Manifestation and Pathogenesis of Sudden Infant Death Syndrome: A Review

Crit Rev Eukaryot Gene Expr. 2020;30(2):111-120. doi: 10.1615/CritRevEukaryotGeneExpr.2020033009.

Abstract

Historically known as "cot death," sudden infant death syndrome (SIDS) is one of the leading causes of postnatal death in infants. According to the Centers for Disease Control and Prevention in 2010, more than 2,000 U.S. infants died from SIDS. Sudden infant death syndrome is the unexplainable death of an infant, less than one year old, that is otherwise healthy. SIDS was first discovered in 1969, and it typically presents in infants with a peak incidence between 2 and 4 months of age. Death by SIDS is typically more prevalent in the winter months, making the infant increasingly vulnerable. Despite witnessing a significant decrease in deaths by SIDS due to awareness campaigns and medical advancements, SIDS remains the leading cause of infant mortality in Western countries, accounting for half of all postnatal deaths. Throughout this paper, we will focus on the environmental factors, physiological factors, and genetic factors that have been postulated to cause an infant to be susceptible to SIDS. The initially postulated pathogenesis of SIDS was explained as the triple risk hypothesis, which states that an increase in SIDS risk presents in situations where there is an overlap of three or more factors. The presence of three or more factors suggests that the trio of factors overrule the infant's threshold for survival; therefore, the infant's homeostasis is unable to protect against the dangers. Death by SIDS has declined considerably from 130.3 deaths per 100,000 live births in 1998 to 38.7 deaths per 100,000 live births in 2014.

Publication types

  • Review

MeSH terms

  • Female
  • Humans
  • Infant
  • Infant Mortality*
  • Male
  • Risk Factors
  • Sudden Infant Death / epidemiology*
  • Sudden Infant Death / genetics*
  • Sudden Infant Death / pathology
  • United States / epidemiology