- Email: [email protected]
SIDS symposium – A perspective for future research
Paediatric Respiratory Reviews 15 (2014) 285–286
Contents lists available at ScienceDirect
Paediatric Respiratory Reviews
Editorial
SIDS symposium – A perspective for future research This update on Sudden infant death syndrome (SIDS) brings together reviews of cardiorespiratory causes for SIDS. The first point to highlight is that research into all causes of the sudden and unexpected death of infants (SUDI) is active, progressing, and doing so because it is needed. The first definition of SIDS in 1969 aimed to focus attention and research on the major cause of post-neonatal infant deaths [1]. Even in current research, the definition of SIDS used to describe the devastating event is ‘‘the sudden death of an infant under one year of age which remains unexplained after a thorough case investigation, including performance of a complete autopsy, examination of the death scene, and review of the clinical history’’ although later definitions include reference to the usual occurrence during sleep times [2,3]. Maintaining uniformity of definitions, and/or of the characteristics of the cases is an ongoing tension and use of the term Sudden Unexpected Death in Infancy (SUDI) is one attempt to include cases ranging from those that remain unexplained following full investigation (SIDS), to those that are fully explained after investigation. Some cases are also called ‘‘unascertained’’ if the pathologist or coroner is unclear about the extent to which the death is explained, often because of incomplete information about the circumstances of death. In the early 1990’s the prone sleep position was identified as a major risk factor in several epidemiological studies. Subsequent public health campaigns reduced the incidence of prone sleeping in infants and follow-up studies showed that this change in behaviour was associated with a 50% or more reduction in the rate of death from SIDS. Figure 1. [4]. But, despite a great reduction in the SIDS rate due to risk-reduction campaigns, SIDS remains the most common single cause of death in the post-neonatal period in developed countries, including Australia.
The underlying cause of SIDS remains unknown, and may be a combination of factors. Since most infants (even with the known risk factors) do not die, it is presumed that those infants who did die have some additional vulnerability that led to their death. The Triple Risk model proposes that infants die of SIDS because they have a developmental abnormality or vulnerability that means they fail to have appropriate protective responses to lifethreatening stressors (e.g. asphyxia, hypoxia, or hypercapnia) as they pass through a critical period of development [5]. Deaths continue to occur, to devastate families, and the threat of such sudden and unexpected death heightens the anxiety of new parents. Despite epidemiological risk showing ongoing links to cigarette smoking and lower socioeconomic status, the families of non-smoking parents in higher soecioeconomic categories continue to be affected. What then do we know about the cause of this phenomenon, how can parents reduce their risk and is there any hope of future screening or elimination of SIDS? Contained within the mini-symposium is a range of up to date reviews of contemporary theories in the aetiology of SIDS. The paper by Galland and Elder reviews biological mechanisms in this triple-risk framework [6]. Machaalani and Waters look specifically at brainstem abnormalities as a possible cause for the vulnerability, and/or failure to respond to an external stressor [7]. Sweeting and Samsarian examine one area of fruitful research, which has been the investigation of specific cardiac abnormalities [8]. Another area that has been researched is that of infectious causes, reviewed by Alfelali and Khandaker [9]. Horne and Nixon examine how physiological studies in infants shed light on the syndrome, as well as putting their role in clinical medicine into perspective [10]. The final update by Fleming et al., provides details of interactions between SIDS deaths and co-sleeping, helping to refine how recommendations can be made in this area [11]. The ongoing need for answers has driven a new generation of parents of these unfortunate infants to campaign in support of the resources that researchers need to continue to investigate the phenomenon, as we expect will continue to occur until a valid screening tool, or marker of risk has been identified. References
Figure 1. Taken from Australian Bureau of statistics. Death rates from SIDS 1989– 1999. http://dx.doi.org/10.1016/j.prrv.2014.09.005 1526-0542/ß 2014 Elsevier Ltd. All rights reserved.
[1] Beckwith JB. Defining the sudden infant death syndrome. Arch Pediatr Adolesc Med 2003;157(3):286–90. [2] Krous HF, et al. Sudden infant death syndrome and unclassified sudden infant deaths: a definitional and diagnostic approach. Pediatrics 2004;114(1): 234–8. [3] Willinger M, James LS, Catz C. Defining the sudden infant death syndrome (SIDS): deliberations of an expert panel convened by the National Institute of Child Health and Human Development. Pediatr Pathol 1991;11(5):677–84. [4] Moon RY. SIDS and other sleep-related infant deaths: expansion of recommendations for a safe infant sleeping environment. Pediatrics 2011;128(5): 1030–9.
286
Editorial / Paediatric Respiratory Reviews 15 (2014) 285–286
[5] Filiano JJ, Kinney HC. A perspective on neuropathologic findings in victims of the sudden infant death syndrome: the triple-risk model. Biol Neonate 1994;65(3–4):194–7. [6] Galland B, Elder D. Unexpected Death in Infancy: Biological Mechanisms. Paediatric Respir Rev 2014;15(4):287–92. [7] Machaalani R, Waters K. Neurochemical abnormalities in the brainstem of the Sudden Infant Death Syndrome (SIDS) victims. Paediatric Respir Rev 2014;15(4):293–300. [8] Sweeting J, Samsarian C. Cardiac Abnormalities and Sudden Infant Death Syndrome. Paediatric Respir Rev 2014;15(4):301–6.
[9] Khandaker G, Jones C. Infection as an hypothesis for Sudden Infant Death Syndrome. Paediatric Respir Rev 2014. [10] Horne R, Nixon G. The role of physiological studies and apnoea monitoring in infants. Paediatric Respir Rev 2014;15(4):312–8. [11] Fleming P, Pease A, Blair P. Bed-sharing and unexpected infant deaths: What is the relationship? in press. doi:10.1016/j.prrv.2014.10.008
Karen A. Waters
Contents lists available at ScienceDirect
Paediatric Respiratory Reviews
Editorial
SIDS symposium – A perspective for future research This update on Sudden infant death syndrome (SIDS) brings together reviews of cardiorespiratory causes for SIDS. The first point to highlight is that research into all causes of the sudden and unexpected death of infants (SUDI) is active, progressing, and doing so because it is needed. The first definition of SIDS in 1969 aimed to focus attention and research on the major cause of post-neonatal infant deaths [1]. Even in current research, the definition of SIDS used to describe the devastating event is ‘‘the sudden death of an infant under one year of age which remains unexplained after a thorough case investigation, including performance of a complete autopsy, examination of the death scene, and review of the clinical history’’ although later definitions include reference to the usual occurrence during sleep times [2,3]. Maintaining uniformity of definitions, and/or of the characteristics of the cases is an ongoing tension and use of the term Sudden Unexpected Death in Infancy (SUDI) is one attempt to include cases ranging from those that remain unexplained following full investigation (SIDS), to those that are fully explained after investigation. Some cases are also called ‘‘unascertained’’ if the pathologist or coroner is unclear about the extent to which the death is explained, often because of incomplete information about the circumstances of death. In the early 1990’s the prone sleep position was identified as a major risk factor in several epidemiological studies. Subsequent public health campaigns reduced the incidence of prone sleeping in infants and follow-up studies showed that this change in behaviour was associated with a 50% or more reduction in the rate of death from SIDS. Figure 1. [4]. But, despite a great reduction in the SIDS rate due to risk-reduction campaigns, SIDS remains the most common single cause of death in the post-neonatal period in developed countries, including Australia.
The underlying cause of SIDS remains unknown, and may be a combination of factors. Since most infants (even with the known risk factors) do not die, it is presumed that those infants who did die have some additional vulnerability that led to their death. The Triple Risk model proposes that infants die of SIDS because they have a developmental abnormality or vulnerability that means they fail to have appropriate protective responses to lifethreatening stressors (e.g. asphyxia, hypoxia, or hypercapnia) as they pass through a critical period of development [5]. Deaths continue to occur, to devastate families, and the threat of such sudden and unexpected death heightens the anxiety of new parents. Despite epidemiological risk showing ongoing links to cigarette smoking and lower socioeconomic status, the families of non-smoking parents in higher soecioeconomic categories continue to be affected. What then do we know about the cause of this phenomenon, how can parents reduce their risk and is there any hope of future screening or elimination of SIDS? Contained within the mini-symposium is a range of up to date reviews of contemporary theories in the aetiology of SIDS. The paper by Galland and Elder reviews biological mechanisms in this triple-risk framework [6]. Machaalani and Waters look specifically at brainstem abnormalities as a possible cause for the vulnerability, and/or failure to respond to an external stressor [7]. Sweeting and Samsarian examine one area of fruitful research, which has been the investigation of specific cardiac abnormalities [8]. Another area that has been researched is that of infectious causes, reviewed by Alfelali and Khandaker [9]. Horne and Nixon examine how physiological studies in infants shed light on the syndrome, as well as putting their role in clinical medicine into perspective [10]. The final update by Fleming et al., provides details of interactions between SIDS deaths and co-sleeping, helping to refine how recommendations can be made in this area [11]. The ongoing need for answers has driven a new generation of parents of these unfortunate infants to campaign in support of the resources that researchers need to continue to investigate the phenomenon, as we expect will continue to occur until a valid screening tool, or marker of risk has been identified. References
Figure 1. Taken from Australian Bureau of statistics. Death rates from SIDS 1989– 1999. http://dx.doi.org/10.1016/j.prrv.2014.09.005 1526-0542/ß 2014 Elsevier Ltd. All rights reserved.
[1] Beckwith JB. Defining the sudden infant death syndrome. Arch Pediatr Adolesc Med 2003;157(3):286–90. [2] Krous HF, et al. Sudden infant death syndrome and unclassified sudden infant deaths: a definitional and diagnostic approach. Pediatrics 2004;114(1): 234–8. [3] Willinger M, James LS, Catz C. Defining the sudden infant death syndrome (SIDS): deliberations of an expert panel convened by the National Institute of Child Health and Human Development. Pediatr Pathol 1991;11(5):677–84. [4] Moon RY. SIDS and other sleep-related infant deaths: expansion of recommendations for a safe infant sleeping environment. Pediatrics 2011;128(5): 1030–9.
286
Editorial / Paediatric Respiratory Reviews 15 (2014) 285–286
[5] Filiano JJ, Kinney HC. A perspective on neuropathologic findings in victims of the sudden infant death syndrome: the triple-risk model. Biol Neonate 1994;65(3–4):194–7. [6] Galland B, Elder D. Unexpected Death in Infancy: Biological Mechanisms. Paediatric Respir Rev 2014;15(4):287–92. [7] Machaalani R, Waters K. Neurochemical abnormalities in the brainstem of the Sudden Infant Death Syndrome (SIDS) victims. Paediatric Respir Rev 2014;15(4):293–300. [8] Sweeting J, Samsarian C. Cardiac Abnormalities and Sudden Infant Death Syndrome. Paediatric Respir Rev 2014;15(4):301–6.
[9] Khandaker G, Jones C. Infection as an hypothesis for Sudden Infant Death Syndrome. Paediatric Respir Rev 2014. [10] Horne R, Nixon G. The role of physiological studies and apnoea monitoring in infants. Paediatric Respir Rev 2014;15(4):312–8. [11] Fleming P, Pease A, Blair P. Bed-sharing and unexpected infant deaths: What is the relationship? in press. doi:10.1016/j.prrv.2014.10.008
Karen A. Waters