A perspective on SIDS pathogenesis. The hypotheses: plausibility and evidence
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OPINION
Open Access
A perspective on SIDS pathogenesis. The hypotheses: plausibility and evidence Paul N Goldwater1,2
Abstract Several theories of the underlying mechanisms of Sudden Infant Death Syndrome (SIDS) have been proposed. These theories have born relatively narrow beach-head research programs attracting generous research funding sustained for many years at expense to the public purse. This perspective endeavors to critically examine the evidence and bases of these theories and determine their plausibility; and questions whether or not a safe and reasoned hypothesis lies at their foundation. The Opinion sets specific criteria by asking the following questions: 1. Does the hypothesis take into account the key pathological findings in SIDS? 2. Is the hypothesis congruent with the key epidemiological risk factors? 3. Does it link 1 and 2? Falling short of any one of these answers, by inference, would imply insufficient grounds for a sustainable hypothesis. Some of the hypotheses overlap, for instance, notional respiratory failure may encompass apnea, prone sleep position, and asphyxia which may be seen to be linked to co-sleeping. For the purposes of this paper, each element will be assessed on the above criteria. Background and leading hypotheses Before committing to this task it is apposite to consider the background and context in which the various hypotheses arose. Beckwith’s 1970 definition of SIDS [1] created the presumption that SIDS babies were normal. Questions arose after Kinney et al. [2] developed their hypothesis based on histopathological abnormalities of the brain, a prenatal origin of these and sudden death occurring during a vulnerable period in infancy. Bergman (1970) [3] had argued against a “single characteristic that ordains an infant for death,” but for an interaction of risk factors with variable probabilities. This approach was supported by Wedgewood (1972) [4] whose hypothesis consisted of host vulnerability, age-specific risks, and precipitating factors. Others have supported a multifactorial approach (Raring 1975) [5], (Rognum and Saugstag 1993) [6]. The triple risk hypothesis of Filiano and Kinney (1994) [7] has been popular with its central focus on brainstem prenatal injury in a subset of SIDS, denoting a not universal finding. The National Institute of Child Health and Development SIDS Strategic Plan 2001 [8], stated Correspondence: [email protected] 1 Microbiology & Infectious Diseases, SA Pathology at the Women’s & Children’s Hospital Full list of author information is available at the end of the article
unequivocally that ‘Knowledge acquired during the past decade supports the general hypothesis that infants who die from SIDS have abnormalities at birth that render them vulnerable to potentially life-threatening challenges during infancy.’ In essence, this states that SIDS is a developmental disorder originating during fetal development. Interest in the brainstem began with Naeye’s (1976) [9] findings of astrogliosis in 50% of SIDS and controls. Hypoxia was
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