Infant Sleeping Position and Sudden Infant Death Syndrome

GENESIS

The postmortem diagnosis of sudden infant death syndrome (SIDS), once known as “cot death,” was introduced midway through the 20th century, but its association with infant sleeping position was not established until the 1990s. SIDS is considered to have a multifactorial and heterogeneous basis whereby some infants are born with risk factors that make them more vulnerable to dying during infancy with additive subtle risk factors. There is a growing body of evidence suggesting that a proportion of SIDS has a genetic underpinning, including a four- to five fold relative risk of SIDS in subsequent siblings and an increased SIDS risk in monozygotic twins compared to dizygotic. Historically, metabolic conditions have been thought to be a substantial proportion of SIDS cases, many of which are now being detected early and treated after the introduction of tandem mass spectrometry–based newborn screening programs. Although morbidity and mortality of conditions such as medium-chain acyl-CoA dehydrogenase (MCAD) deficiency has significantly reduced, neonatal death in individuals with early disease manifestation and severe hypoglycemia may still occur. Decompensation due to MCAD deficiency has been reported in the first hours and days of life before any metabolic screening results become available, with episodes that lead to death in up to 5% of affected patients. Rigorous cardiac genetic evaluations have not been historically recommended unless the circumstances at the time of death or family history are suggestive of an arrhythmic death.

Although rates of SIDS have decreased by 50% since the 1990s, African-American and Native-American infants are more than twice as likely to die of SIDS than are White babies. A metaanalysis of 217 articles found 7 qualitative studies that surveyed African-American mothers and found several themes: many tended to believe that SIDS is a random occurrence and is not preventable, so they may feel that there was little reason to make their infant sleep in a cold, hard crib when they could sleep in a warm, comfortable bed with them. In a 2022 retrospective study of infant mortality in the District of Columbia, 89% were African American and 63% involved bed sharing, despite more than half of those cases having a known safe sleep surface available. Nurses should work with Black mothers to understand their cultural beliefs while educating them about safe sleep practices. Some genetic variants have been proposed as risk factors for SIDS; for example, the carnitine palmitoyltransferase 1 ( CPT1A ) p.P479L variant common in Aboriginal populations on the west and north coasts of Alaska and Canada and in northeast Siberia and Greenland, although the association may be more prevalent on the basis of drift, positive selection, or a founder effect, and more likely has a noncausal association with infant death owing to a range of social and environmental risk factors that also occur at higher rates in the population. Currently, whole-exome or whole-genome sequencing techniques are largely used postmortem in an otherwise healthy infant. These broad tests do not have adequate predictive value and are still cost-prohibitive for universal use after the death of an infant.

The leading model of SIDS is the “triple-risk model,” which postulates that SIDS occurs in a biologically vulnerable infant during a critical developmental period when triggered by a stressor or external risk factor. Infant sleeping position has emerged as a major risk factor for SIDS. It has been hypothesized that abnormalities in the arcuate nucleus, which controls breathing and waking, might be involved in some cases of SIDS. Normal infants sense inadequate air intake, which triggers them to awaken, cry, and change cardiorespiratory function to compensate for insufficient oxygen and excess carbon dioxide. This situation might result from infants sleeping on their stomachs and rebreathing exhaled air that is trapped in underlying bedding, and a baby with defective functioning of the arcuate nucleus might lack this protective mechanism and succumb to SIDS. There are also other predisposing factors for SIDS, such as chronic hypoxia induced by maternal cigarette smoking during pregnancy or concurrent respiratory infection in the infant. Also, more SIDS cases occur in the colder months, when such infections are more common. Increases in cellular and protein immune responses also have been suggested to play a role, along with the microbiome in the gut. Arousal thresholds are significantly higher in both active and quiet sleep when infants sleep prone at 2–3 weeks or 2–3 months (the age of peak susceptibility to SIDS) but not at 5–6 months (the age when susceptibility to SIDS is decreased). Thus the prone position significantly impairs arousal from sleep during the time when infants are most likely to die from SIDS, which is the major cause of death for infants between 1 and 12 months of age.