 weeks of gestation, especially at late and post neonatal ages, and for congenital anomaly and sudden infant death.
The risk of stillbirth and infant death by each additional week of expectant management in twin pregnancies
2015, American Journal of Obstetrics and Gynecology
The objective of the study was to compare the fetal/infant mortality risk associated with each additional week of expectant management with the mortality risk of immediate delivery in women with twin gestations.
A retrospective cohort study was performed utilizing 2006–2008 National linked birth certificate and death certificate data. The incidence of stillbirth and infant death were determined for each week of pregnancy from 32 0/7 weeks’ through 40 6/7 weeks’ gestation. Pregnancies complicated by fetal anomalies were excluded. These measures were combined to estimate the theoretic risk of remaining pregnant an additional week by adding the risk of stillbirth during the extra week of pregnancy with the risk of infant death encountered with delivery during the following week. This composite fetal/infant mortality risk was compared with the risk of infant death associated with delivery at the corresponding gestational age.
The risk of stillbirth increased with increasing gestational age, for example, between 37 and 38 weeks’ gestation (12.5 per 10,000 vs 22.5 per 10,000; P < .05). As expected, the risk of infant death following delivery gradually decreased as pregnancies approached term gestation. Week-by-week differences were statistically significant (P < .05) between 32 and 36 weeks with decreasing risk of infant death at advancing gestational ages. The composite risk of stillbirth and infant death associated with an additional week of pregnancy had a significant increase from 37 to 38 weeks’ gestation (43.9 per 10,000 vs 59.2 per 10,000; P < .05). At 37 weeks’ gestation, the relative risk of mortality was statistically significantly lower with immediate delivery as compared with expectant management (relative risk, 0.87; 95% confidence interval, 0.77–0.99).
Our results suggest that fetal/infant death risk is minimized at 37 weeks’ gestation; however, individual maternal and fetal characteristics must also be taken into account when determining the optimal timing of delivery for twin pregnancies.
The physiological determinants of Sudden Infant Death Syndrome
2013, Respiratory Physiology and Neurobiology
Citation Excerpt :
Mechanical and drug interventions will also alter postnatal respiratory development (Sweet and Halliday, 2005; O’Reilly et al., 2013). Intriguing epidemiological findings from two groups have shown that preterm infants succumb to SIDS at earlier post-conceptional ages than term infants (45 versus 55 weeks, respectively) but later postnatal ages (20 versus 15 weeks, respectively) (Halloran and Alexander, 2006; Malloy, 2013). This distinct high-risk time period should not only be a consideration while conducting preterm studies, but may also be used to identify developmental changes correlated with SIDS risk in preterm versus term populations.
It is well-established that environmental and biological risk factors contribute to Sudden Infant Death Syndrome (SIDS). There is also growing consensus that SIDS requires the intersection of multiple risk factors that result in the failure of an infant to overcome cardio-respiratory challenges. Thus, the critical next steps in understanding SIDS are to unravel the physiological determinants that actually cause the sudden death, to synthesize how these determinants are affected by the known risk factors, and to develop novel ideas for SIDS prevention. In this review, we will examine current and emerging perspectives related to cardio-respiratory dysfunctions in SIDS. Specifically, we will review: (1) the role of the preBötzinger complex (preBötC) as a multi-functional network that is critically involved in the failure to adequately respond to hypoxic and hypercapnic challenges; (2) the potential involvement of the preBötC in the gender and age distributions that are characteristic for SIDS; (3) the link between SIDS and prematurity; and (4) the potential relationship between SIDS, auditory function, and central chemosensitivity. Each section underscores the importance of marrying the epidemiological and pathological data to experimental data in order to understand the physiological determinants of this syndrome. We hope that a better understanding will lead to novel ways to reduce the risk to succumb to SIDS.
The risk of stillbirth and infant death by each additional week of expectant management stratified by maternal age
2013, American Journal of Obstetrics and Gynecology
The objective of the study was to examine fetal/infant mortality by gestational age at term stratified by maternal age.
A retrospective cohort study was conducted using 2005 US national birth certificate data. For each week of term gestation, the risk of mortality associated with delivery was compared with composite mortality risk of expectant management. The expectant management measure included stillbirth and infant death. This expectant management risk was calculated to estimate the composite mortality risk with remaining pregnant an additional week by combining the risk of stillbirth during the additional week of pregnancy and infant death risk following delivery at the next week. Maternal age was stratified by 35 years or more compared with women younger than 35 years as well as subgroup analyses of younger than 20, 20-34, 35-39, or 40 years old or older.
The fetal/infant mortality risk of expectant management is greater than the risk of infant death at 39 weeks’ gestation in women 35 years old or older (15.2 vs 10.9 of 10,000, P < .05). In women younger than 35 years old, the risk of expectant management also exceeded that of infant death at 39 weeks (21.3 vs 18.8 of 10,000, P < .05). For women younger than 35 years old, the overall expectant management risk is influenced by higher infant death risk and does not rise significantly until 41 weeks compared with women 35 years old or older in which it increased at 40 weeks.
Risk varies by maternal age, and delivery at 39 weeks minimizes fetal/infant mortality for both groups, although the magnitude of the risk reduction is greater in older women.
Altered placental development in pregnancies resulting in sudden infant death syndrome (SIDS)
2012, Early Human Development
Citation Excerpt :
Although the etiological factor(s) is unknown, a suboptimal intrauterine environment during pregnancy is hypothesised to lead to compromised fetal development in utero thus predisposing a vulnerable infant to an increased risk of SIDS postnatally. Principal epidemiological research supporting a prenatal origin of SIDS stems from not only its close association with maternal risk factors during pregnancy including maternal cigarette smoking [2], maternal anaemia [3], drug and alcohol consumption [4], but also its close association with common obstetric complications of pregnancy such as pre-eclampsia (PE) [5], intrauterine growth restriction (IUGR) [6] and preterm birth (PTB) [7]. Human pathological evidence for a prenatal origin is provided by quantitative studies demonstrating that a subset of SIDS infants is developmentally compromised and has delayed and/or arrested organogenesis in organs critical for survival ex utero including the, brain, kidney, diaphragm, phrenic nerve and lungs (although maturation of terminal ducts occurs postnatally) [1,8–13].
Sudden infant death syndrome (SIDS) is postulated to be a developmental disorder originating during fetal life in utero. Knowledge regarding the intrauterine environment in which SIDS infants develop is, however, inadequate and how the placenta develops prior to a SIDS event has not been studied.
To investigate the morphological development of the placenta obtained from full-term infants who subsequently succumbed to SIDS.
To estimate the percentage and total volumes of the chorionic villi and villous trophoblast membrane using stereological techniques.
Placentas were obtained retrospectively from normal birthweight (SIDS-NBW n = 18) and small-for-gestational age (SIDS-SGA, n = 14) infants who had succumbed to SIDS, and compared to either control (n = 8) or SGA placentas (n = 7), respectively.
SIDS-NBW placentas displayed evidence of augmented villous growth shown by significantly greater volumes of placental chorionic villi (gas-exchanging (GE) villi) in comparison to controls; this was not observed for SIDS-SGA placentas. However, both SIDS-NBW and SIDS-SGA placentas displayed significantly greater volumes of the cytotrophoblast (CT) (SIDS-NBW only), syncytiotrophoblast (SIDS-SGA only) and syncytial knots (SCT-K) and those displaying apoptotic syncytial nuclei (AP SCT-K). In contrast, SGA placentas displayed significantly reduced volumes of chorionic villi, GE villi and the villous trophoblast indicating a SIDS-specific effect associated with augmented placental growth.
Our findings provide initial evidence that placental abnormality, although not necessarily causative, may precede a subset of SIDS cases supporting the hypothesis that the origins of SIDS begin during fetal life in utero.
Antagonism of progesterone receptor suppresses carotid body responses to hypoxia and nicotine in rat pups
2012, Neuroscience
We tested the hypothesis that antagonism of progesterone receptor (PR) in newborn rats alters carotid body and respiratory responses to hypoxia and nicotinic receptor agonists. Rats were treated with the PR antagonist mifepristone (daily oral gavage 40 μg/g/d) or vehicle between postnatal days 3 and 15. In 11–14-day-old rats, we used in vitro carotid body/carotid sinus nerve preparation and whole body plethysmography to assess the carotid body and ventilatory responses to hypoxia (65 mmHg in vitro, 10% O2 in vivo) and to nicotinic receptor agonists (as an excitatory modulator of carotid body activity—nicotine 100 μM for in vitro studies, and epibatidine 5 μg/kg, i.p., which mainly acts on peripheral nicotinic receptors, for in vivo studies). The carotid body responses to hypoxia and nicotine were drastically reduced by mifepristone. Compared with vehicle, mifepristone-treated rats had a reduced body weight. The ventilatory response to epibatidine was attenuated; however, the hypoxic ventilatory response was similar between vehicle and mifepristone-treated pups. Immunohistochemical staining revealed that mifepristone treatment did not change carotid body morphology. We conclude that PR activity is a critical factor ensuring proper carotid body function in newborn rats.

View all citing articles on Scopus

View full text

Preterm Delivery and Age of SIDS Death

Purpose

Methods

Results

Conclusions

Introduction

Section snippets

Study Population

Results

Discussion

J Pediatr

J Pediatr

J Pediatr

Clin Perinatol

J Pediatr

Am J Obstet Gynecol

Obstet Gynecol

Obstet Gynecol

Deaths: Preliminary data for 2002

Natl Vital Stat Rep

Defining the sudden infant death syndrome: Deliberations of an expert panel convened by the National Institute of Child Health and Human Development

Pediatr Pathol

Infant mortality statistics from the 1998 period linked birth/infant death data set

Natl Vital Stat Rep

Deaths: Final data for 1996

Natl Vital Stat Rep

Factors associated with caregivers' choice of infant sleep position, 1994–1998: The National Infant Sleep Position Study

JAMA

Secular changes in sleep position during infancy: 1995–1998

Pediatrics

Prematurity, sudden infant death syndrome, and age of death

Pediatrics

Are race and length of gestation related to age at death in the sudden infant death syndrome

Paediatr Perinatal Epidemiol

US Department of Health and Human Services, Centers for Disease Control and Prevention. 1995–1998 Birth Cohort Linked Birth/Infant Death Data Set

Seasonal variation in adolescent conceptions, induced abortions, and late initiation of prenatal care

Public Health Rep

1994-6 U.S. singleton birth weight percentiles for gestational age by race, Hispanic origin, and gender

Matern Child Health J

Nonparametric Statistical Methods

Sudden, unexpected death in infants: An epidemiologic study

Am J Epidemiol

Postneonatal sudden unexplained death in California: A cohort study

Am J Epidemiol

Studies of the sudden infant death syndrome in King County, Washington. III. Epidemiology

Pediatrics

Evidence for an exponentially increasing incidence of sudden infant death syndrome with decreasing birth weight

Pediatr Res

Age at death and risk factors in sudden infant death syndrome

Aust Paediatr J