Sudden Infant Death Syndrome Cases Research Articles

Duration of Breastfeeding and Risk of SIDS: An Individual Participant Data Meta-analysis.

Sudden infant death syndrome (SIDS) is a leading cause of postneonatal infant mortality. Our previous meta-analyses showed that any breastfeeding is protective against SIDS with exclusive breastfeeding conferring a stronger effect.The duration of breastfeeding required to confer a protective effect is unknown. To assess the associations between breastfeeding duration and SIDS. Individual-level data from 8 case-control studies. Case-control SIDS studies with breastfeeding data. Breastfeeding variables, demographic factors, and other potential confounders were identified. Individual-study and pooled analyses were performed. A total of 2267 SIDS cases and 6837 control infants were included. In multivariable pooled analysis, breastfeeding for <2 months was not protective (adjusted odds ratio [aOR]: 0.91, 95% confidence interval [CI]: 0.68-1.22). Any breastfeeding ≥2 months was protective, with greater protection seen with increased duration (2-4 months: aOR: 0.60, 95% CI: 0.44-0.82; 4-6 months: aOR: 0.40, 95% CI: 0.26-0.63; and >6 months: aOR: 0.36, 95% CI: 0.22-0.61). Although exclusive breastfeeding for <2 months was not protective (aOR: 0.82, 95% CI: 0.59-1.14), longer periods were protective (2-4 months: aOR: 0.61, 95% CI: 0.42-0.87; 4-6 months: aOR: 0.46, 95% CI: 0.29-0.74). The variables collected in each study varied slightly, limiting our ability to include all studies in the analysis and control for all confounders. Breastfeeding duration of at least 2 months was associated with half the risk of SIDS. Breastfeeding does not need to be exclusive to confer this protection.

A Retrospective Study of the Investigation of Homicidal Childhood Asphyxial Deaths.

As one of the leading causes of traumatic deaths in newborns, infants, and young children, there is no anatomic or microscopic feature that is pathognomonic for asphyxial deaths. Instead, pathologists rely on investigation information, including confessions and/or witness statements, and potential evidence at the scene. Twenty cases of homicidal newborn, infant, and young children asphyxial deaths were reviewed, which included death and police investigation reports and autopsy reports, as well as histology slides of lung sections. This series of homicidal asphyxial deaths highlight that, in a vast majority of such cases, the final cause and manner of death rulings are dependent on confession by the perpetrator. Furthermore, this series highlights the possible role of histology to help forensic pathologists better certify asphyxial deaths. Finally, this series emphasizes important investigation points and considerations at autopsy during the investigation of asphyxial deaths in newborns, infants, and young children.

Noteworthy Professional News

FIRST NEONATAL MRI DEVICE CLEARED BY FDA The first neonatal magnetic resonance imaging (MRI) device designed to scan the head and brain of a neonate has received clearance from the US Food and Drug Administration. The MRI machine uses strong magnetic fields and radio waves to generate the images needed to view the head and the brain. The images are produced when protons in fat and water molecules line up in the body, producing scans that are useful in the diagnosis of many neurological diseases.1Embrace Neonatal MRI System was designed for infants with a head circumference of up to 38 cm and weight of 1 to 4.5 kg; the machine was designed in such a way to allow a temperature-controlled incubator to be placed directly into the machine, limiting temperature fluctuations. If the infant does exhibit signs of distress, removal of the infant from the machine takes only approximately 30 seconds. The Embrace Neonatal MRI System is contraindicated for patients weighing more than 4.5 kg, those with a head circumference of more than 38 cm, and infants with metallic or electronically active implants. The MRI system can be placed directly in the neonatal intensive care unit because the machine does not require a safety zone.2 NEW BREAST PUMP KIT CLEANING INSTRUCTIONS New guidelines for how to keep breast pump kits clean have been released following the tragic death of an infant who was 29 weeks old.3,4 The infant developed sepsis at the age of 21 days of life demonstrating positive Cronobacter sakazakii in both her blood and her cerebrospinal fluid. Despite aggressive treatment, the infant developed global developmental delay and required a ventriculoperitoneal shunt and a gastrostomy feeding tube. After extensive investigation, one of the potential contributing factors to the sepsis was the breast pump kit that became contaminated with C sakazakii. Without adequate cleaning or sanitation, the infant was exposed to the deadly bacterial infection. Thus, the Centers for Disease Control and Prevention has introduced new guidelines for parents to facilitate more hygienic expression and handling of human milk.4 Before using the breast pump kit, always wash hands with soap and water. Then assemble and inspect the kit to ensure that no mold or dirt is directly visible in the tubing. Finally, clean pump dial, power switch, and countertop with disinfectant wipes. After using the breast pump, store the milk safely, clean the pumping area, take apart the breast pump, rinse the pump parts, and clean the pump parts either in the dishwasher or by hand. Finally, after cleaning for extra protection, sanitize the pump parts, washbasin, and bottlebrush at least once daily after they have been cleaned. Ensure that items are stored in a clean dry area until needed.3 HIGH PERIPHERAL SEROTONIN IN INFANTS WITH SUDDEN INFANT DEATH SYNDROME MAY BE A PERIPHERAL BIOMARKER The incidence of sudden infant death syndrome (SIDS) even after the national Back to Sleep campaign continues to remain at 0.4 per 1000 live births, which is the leading cause of postneonatal infant mortality.5 SIDS is defined as an infant who dies suddenly without explanation despite a complete autopsy, an examination of the death scene, and a review of the clinical history.6 Infants with SIDS appear to have what is called the triple risk hypothesis: underlying vulnerability (poverty, prematurity, gender, race); critical developmental period (infancy); and an outside stressor that precipitates sudden death (asphyxia due to prone sleeping).7–10 The infants with SIDS appear to have respiratory and cardiac abnormalities within the brainstem, combined with the environmental stressors (sleeping position, temperature, exposure to tobacco smoke, sleep state) and a “terminal cascade of hypoxia, bradycardia, apnea, and death,” thus the infants suffer irreversible injury and death occurs.10(p778),11 A new study sought to determine whether peripheral serum serotonin (5-hydroxytryptamine [5-HT]) levels are altered in SIDS cases compared with deceased infants with known causes, since no known peripheral biomarkers exist for SIDS.12 Sixty-one SIDS cases were identified and 15 control infants were also recruited following a thorough investigation using the postulated triple risk hypothesis. Postmortem results indicated that the serum 5-HT levels for SIDS cases was 177.2 + 15.1 with control infants having 5-HT levels of 91.1 ng/mL + 30.6 ng/ml, which was statistically significant difference. Results confirm that increased serum 5-HT levels in SIDS infants were present when compared with other infants who died within the first year of life. The high levels of serum 5-HT may serve as a potential biomarker for infants.12 Potential use for this may allow for differentiation of different types of neonatal death, allowing for correct diagnosis.

SIDS: EPIDEMIOLOGY, INFANT PHYSIOLOGY AND SALIVA ASPIRATION

A sudden infant death syndrome (SIDS) is diagnosed in the case of a sudden and unexpected death of an infant during sleep and where an autopsy shows no obvious pathological lesions or injuries. Although literature indicates a wide range of risk factors, there is no single opinion on the specific cause of SIDS. This paper describes a study of 191 infant deaths in which the State Forensic Medicine Service established 29 SIDS cases. Microscopical and histological results of samples taken from sections of the respiratory system reveal serous fluid in the alveoli and change specific to asphyxia in all autopsy cases of infants diagnosed with SIDS. The risk of SIDS is highest in infants aged 1–4 months. Salivary gland secretion increases with the development of infant physiology, and this increase coincides with infant teething. However, in this phase, an infant’s swallowing reflex is still to form completely. Findings suggest that the serous fluid found in the alveoli was from the salivary glands, and thus, saliva aspiration may be associated with infant deaths due to SIDS.

Abnormalities in substance P neurokinin-1 receptor binding in key brainstem nuclei in sudden infant death syndrome related to prematurity and sex.

Sudden infant death syndrome (SIDS) involves failure of arousal to potentially life threatening events, including hypoxia, during sleep. While neuronal dysfunction and abnormalities in neurotransmitter systems within the medulla oblongata have been implicated, the specific pathways associated with autonomic and cardiorespiratory failure are unknown. The neuropeptide substance P (SP) and its tachykinin neurokinin-1 receptor (NK1R) have been shown to play an integral role in the modulation of homeostatic function in the medulla, including regulation of respiratory rhythm generation, integration of cardiovascular control, and modulation of the baroreceptor reflex and mediation of the chemoreceptor reflex in response to hypoxia. Abnormalities in SP neurotransmission may therefore result in autonomic dysfunction during sleep and contribute to SIDS deaths. [125I] Bolton Hunter SP autoradiography was used to map the distribution and density of the SP, NK1R to 13 specific nuclei intimately related to cardiorespiratory function and autonomic control in the human infant medulla of 55 SIDS and 21 control (non-SIDS) infants. Compared to controls, SIDS cases exhibited a differential, abnormal developmental profile of the SP/NK1R system in the medulla. Furthermore the study revealed significantly decreased NK1R binding within key medullary nuclei in SIDS cases, principally in the nucleus tractus solitarii (NTS) and all three subdivisions of the inferior portion of the olivo-cerebellar complex; the principal inferior olivary complex (PIO), medial accessory olive (MAO) and dorsal accessory olive (DAO). Altered NK1R binding was significantly influenced by prematurity and male sex, which may explain the increased risk of SIDS in premature and male infants. Abnormal NK1R binding in these medullary nuclei may contribute to the defective interaction of critical medullary mechanisms with cerebellar sites, resulting in an inability of a SIDS infant to illicit appropriate respiratory and motor responses to life threatening challenges during sleep. These observations support the concept that abnormalities in a multi-neurotransmitter network within key nuclei of the medullary homeostatic system may underlie the pathogenesis of a subset of SIDS cases.

Sudden infant death syndrome and inherited cardiac conditions.

Sudden infant death syndrome (SIDS) is the leading cause of post-neonatal infant mortality in developed countries, characterized by the death of infants for no obvious reason and without prior warning. The complex interaction of multiple factors in the pathogenesis of SIDS is illustrated by the 'triple risk hypothesis', which proposed that SIDS results from a convergence of three overlapping risk factors: a critical developmental period, an exogenous stressor, and underlying genetic and/or nongenetic vulnerability in the infant. Rare variants in genes associated with inherited arrhythmia syndromes and cardiomyopathies have been proposed as the substrate for an infant's critical vulnerability in a small subset of SIDS cases. Given the potential risk of inherited cardiac disease, current guidelines recommend post-mortem genetic testing (molecular autopsy) and cardiological investigation of the surviving family, complemented by targeted genetic testing if appropriate. In this Review, we highlight the latest developments in understanding the spectrum and prevalence of cardiac-mediated SIDS, and discuss the clinical implications of SIDS in the surviving family and the general population.

Exploring the possible relationship between ambient heat and sudden infant death with data from Vienna, Austria.

A non-linear relationship between maximum ambient temperature and number of sudden infant death syndrome (SIDS) cases had been reported for Montreal, Canada, for the warm season. In particular, high maximum ambient temperatures were found to be extra-hazardous for infants. The study was replicated with data from Vienna, Austria, applying the same statistical approach. Vienna is roughly comparable to Montreal with regard to temperatures in the warm season, size of population, and number of SIDS cases. Although the Viennese study was powerful enough to detect even smaller effects, the Montrealean results could not be confirmed. The Viennese results do not support the hypothesis of a strong effect of maximum ambient temperature on the risk of SIDS during the warm season.

Ambient Temperature and Sudden Infant Death Syndrome in the United States.

Sudden infant death syndrome (SIDS) is a leading cause of infant mortality in the United States. While thermal stress is implicated in many risk factors for SIDS, the association between ambient temperature and SIDS remains unclear. We obtained daily individual-level infant mortality data and outdoor temperature data from 1972 to 2006 for 210 US cities. We applied a time-stratified case-crossover analysis to determine the effect of ambient temperature on the risk of SIDS by season. We stratified the analysis by race, infant age, and climate. There were a total of 60,364 SIDS cases during our study period. A 5.6°C (10°F) higher daily temperature on the same day was associated with an increased SIDS risk of 8.6% (95% confidence interval [CI] = 3.6%, 13.8%) in the summer, compared with a 3.1% decrease (95% CI = -5.0%, -1.3%) in the winter. Summer risks were greater among black infants (18.5%; 95% CI = 9.3%, 28.5%) than white infants (3.6%; 95% CI = -2.3%, 9.9%), and among infants 3-11 months old (16.9%; 95% CI = 8.9%, 25.5%) than infants 0-2 months old (2.7%; 95% CI = -3.5%, 9.2%). The temperature-SIDS association was stronger in climate clusters in the Midwest and surrounding northern regions. Temperature increases were associated with an elevated risk of SIDS in the summer, particularly among infants who were black, 3 months old and older, and living in the Midwest and surrounding northern regions.

Factors influencing maternal decision-making for the infant sleep environment in families at higher risk of SIDS: a qualitative study

ObjectiveQualitative interviews with mothers of babies at higher risk of sudden infant death syndrome (SIDS) were carried out to understand their views and decision-making process on the infant sleep environment...

Active sleep unmasks apnea and delayed arousal in infant rat pups lacking central serotonin.

Sudden infant death syndrome (SIDS), occurring during sleep periods, is highly associated with abnormalities within serotonin (5-HT) neurons, including reduced 5-HT. There is evidence that future SIDS cases experience more apnea and have abnormal arousal from sleep. In rodents, a loss of 5-HT neurons is associated with apnea in early life and, in adulthood, delayed arousal. As the activity of 5-HT neurons changes with vigilance state, we hypothesized that the degree of apnea and delayed arousal displayed by rat pups specifically lacking central 5-HT varies with state. Two-week-old tryptophan hydroxylase 2-deficient (TPH2-/-) and wild-type (WT) rat pups were placed in plethysmographic chambers supplied with room air. At the onset of active (AS) or quiet (QS) sleep, separate groups of rats were exposed to hypercapnia (5% CO2) or mild hypoxia (~17% O2) or maintained in room air. Upon arousal, rats received room air. Apnea indexes and latencies to spontaneous arousal from AS and QS were determined for pups exposed only to room air. Arousal latencies were also calculated for TPH2-/- and WT pups exposed to hypoxia or hypercapnia. Compared with WT, TPH2-/- pups hypoventilated in all states but were profoundly more apneic solely in AS. TPH2-/- pups had delayed arousal in response to increasing CO2, and AS selectively delayed the arousal of TPH2-/- pups, irrespective of the gas they breathed. Thus infants who are deficient in CNS 5-HT may be at increased risk for SIDS in AS because of increased apnea and delayed arousal compared with QS.NEW & NOTEWORTHY Sudden infant death syndrome (SIDS) occurs during sleep and is associated with central serotonin (5-HT) deficiency. We report that rat pups deficient in central 5-HT (TPH2-/-) are profoundly more apneic in active sleep (AS) but not quiet sleep (QS). Unlike control pups, the arousal of TPH2-/- pups in air, CO2, and hypoxia was delayed in AS compared with QS. Thus for infants deficient in central 5-HT, the risk of SIDS may be higher in AS than in QS.

Medullary Serotonin Neuron Abnormalities in an Australian Cohort of Sudden Infant Death Syndrome.

Serotonin (5-hydroxytryptamine [5-HT]) neurons in the medulla oblongata project extensively to key autonomic and respiratory nuclei in the brainstem and spinal cord regulating critical homeostatic functions. Multiple abnormalities in markers of 5-HT function in the medulla in sudden infant death syndrome (SIDS) have been reported, informing the hypothesis that at least a subset of SIDS cases is caused by deficits in 5-HT function resulting in impaired homeostatic responses to potentially life-threatening events during sleep. To investigate medullary 5-HT defects in SIDS further, we undertook qualitative analysis immunohistochemical assessment of 5-HT neuron expression within the medulla of SIDS infants (n41) and nonSIDS controls (n = 28) in an independent cohort from Forensic Science South Australia. Compared with controls SIDS cases had significantly higher 5-HT neuron numbers and density in addition to significantly altered 5-HT neuron morphology. Thus, for the first time, we replicated and corroborated previous observations of a significant abnormality in medullary 5-HT neuron expression in SIDS in a separate independent SIDS cohort. This study further supports the hypothesis that medullary 5-HT defects contribute to the pathogenesis of a subset of SIDS victims and provides additional evidence of a more complex abnormality in 5-HT neuron dysfunction specifically within the different caudal and rostral medullary 5-HT domains.

Postmortem genetic analysis of sudden unexpected death in infancy: neonatal genetic screening may enable the prevention of sudden infant death.

Tandem mass screening has recently been started in Japan, but genetic screening has yet to be widely performed in neonates and many unexpected deaths are still being reported. We previously reported two cases of sudden infant death that may have been prevented had newborn screening been performed. In this study, we retrospectively reviewed 71 cases of sudden infant death for 66 arrhythmia- and 63 metabolic disease-related genes to identify how many cases of sudden infant death may have been prevented had mass screening been performed. Next-generation sequencing revealed that six cases had arrhythmia-related gene variants and five cases had metabolic disease-related gene variants. Had genetic screening been performed in addition to biochemical and physiological screening during the neonatal period to identify those at risk of arrhythmia or metabolic disease, these infants could have been diagnosed and treated, preventing their deaths. As such, screening of newborns may prevent sudden infant death.

Long QT syndrome: the necessity and practicability of electrocardiogram screening in infancy

The occurrence rate of long QT syndrome is 1/2 000, which accounts for approximately 10% of cases of the sudden infant death syndrome.The morbidity is decreased after receiving appropriate therapy in early stage.Electrocardiogram (ECG) screening, with reliable results, is simple and feasible in infancy and can be used to conduct appropriate genetic testing.Neonatal screening is controversial because of individual differences in ECG results.Even there are some defects, it is still necessary to perform neonatal ECG screening which can improve prognosis in children with long QT syndrome. Key words: Long QT syndrome; Infant; Sudden cardiac death; Electrocardiogram screening

High serum serotonin in sudden infant death syndrome

Sudden infant death syndrome (SIDS), the leading cause of postneonatal infant mortality, likely comprises heterogeneous disorders with the common phenotype of sudden death without explanation upon postmortem investigation. Previously, we reported that ∼40% of SIDS deaths are associated with abnormalities in serotonin (5-hydroxytryptamine, 5-HT) in regions of the brainstem critical in homeostatic regulation. Here we tested the hypothesis that SIDS is associated with an alteration in serum 5-HT levels. Serum 5-HT, adjusted for postconceptional age, was significantly elevated (95%) in SIDS infants (n = 61) compared with autopsied controls (n = 15) [SIDS, 177.2 ± 15.1 (mean ± SE) ng/mL versus controls, 91.1 ± 30.6 ng/mL] (P = 0.014), as determined by ELISA. This increase was validated using high-performance liquid chromatography. Thirty-one percent (19/61) of SIDS cases had 5-HT levels greater than 2 SDs above the mean of the controls, thus defining a subset of SIDS cases with elevated 5-HT. There was no association between genotypes of the serotonin transporter promoter region polymorphism and serum 5-HT level. This study demonstrates that SIDS is associated with peripheral abnormalities in the 5-HT pathway. High serum 5-HT may serve as a potential forensic biomarker in autopsied infants with SIDS with serotonergic defects.

Sudden unexplained death in children

Sudden unexplained death in children

The gene encoding the inwardly rectifying potassium channel Kir4.1 may be involved in sudden infant death syndrome.

Disturbances in brain function and development may play a role in sudden infant death syndrome (SIDS). This Norwegian study aimed to test the hypothesis that specific variants of genes involved in water transport and potassium homeostasis would be predisposing factors for SIDS. Genetic variation in the genes encoding aquaporin-4 (AQP4), Kir4.1 (KCNJ10) and α-syntrophin was analysed in 171 SIDS cases (62.6% male) with a median age of 15.5 (2-52) weeks and 398 adult controls (70.6% male) with a median age of 44 (11-91) years. All the subjects were Caucasians who were autopsied from 1988 to 2013. The CC genotype of rs72878794 in the AQP4 gene and a combination of the CC genotype in rs17375748, rs1130183, rs12133079 and rs1186688 in KCNJ10 (4xCC) were found to be associated with SIDS. The SIDS cases with the 4xCC SNP combination were younger than the SIDS cases with other genotype combinations (p = 0.006). This study indicates that genetic variations in KCNJ10 and AQP4 may be predisposing factors for SIDS. Alterations in the expression of the AQP4/Kir4.1 complex can disrupt water and ion homeostasis, which may influence brain development and facilitate brain oedema formation This may be especially unfavourable during the first weeks of life.

Ten Percent of SIDS Cases are Murder - or are They?

Sudden infant death syndrome (SIDS) has been used as a cause of death for over four decades. It has allowed deaths of infants to be registered as natural. Within this group of deaths, a certain number have been recognized to be homicides from inflicted smothering rather than being natural or accidental deaths. Research has been conducted using confidential inquires to determine how frequent homicide is in cases called SIDS. This paper traces the history of quoted rates of homicide. Early work suggested the figure was between 2-10% of all SIDS cases, though other workers have suggested figures as high as 20-40%. With the fall in the rate of infant deaths following the "Back to Sleep" campaigns, these figures have been reevaluated. If the higher figures were correct that 20-40% of SIDS were homicides, the fall in infant deaths would be expected to be less than it has been. Current data suggests a much lower figure than 10% of current cases, with much lower overall rates of infant deaths. As well as 10% of SIDS cases having been stated to be homicides, a related question is whether multiple deaths classified as SIDS are really homicides. The paper discusses the maxim that one death is a tragedy, two is suspicious, and three deaths indicate homicide. The paper also looks at court cases and the approach that has been made in prosecutions of sudden unexpected death in infancy as multiple murder.

A single-centre review of suspected sudden infant death cases.

This study aimed to establish the number of deaths in infants under 1 year of age that were being reported for medico-legal examination at a single large academic centre in Hungary, as well as the method of these investigations with special emphasis on histopathology, ancillary techniques and the adherence of our current practice to international recommendations. A single-centre, retrospective audit was conducted on all suspected sudden infant death cases. After the review there were eight infectious background sudden infant death syndrome (SIDS) cases, infectious respiratory tract disease in 14 cases, cardiac septal tumour in one case, and hepatic, possibly metabolic, disorder in one case. Our study has highlighted that even in a single institution there is a huge heterogeneity of approaches which needs standardisation. A reclassification of infant cases according to the San Diego definition resulted in a decreased number of SIDS cases in our material. The San Diego definition and related international recommendations were found to be practical and the classification provides a guide to the standardisation of current practice.

The Sudden Death in the Young Case Registry: Collaborating to Understand and Reduce Mortality.

Knowledge gaps persist about the incidence of and risk factors for sudden death in the young (SDY). The SDY Case Registry is a collaborative effort between the National Institutes of Health, the Centers for Disease Control and Prevention, and the Michigan Public Health Institute. Its goals are to: (1) describe the incidence of SDY in the United States by using population-based surveillance; (2) compile data from SDY cases to create a resource of information and DNA samples for research; (3) encourage standardized approaches to investigation, autopsy, and categorization of SDY cases; (4) develop partnerships between local, state, and federal stakeholders toward a common goal of understanding and preventing SDY; and (5) support families who have lost loved ones to SDY by providing resources on bereavement and medical evaluation of surviving family members. Built on existing Child Death Review programs and as an expansion of the Sudden Unexpected Infant Death Case Registry, the SDY Case Registry achieves its goals by identifying SDY cases, providing guidance to medical examiners/coroners in conducting comprehensive autopsies, evaluating cases through child death review and an advanced review by clinical specialists, and classifying cases according to a standardized algorithm. The SDY Case Registry also includes a process to obtain informed consent from next-of-kin to save DNA for research, banking, and, in some cases, diagnostic genetic testing. The SDY Case Registry will provide valuable incidence data and will enhance understanding of the characteristics of SDY cases to inform the development of targeted prevention efforts.

Is it Time for a Sudden Infant Death Syndrome (SIDS) Awareness Campaign? Community Stakeholders’ Perceptions of SIDS

ABSTRACTSudden infant death syndrome (SIDS) remains a leading cause of infant death in the United States, and in Virginia. We sought to gauge the perceptions among community-identified stakeholders regarding community resource needs to reduce SIDS. Snowball sampling identified important community stakeholders to be interviewed as key informants. A semi-structured interview was delivered to determine resource needs to reduce SIDS, and whether high-risk community members were aware of SIDS risk factors. Interviews were conducted in two geographic areas with higher than average rates of infant mortality: Winchester City, VA; Page County, VA. Seventy-four interviews were completed with stakeholders in healthcare, social services, and a variety of other organizations. The majority of respondents perceive that high-risk community members are not aware of factors that can lead to SIDS (50%). Participants suggested that more “education” is needed to further reduce SIDS rates in their communities (73%). Respondents detailed that more pervasive, strategic, and multi-channelled education is necessary to reduce cases of SIDS. Community leaders perceive that high-risk community members are not fully aware of risk factors that can lead to SIDS. Maternal/child health stakeholders in these Virginia locales suggested more community-based education as a potential solution.