In developed countries Sudden Infant Death Syndrome (SIDS) is the most common cause of death for infants between the age of 1 month and 1 year. The etiology of SIDS is likely to be multifactorial, and current paradigms often describe three overlapping elements of risk. Those elements are a critical developmental period, a vulnerable infant and one or more exogenous stressors.
In the “Triple-risk Model”, SIDS infants are described as having an underlying vulnerability in cardio-respiratory control in the central nervous system during a critical period when autonomic control is developing. This vulnerability might affect the response to exogenous stressors, including prone sleep position, hypoxia and increased carbon dioxide.
In the “Common Bacterial Hypothesis” and “Fatal Triangle”, the focus is on the stressors. A combination of common respiratory infections can cause SIDS in an infant during a developmentally vulnerable period. This theory also includes three factors of vulnerability: a genetic predisposition, vulnerable developmental age and infectious stressors. In the “Fatal Triangle” theory, infection, inflammation and genetics each play a role in triggering a SIDS fatality.
From our work in an animal model we have found that rat pups die from a combination of infectious insults, during a critical time of development. This is exacerbated by perinatal nicotine exposure, a condition shown to alter the autonomic response in exposed offspring. We are proposing that shock and cardiovascular collapse is a key element that links these theories.