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1533 results in The University of Adelaide Press

Page 2 of 77

  • 33 - Animal Models: Illuminating the Pathogenesis of Sudden Infant Death Syndrome

    • By Aihua Li, Department of Molecular and Systems Biology, Geisel School of Medicine at Dartmouth, Lebanon, USA, Robert A Darnall, Department of Molecular and Systems Biology, Geisel School of Medicine at Dartmouth, Lebanon, USA Department of Pediatrics, Geisel School of Medicine at Dartmouth, Lebanon, USA, Susan Dymecki, Department of Genetics, Harvard Medical School, Boston, USA, James C Leiter, Department of Molecular and Systems Biology, Geisel School of Medicine at Dartmouth, Lebanon, USA
  • Edited by Jodhie R. Duncan, University of Melbourne, Roger W. Byard, University of Adelaide
  • Book:
    SIDS Sudden Infant and Early Childhood Death
    Published by:
    The University of Adelaide Press
    Published online:
    20 July 2018
    Print publication:
    30 April 2018, pp 759-828

  • Summary

    Introduction

    Three research areas derived from human studies of epidemiology, pathology, and sleep in infants have made contributions to our understanding of sudden infant death syndrome (SIDS). Epidemiological studies of infants who died of SIDS have identified a variety of risk factors associated with increased and decreased risk of SIDS (1-7), including prone sleeping position (8, 9), maternal cigarette smoking during pregnancy, and heat stress in the infant, often related to overheated environments, excessive bed clothing, or other unsafe sleeping practices (8, 10, 11). Additional risk factors include a recent upper respiratory tract infection, bed sharing, prematurity, and intrauterine and/or postnatal hypoxic stress.

    Similar progress in understanding the origins of SIDS has been made by pathologists analysing the brains of infants who died and were classified as SIDS. Analyses of brain tissue from these infants have consistently revealed a high prevalence of abnormalities in the brainstem serotoninergic system including an increased number of serotonergic neurons, a higher proportion of serotonergic neurons displaying immature morphology, decreased tissue levels of serotonin (5-HT) and its synthetic enzyme, tryptophan hydroxylase 2 (TPH2), and decreased 5-HT receptor binding intensity both in serotonergic nuclei themselves and in several nuclei that are important in cardiorespiratory control (9, 12-16). Similar serotonin system deficits have been described in infants who died of asphyxia (17). There has been persistent speculation that infants who died of SIDS suffered from hypoxia (i.e. low oxygen levels) at some time preceding death (18-22), and hypoxia appeared to delay maturation of the brain in infants who died of SIDS (19-21, 23, 24).

    Finally, sleep studies in the infants who subsequently died of SIDS have revealed a sequence of repetitive episodes of hypoxia preceding, or following, apnea and/or bradycardia, followed by autoresuscitative efforts to restore normal breathing and arouse from sleep (25-28). Death occurred when the autoresuscitation or arousal following prolonged apnea failed to restore regular breathing and adequate oxygenation. Many infants experienced sequences of multiple hypoxic apneic events from which they recovered, only to succumb to a final event in which autoresuscitation and/or arousal failed.

  • 22 - Autonomic Cardiorespiratory Physiology and Arousal of the Fetus and Infant

    • By Rosemary Sc Horne, The Ritchie Centre, Monash University and Hudson Institute of Medical Research, Melbourne, Australia
  • Edited by Jodhie R. Duncan, University of Melbourne, Roger W. Byard, University of Adelaide
  • Book:
    SIDS Sudden Infant and Early Childhood Death
    Published by:
    The University of Adelaide Press
    Published online:
    20 July 2018
    Print publication:
    30 April 2018, pp 449-490

  • Summary

    Introduction

    Despite intensive research over the past decades, the mechanisms which lead to sudden infant death syndrome (SIDS) still remain elusive. SIDS is presumed to occur in an apparently healthy infant during a period of sleep (1). A failure of cardiorespiratory control mechanisms, together with an impaired arousal from sleep response, are believed to play an important role in the final event of SIDS. Sleep has a marked influence on respiratory and cardiovascular control in both adults and infants, although sleep states, sleep architecture, and arousal from sleep processes in infants are very different from those of adults and undergo significant maturation during the first year of life, particularly in the first six months when SIDS risk is greatest (2).

    Arousal from sleep involves both physiological and behavioral responses and has long been considered a vital survival response for restoring homeostasis in reaction to various life-threatening situations, such as prolonged hypoxia or hypotension (3). There are two distinct arousal types defined in infants, subcortical activation and full cortical arousal, which reflect the hierarchical activation from the brainstem (including heart rate, blood pressure, and ventilation changes) to the cortex (4). Any impairment of these protective responses may render an infant vulnerable to the respiratory and cardiovascular instabilities that are common during infancy and that have been postulated to occur in SIDS. In support of this possibility, extensive physiological and neuropathological studies have provided compelling evidence that impaired cardiovascular control, with a concomitant failure to arouse from sleep, are involved in the final events leading to SIDS. The first six months of life are a critical period of development when rapid maturation of the brain, cardiorespiratory system, and sleep state organization are all taking place (2, 5). Thus, the investigation of sleep physiology in healthy infants during this high-risk period provides important insights into the likely mechanisms involved in the pathogenesis of SIDS.

    Development of Sleep

    The maturation of sleep is one of the most important physiological processes occurring during the first year of life and is particularly rapid during the first six months after birth (5). Behavioral states in infants are defined by physiological and behavioral variables that are stable over time and occur repeatedly in an individual infant and also across infants (6). The emergence of sleep states is dependent on the central nervous system and is a good and reliable indicator of normal and abnormal development (7).

  • 4 - Sudden Infant Death Syndrome: History

    • By Leanne Raven, Faculty of Science, Health, Education and Engineering, University of Sunshine Coast, Queensland, Australia
  • Edited by Jodhie R. Duncan, University of Melbourne, Roger W. Byard, University of Adelaide
  • Book:
    SIDS Sudden Infant and Early Childhood Death
    Published by:
    The University of Adelaide Press
    Published online:
    20 July 2018
    Print publication:
    30 April 2018, pp 73-84

  • Summary

    Introduction

    Over the last century human life expectancy has increased in many countries throughout the world. After World War II it was still accepted by the medical and scientific community that an infant could die suddenly and unexpectedly from no known cause (1). In the 1960s, this view began to be challenged and in 1963 and 1969 two international conferences were held to focus on the etiology of sudden infant death syndrome (SIDS), and the first working definition of SIDS was established (1).

    However, given the overall decline in perinatal mortality during the last century due to medical advancements and higher standards of living, our societal expectations have changed. It has now become the norm that children will thrive and grow to outlive their parents, when 100 years ago this was frequently not the case. With our increased knowledge about how the human body functions and about how to prevent childhood diseases, it has become unthinkable that in the 21st century a healthy child would die in their sleep from SIDS, and yet this still happens to many families. Indeed, SIDS remains the leading cause of infant mortality in Western countries, contributing to half of all post-neonatal deaths (2, 3).

    For any parent there could be no greater nightmare than the silent tragedy of SIDS. When a child's death is attributed to SIDS, a diagnosis of exclusion, the infant's death remains unexplained even after a thorough investigation, including performance of a complete autopsy and review of the circumstances of death and clinical history (4). It has been estimated by Red Nose that, on average, at least 60 people are impacted by a child's death to SIDS. The parents, siblings, and extended family are at the core of this experience, with friends, work colleagues, first responders, coroners, and health professionals included in the network of those impacted. SIDS communities have formed in every country as a result of these tragedies, often through the significant leadership and unrelenting passion of the families and individuals who have lived through the experience of SIDS. These families have embarked on a quest for answers as to why this tragedy happened to them, with their journey often involving activities undertaken in honor and memory of their beloved children.

  • 31 - The Genetics of Sudden Infant Death Syndrome

  • Edited by Jodhie R. Duncan, University of Melbourne, Roger W. Byard, University of Adelaide
  • Book:
    SIDS Sudden Infant and Early Childhood Death
    Published by:
    The University of Adelaide Press
    Published online:
    20 July 2018
    Print publication:
    30 April 2018, pp 711-730

  • Summary

    Introduction

    Despite a decrease in the mortality rates of sudden infant death syndrome (SIDS) over the past decades, SIDS is still one of the leading causes of post-neonatal and infant death. In the United States, 8% of all infant deaths are attributed to SIDS, only behind congenital malformations and chromosomal abnormalities (21%) and disorders relating to prematurity and low birth weight (17%) (1). While efforts have been made to reduce the role of environmental factors, such as sleep environment and smoking, this persistent mortality highlights the importance of intrinsic factors involved in SIDS, including genetic changes that predispose infants to, or are directly responsible for, SIDS (2, 3). In addition, the incidence of SIDS in families where one infant has died from SIDS is increased by over fivefold, providing further evidence of a role for genetic factors (4, 5).

    A role for genetic factors in SIDS is consistent with the Triple Risk Model of SIDS, with genetic factors contributing to the “vulnerable infant”. The Triple Risk Model hypothesizes that three elements are present for SIDS to occur (6):

  • 1. Critical developmental period: Mortality from SIDS clusters during certain ages. Developmental changes in autonomic control co-incide with periods of increased susceptibility to SIDS.

  • 2. Vulnerable infant: Understood largely in terms of associated risk factors such as race or exposure to alcohol or tobacco during pregnancy; infants dying from SIDS have been shown to have differences in autonomic responses that impair their ability to respond to challenges in the sleep environment. In addition, genetic conditions, such as a cardiac channelopathy, a metabolic condition, or a seizure disorder, may cause the infant to be vulnerable and at greater risk of SIDS.

  • 3. Exogenous stressor(s): Stressors associated with SIDS include overheating, secondhand tobacco smoke, upper respiratory tract infection, bed sharing, and prone sleeping position (6).

    • According to the Triple Risk Model, although most babies encounter and survive environmental stressors, a vulnerable infant who becomes challenged during a critical period may not be able to overcome the stressor, leading to SIDS. Thus, SIDS can be seen as representing a severe, lethal phenotype with genetic causes that contribute to the vulnerable infant. Genomic approaches to SIDS attempt to understand genetic mechanisms causing or contributing to this infant vulnerability.

  • 2 - Sudden Infant Death Syndrome: An Overview

    • By Jhodie R Duncan, School of Medicine, The University of Adelaide, Adelaide, Australia and Florey Institute of Neuroscience and Mental Health, Victoria, Australia, Roger W Byard, School of Medicine, The University of Adelaide, Adelaide, Australia and Florey Institute of Neuroscience and Mental Health, Victoria, Australia
  • Edited by Jodhie R. Duncan, University of Melbourne, Roger W. Byard, University of Adelaide
  • Book:
    SIDS Sudden Infant and Early Childhood Death
    Published by:
    The University of Adelaide Press
    Published online:
    20 July 2018
    Print publication:
    30 April 2018, pp 15-50

  • Summary

    Introduction

    The term sudden infant death syndrome (SIDS) was first proposed in 1969 in order to focus attention on a subgroup of infants with similar clinical features whose deaths occurred unexpectedly in the postnatal period (1). Today the definition of SIDS refers to death in a seemingly healthy infant younger than 1 year of age whose death remains unexplained after a thorough case investigation including a complete autopsy, review of medical and clinical history, and death scene investigation (2). SIDS is typically associated with a sleep period (3) with death presumed to have occurred during sleep itself or in the transition between sleep and waking (4). This led to application of the terms “cot” or “crib” death; however, these terms are rarely used today. Furthermore, while the definition is inclusive of infants up to 1 year of age, approximately 95% of SIDS deaths occur in the first six months of life with a peak incidence in infants aged between 2 to 4 months (5). While there are distinctive features associated with the syndrome there are no diagnostic features that can be attributed to a SIDS death. Indeed, application of the term relies on a process of elimination and when no known cause of death or contributing factors can be determined, the term SIDS is usually applied. Thus, while the debate continues regarding the definition and use of the term SIDS, and no one definition has been universally accepted, one certainty persists, and that is that SIDS still remains a diagnosis of exclusion (1).

    History

    Sudden death in a seemingly healthy infant during sleep is not a phenomenon of modern times, with cases being recorded throughout history for thousands of years. Indeed, one of the first cases is mentioned in the Bible (1 Kings 3:19). However, these deaths have generally been attributed to overlaying, as it was common practice to sleep in the same bed as a child. Indeed, the death of an infant by “overlay” was considered such an issue that by the seventh century the event was a punishable offence (6), with the introduction of a “protective” wooden arcuccio for infants to sleep in during the 18th century in Europe with severe penalties if the infant died in a co-sleeping arrangement and the frame was not used (7).

  • 29 - Abnormalities of the Hippocampus in Sudden and Unexpected Death in Early Life

    • By Hannah C Kinney, Department of Pathology, Boston Children's Hospital and Harvard Medical School, Boston, USA, Robin L Haynes, Department of Pathology, Boston Children's Hospital and Harvard Medical School, Boston, USA, Dawna D Armstrong, Retired Professor Pathology Baylor College of Medicine, Department of Pathology, Houston, USA, Richard D Goldstein, Department of Psychosocial Oncology and Palliative Care, Dana-Farber Cancer Institute, Department of Medicine, Boston Children's Hospital and Harvard Medical School, Boston, USA
  • Edited by Jodhie R. Duncan, University of Melbourne, Roger W. Byard, University of Adelaide
  • Book:
    SIDS Sudden Infant and Early Childhood Death
    Published by:
    The University of Adelaide Press
    Published online:
    20 July 2018
    Print publication:
    30 April 2018, pp 661-688

  • Summary

    Introduction

    The terrifying aspect of the sudden infant death syndrome (SIDS) is that it occurs in infants who seem healthy and then die without warning when put down to sleep. SIDS is not typically witnessed and it is surmized that death occurs during sleep, or during one of the many transitions to waking that occur during normal infant sleep-wake cycles (1). Multiple sleep-related mechanisms have been proposed to cause SIDS (1, 2). These mechanisms include suffocation/asphyxiation in the face-down sleep position, central and/or obstructive sleep apnea, impaired-state-dependent responses to hypoxia and/ or hypercarbia, inadequate autoresuscitation, defective autonomic regulation of blood pressure or thermal responses, and abnormal arousal to life-threatening challenges during sleep.

    In this chapter, we review the hypothesis and the neuropathologic evidence that SIDS is precipitated by a dentate gyrus-related seizure or a limbic-related instability that involves the central homeostatic network (CHN). We begin with an overview of this hypothesis, and then review our neuropathologic evidence for an epileptiform hippocampal lesion in the brain of a subset of SIDS infants and young children (41-50% respectively) who died suddenly and unexpectedly (3-5). We then consider the putative mechanism whereby dentate lesions cause seizures, the role of the hippocampus as part of the CHN in stress responses (such as the face-down sleep position), and the potential interactions of brainstem serotonergic (5-HT) deficits and the hippocampus in the pathogenesis of sudden death in infants. We conclude with further directions for research into the role of the hippocampus in sudden and unexpected death in early life.

    The Limbic Seizure-Related Hypothesis in SIDS

    In 1986, Harper suggested that some SIDS deaths may be due to a fatal seizure during sleep that arises in forebrain-limbic-related circuits (6). This hypothesis arose from the recognition of the following inter-related phenomena: limbic regions are particularly susceptible to epileptogenesis; sleep states lower the threshold for seizure; and SIDS is linked to sleep and arousal. Sleep itself is thought to be a precarious state, in part because of the loss of the major “back-up” forebrain systems of waking which influence the final common pathways in the brainstem that mediate central cardiorespiratory function during sleep. Forebrain limbic regions, such as the hippocampus and amygdala, which are part of the CHN, modulate brainstem cardiorespiratory control in a manner influenced by the sleep-waking cycles.

  • 12 - Preventive Strategies for Sudden Infant Death Syndrome

  • Edited by Jodhie R. Duncan, University of Melbourne, Roger W. Byard, University of Adelaide
  • Book:
    SIDS Sudden Infant and Early Childhood Death
    Published by:
    The University of Adelaide Press
    Published online:
    20 July 2018
    Print publication:
    30 April 2018, pp 217-256

  • Summary

    Introduction

    The impact on sudden infant death rates of the “Back to Sleep” or “Reduce the Risk” campaigns introduced across many countries in the late 1980s and early 1990s has been hailed as one of the great public health success stories of the 20th century (1, 2). Many countries around the world saw substantial reductions in their sudden infant death syndrome (SIDS) rates around the time of introduction of the campaigns (Figure 12.1), with falls of between 42% and 92% (Figure 12.2). The rate of SIDS was halved in the United Kingdom (UK) in just one year, and in New Zealand in two years (1, 3). Instituting a “Back to Sleep” campaign has been estimated to have saved 3,000 lives in New Zealand, 17,000 lives in the UK, and 40,000 lives in the United States (3).

    Since the initial drop-off immediately after the “Back to Sleep” campaigns, the rate of SIDS has continued to decline in line with overall post-neonatal mortality (4). For example, in England and Wales, SIDS rates fell from an average of 2.27 per 1,000 live births in 1986-88 to 0.66 per 1,000 live births in 1993-95 and 0.32 per 1,000 live births in 2012-14 (5). These reductions have been accompanied by a shift in the demographics of SIDS cases, such that most cases now occur in high-risk families with multiple recognized risk factors (6). As a result, SIDS rates are much higher in families from deprived socioeconomic backgrounds and particular population groups, such as the Māori population in New Zealand (7) or the Indigenous and black populations in the United States (8). While these campaigns appear to have effectively reached some segments of our population and resulted in behavioral change, this is not universal.

    In order to better understand how we can reach those higher-risk groups and achieve further reductions in SIDS rates, we need a better understanding of the nature and impact of preventive strategies. In this chapter we will outline the principles of public health approaches to prevention and the evidence base for different strategies; in light of this, we will consider the evidence for current approaches to further reduce the risk of SIDS.

  • 6 - The Role of Death Review Committees

    • By Sharyn Watts, South Australian Child Death and Serious Injury Review Committee, Department for Education and Child Development, Adelaide, Australia
  • Edited by Jodhie R. Duncan, University of Melbourne, Roger W. Byard, University of Adelaide
  • Book:
    SIDS Sudden Infant and Early Childhood Death
    Published by:
    The University of Adelaide Press
    Published online:
    20 July 2018
    Print publication:
    30 April 2018, pp 117-122

  • Summary

    Introduction

    A 5-month-old infant placed to sleep in a partially inflated plastic bed was found, unresponsive, with her face pressed against the plastic in a trough created between the base and the side of the inflatable bed (1). The infant's death was attributed to suffocation. Byard (2006) reviewed the circumstances of this death and recommended assessment of these types of inflatable beds by product safety experts (1).

    Details about the circumstances and cause of this death were also collected by the South Australian Child Death and Serious Injury Review Committee, which undertook its own in-depth review. The result of this review was to recommend to the South Australian government that it request the relevant national regulatory body to amend regulations about children's portable cots to incorporate the requirement that “no component of a portable folding cot be inflatable” (2). This change in national regulations was achieved three years after the infant's death.

    Child Death Review in South Australia

    Since 2005, the Child Death and Serious Injury Review Committee (“the Committee”) has been responsible for reviewing the circumstances and causes of all child deaths in the state of South Australia. Similar teams and committees are now well established in other states and territories in Australia and in other countries including Canada, New Zealand, the United Kingdom, and the United States.

    In South Australia, the Committee consists of a multidisciplinary team with expertise in fields such as pediatrics, education, disability, psychology, social work, child protection, public health, and justice who come together to consider the information that has been gathered about an infant's death. This broad base of knowledge and experience leads to a comprehensive overview of the circumstances of the death and identification of systemic issues that may have contributed to the quality of service provision to that infant and their family. The review process can also identify the absence of particular services, or of regulatory or legislative mechanisms which, if present, may have resulted in a different outcome for the infant.

    At the conclusion of a death review, the Committee can make recommendations to government about changes to legislation, policy, or practice which could potentially lead to a reduction in the risk of deaths occurring under similar circumstances, such as the change to portable cot regulations.

  • 28 - Neuropathology of Sudden Infant Death Syndrome: Hypothalamus

    • By Karen A Waters, The Children's Hospital at Westmead and The University of Sydney, Camperdown, NSW, Australia, Nicholas J Hunt, The University of Sydney, Camperdown, NSW, Australia, Rita MacHaalani, The University of Sydney, Camperdown, NSW, Australia
  • Edited by Jodhie R. Duncan, University of Melbourne, Roger W. Byard, University of Adelaide
  • Book:
    SIDS Sudden Infant and Early Childhood Death
    Published by:
    The University of Adelaide Press
    Published online:
    20 July 2018
    Print publication:
    30 April 2018, pp 641-660

  • Summary

    Introduction

    Since deaths attributed to sudden infant death syndrome (SIDS) occur during sleep, failure to arouse in a stressful situation comprises one component in the proposed mechanism of death. While the infant was previously apparently healthy, the hypothesis underpinning neuropathological studies is that an underlying defect in the infant's brain has contributed to death. The defect in infants who do not arouse may be developmental, inherited, or secondary to previous non-fatal insults. The brainstem and hypothalamus are two regions housing nuclei with important roles in stress responses and arousal mechanisms. This chapter focuses on studies of the hypothalamus and how deficits in this region may contribute to SIDS.

    The hypothalamus is a small but complex part of the brain with important roles in the homeostasis of energy balance, circadian rhythms, and stress responses, as well as growth and reproductive behaviors (1). As a regulatory center for so many functions, it receives input from, and transmits output to, a large number of other brain regions. Thus, as the hypothalamus controls many physiological functions, and is highly interconnected with other brain regions, it is an excellent candidate for abnormalities contributing to the pathogenesis of SIDS.

    The hypothalamus was evaluated early in the 1990s in SIDS infants (2, 3). At that time, fewer neurotransmitters had been identified compared to today. But even without our current understanding (e.g. of the orexins which were discovered in 1998), the hypothalamus was of interest in SIDS because of its known role in the regulation of sleep. Findings at that time included increased tryptophan content and decreased serotonin, increased serotonin receptor binding, and increased monoamine oxidase-A (MOA) activity, with decreased choline acetyltransferase (ChAT) activity (2) (see Table 28.1).

    Updating our knowledge of the hypothalamus and its potential role in SIDS is important, because our understanding of the hypothalamus is now more sophisticated with regards to its structure, functions, and development (1). In addition, a series of recent studies have made important advances in our understanding of abnormalities in the hypothalamus of SIDS infants.

  • 11 - Shared Sleeping Surfaces and Dangerous Sleeping Environments

    • By Jeanine Young, School of Nursing, Midwifery, and Paramedicine, University of the Sunshine Coast, Queensland, Australia, Rebecca Shipstone, School of Nursing, Midwifery, and Paramedicine, University of the Sunshine Coast, Queensland, Australia
  • Edited by Jodhie R. Duncan, University of Melbourne, Roger W. Byard, University of Adelaide
  • Book:
    SIDS Sudden Infant and Early Childhood Death
    Published by:
    The University of Adelaide Press
    Published online:
    20 July 2018
    Print publication:
    30 April 2018, pp 187-216

  • Summary

    Introduction

    Whether, and in what circumstances, the risk of sudden unexpected death in infancy (SUDI) is increased when an infant shares a sleep surface with another person has been the subject of extensive and vexed debate over the past two decades (1-6). This is largely because of opposing views as to the potential benefits and risks associated with this practice. Researchers remain divided on their stance towards shared sleeping and SUDI. While the United States American Academy of Pediatrics has strongly recommended against sharing a sleep surface with an infant for many years (7-9), a number of researchers in the United Kingdom and Australia question labeling a common sleeping practice a “risk factor” to be advised against. Instead the circumstances, rather than the shared sleeping itself, are recognized as the potential risk (3, 10-12). Whatever one's personal standpoint, from a clinical perspective, parents are entitled to clear information about the risks and benefits of shared sleeping to enable them to make a well-informed decision concerning the infant care practices they adopt. Health professionals, in both hospital and community settings, play a pivotal role in ensuring that parents are provided with this information, ideally in a non-judgemental manner that is relevant to their specific circumstances.

    This chapter commences by defining the important terms used throughout. Second, it examines the prevalence of shared sleeping in both Western and non-Western countries and cultures. Third, it reviews the evidence base concerning the benefits and the risks of sharing a sleep surface with an infant. Fourth, the use of a risk-minimization, as opposed to a risk-elimination, approach in the provision of safe sleeping advice and education is discussed. Finally, the recent move towards devices designed to overcome the risk associated with “direct” shared sleeping, while still maintaining the close motherinfant proximity needed to facilitate breastfeeding, is discussed.

    Definitions

    Various terms have been used in the literature to define environments in which an infant sleeps in close proximity to a caregiver, including co-sleeping, bed sharing, and room sharing.

  • 8 - Parental Grief

    • By Richard D Goldstein, Division of General Pediatrics, Department of Medicine, Boston Children's Hospital and Harvard Medical School, Boston, USA
  • Edited by Jodhie R. Duncan, University of Melbourne, Roger W. Byard, University of Adelaide
  • Book:
    SIDS Sudden Infant and Early Childhood Death
    Published by:
    The University of Adelaide Press
    Published online:
    20 July 2018
    Print publication:
    30 April 2018, pp 143-154

  • Summary

    Introduction

    A seemingly healthy infant dies suddenly and unexpectedly. A parent or someone the parent trusted with their infant was nearby, but the moment of death went unwitnessed. The forensic process ensues, including parent and guardian interviews, a death scene investigation, and autopsy. But another highly consequential process also begins: the process through which the infant's parents contend with their profound loss. As they seek an explanation, and the typically inconclusive results of the forensic process become known, they will experience intense emotions and a crisis of meaning. They will continue to face the complexities of coping with their loss for the rest of their lives. Medical relationships during involvement with sudden infant death syndrome (SIDS) begin and occur in a context of grief.

    Medical and investigative interactions occur at the time of death, during the investigations, and as results are shared. Bereavement-related supportive services may be available; they may or may not meet the parents’ needs (a situation which is explored in more detail in Chapter 7). There is rarely a plan or anticipatory guidance provided for the future once the death investigation is concluded. The family's usual medical care providers may not feel qualified to offer their assessment or advice, provided they even become aware of the challenges the family faces. All of these services and interactions will be influenced by the parents’ grief, just as their grief will be influenced by the interactions. We can improve our care in this area with an awareness of the parents’ emotional state and their needs. In the following, we present the state of knowledge about psychological coping following the loss of a young child and the process of grief that is seen.

    Important Concepts

    Grief is the emotional adaptation to loss and the way it is expressed. Those who interact with parents around the time of unexpected infant death would agree that the emotional state of the parents is extremely raw and intense. First moments in dealing with significant losses are predictably overwhelming but, from the perspective of grief research, the quality of grief in this setting underscores important concepts at the heart of the current theoretical understanding of grief.

  • 26 - Brainstem Neuropathology in Sudden Infant Death Syndrome

    • By Fiona M Bright, School of Medicine, the University of Adelaide, Adelaide, Australia, Robert Vink, Sansom Institute for Health Research, University of South Australia, Adelaide, Australia, Roger W Byard, School of Medicine, The University of Adelaide, Adelaide, Australia and Florey Institute of Neuroscience and Mental Health, Victoria, Australia
  • Edited by Jodhie R. Duncan, University of Melbourne, Roger W. Byard, University of Adelaide
  • Book:
    SIDS Sudden Infant and Early Childhood Death
    Published by:
    The University of Adelaide Press
    Published online:
    20 July 2018
    Print publication:
    30 April 2018, pp 589-614

  • Summary

    Introduction

    Sudden infant death syndrome (SIDS) has a complex and heterogeneous pathogenesis, with multiple abnormalities in a number of physiological functions and systems including neurological, cardiovascular, respiratory, gastrointestinal, nutritional, endocrine, metabolic, infectious, immunological, environmental, and genetic (1-7). Typically, without warning, an apparently healthy infant is found deceased sometime after being placed to sleep (8). there are many theories involving animal and human studies that have attempted to understand the pathophysiology of SIDS. Unfortunately, to date, there are no biomarkers available to aid in the prevention or definitive diagnosis of SIDS. the aim of much scientific research has been to determine the mechanisms of failure in SIDS infants that are undetectable prior to death and that remain just as unclear following death. While the precise cause of death in infants dying of SIDS has not been identified, there is considerable evidence that the syndrome results from a combination of circumstances involving [1] a cardiorespiratory challenge that occurs in [2] a neurologically compromised infant at [3] a specific period of postnatal development (3, 9, 10). The following chapter will focus on the failure of cardiorespiratory and autonomic control associated with neuropathology of the brainstem in SIDS.

    An important step in understanding the complex pathophysiology of SIDS was the establishment of the Triple Risk Model, which successfully conceptualized the epidemiological, physiological, and neuropathological data associated with SIDS. the Triple Risk Model proposes three coinciding factors: [1] an underlying vulnerability of the infant; [2] a critical developmental period in homeostatic control that the infant is transitioning through; and [3] the application of an exogenous stressor/s such as an asphyxiating environment (11). the model implies that an infant may be most at risk of SIDS when all three factors are simultaneously present (8, 11). All three factors contribute to the risk of an adverse event that occurs suddenly in an otherwise “healthy” infant. therefore, consideration of the Triple Risk Model is of key importance to SIDS research, with the model providing a foundation upon which researchers can build in the generation of research hypotheses.

  • 16 - An Australian Perspective

    • By Jane Freemantle, Melbourne School of Population and Global Health, The University of Melbourne, Victoria, Australia, Louise Ellis, Red Nose, Melbourne, Victoria, Australia
  • Edited by Jodhie R. Duncan, University of Melbourne, Roger W. Byard, University of Adelaide
  • Book:
    SIDS Sudden Infant and Early Childhood Death
    Published by:
    The University of Adelaide Press
    Published online:
    20 July 2018
    Print publication:
    30 April 2018, pp 349-374

  • Summary

    Introduction

    An accurate picture of mortality informs a society as to its social progress within each community, as mortality is a key indicator of effective public health policies and programs. Data on the causes of sudden infant and childhood mortality also reflect a broader set of social, economic, and political issues (1). As an example, sudden infant and child mortality is a key indicator of an important public health issue, given that some of the causes of infant and childhood mortality are potentially preventable. Effective prevention strategies and relevant health policy require a comprehensive and accurate profile of mortality, which, in turn, requires a better understanding of the epidemiology and mechanisms involved. This profile should include not only the patterns and trends of mortality over time, but also measurements of the indicators that have the potential to contribute to premature mortality among infants and children. These factors should include perinatal, maternal, and infant indicators; the specific causes of death; and the role of the geographical location as an indicator of excess sudden infant and child mortality (2).

    This chapter will outline the Australian perspective associated with sudden infant death syndrome (SIDS) and sudden infant and early childhood death. It will comment on the patterns and trends of sudden infant and early childhood mortality reported for all Australians and then focus on the First Peoples of Australia, the Aboriginal and Torres Strait Islander population, within the limitations of the availability of an accurate ascertainment of the Indigenous population. With respect to Aboriginal and Torres Strait Islander peoples, in this chapter the authors follow the Australian Institute of Health and Welfare (AIHW) principal that “[t]o acknowledge the separate Indigenous peoples of Australia, the term ‘Aboriginal and Torres Strait Islander people’ is preferred … [H]owever, the term ‘Indigenous’ is used interchangeably when referring to Indigenous status or when assists readability” (3).

    The chapter will conclude with a case study that describes a health promotion project that was introduced in Western Australia (WA) in 2005: Reducing the Risks of SIDS in Aboriginal Communities (RROSIAC). This project addresses the high rates of sudden unexpected death in infants (SUDI) in WA Aboriginal and Torres Strait Islander people in rural and remote communities, which have continued despite decreasing rates among non-Indigenous communities following the Red Nose SUDI risk reduction campaigns.

  • 9 - Promoting Evidence-Based Public Health Recommendations to Support Reductions in Infant and Child Mortality: The Role of National Scientific Advisory Groups

    • By Jeanine Young, School of Nursing, Midwifery, and Paramedicine, University of the Sunshine Coast, Queensland, Australia
  • Edited by Jodhie R. Duncan, University of Melbourne, Roger W. Byard, University of Adelaide
  • Book:
    SIDS Sudden Infant and Early Childhood Death
    Published by:
    The University of Adelaide Press
    Published online:
    20 July 2018
    Print publication:
    30 April 2018, pp 155-168

  • Summary

    Introduction

    Public health programs are tasked with using the best available evidence to make informed decisions in supporting campaigns, guidelines, policies, and advice in order to improve the health and wellbeing of countries, communities, families, and individuals (1). Public health programs, which focus on reducing preventable infant and child mortality, target modifiable factors that parents, caregivers, and health professionals can influence the most in order to promote the optimal conditions in which infants and children may survive, grow, and thrive (2, 3). The “Reduce the Risk of Sudden Infant Death Syndrome (SIDS)” and subsequent “Safe Sleeping” campaigns (4, 5) are key components of successful public health programs, which promote evidence-based risk reduction strategies to reduce infant mortality (2, 6). Although national campaigns and programs may vary in style, number, and content of key messages, countries that have adopted similar risk reduction programs, and in particular the advice to sleep babies on their backs, have experienced marked reductions in sudden and unexpected infant deaths (2, 4, 5, 7).

    Essentials of an Evidence-Based Public Health Approach

    Evidence underpinning public health recommendations comes from a systematic study of completed, peer reviewed, and publicly available research (1, 8). To ensure that public health practice is underpinned by evidence, it has been proposed that five key activities need to be undertaken (1). These activities include [1] evaluating needs for new or improved programs or practices; [2] identifying the best available evidence on programs and practices that potentially meet the needs; [3] collecting the best available information on appropriate programs and practices; [4] selecting programs that fit together with community and population needs and values; and [5] evaluating the impact on health and wellbeing of putting selected programs into practice (1, 9). In addition, high-quality programs are those which deliver public health initiatives that have been demonstrated to be population-centered, equitable, proactive, health promoting, risk-reducing, vigilant, transparent, effective, and efficient (9, 10).

    The Role of Scientific Advisory Groups

    Governments and public health organizations have recognized the importance of expert advice in facilitating efficient access to the best available evidence to support sound public health practice and policy making (11, 12). Access to, and knowledge of, good clinical practice also requires an understanding of the needs of stakeholder groups and the systems they work within, in order to translate evidence into practice.

  • 18 - A United Kingdom Perspective

  • Edited by Jodhie R. Duncan, University of Melbourne, Roger W. Byard, University of Adelaide
  • Book:
    SIDS Sudden Infant and Early Childhood Death
    Published by:
    The University of Adelaide Press
    Published online:
    20 July 2018
    Print publication:
    30 April 2018, pp 395-408

  • Summary

    Introduction

    Sudden infant death syndrome (SIDS) is still a leading cause for infant mortality in the United Kingdom (UK) despite the significant reduction in cases since the 1990s. Currently, there are ongoing public health campaigns aimed at promoting safer sleep, as the majority of SIDS cases in the UK occur in unsafe sleep environments. There is little uniformity of practice nationally about which deaths should be classified as SIDS or “unascertained”, with very few deaths recognized as being due to accidental asphyxia. The investigation of sudden and unexpected death in infancy (SUDI) has changed considerably since the early 2000s. Joint agency investigation by police, healthcare, and social care is now standard, with local review of all child deaths mandatory.

    Incidence

    UK rates

    SIDS is a prominent cause of death for infants in the UK (1). There were 247 unexplained deaths of children under 2 years of age in 2014; of these, 230 were unexplained infant deaths, giving a rate of 0.30 deaths per 1,000 live births, the lowest on record (2). There were 17 unexplained deaths of children aged between 12 and 24 months, accounting for 6.9% of all unexplained deaths of children younger than 2 years. Much higher rates of deaths in the 1970s and 1980s (2.30 deaths per 1,000 live births, or 1,593 deaths in 1988) (3) led to a concerted effort to identify modifiable risk factors and translate these into advice for parents. As in other countries, associations between unexplained infant deaths and the prone sleeping position, smoking during pregnancy, and overwrapping led to educational campaigns for parents, the successful implementation of which has led to a rapid decline in these deaths in the last 25 years.

    The UK “Back to Sleep” campaign

    The introduction of the “Back to Sleep” campaign in the UK in 1991 (see Figure 18.1) led to a dramatic fall in the number of infants dying (see Figures 18.2 and 18.3). The campaign in the UK was promoted at a national level and included a strong media element, as well as guidance for health professionals, to change their recommendations to parents. Anne Diamond, who was a popular TV presenter at the time, had a son, Sebastian, who died of SIDS in 1991. She campaigned strongly for the changes to advice (4), which eventually included a television advertisement in collaboration with the Department of Health (5).

  • 1 - Sudden Infant Death Syndrome: Definitions

    • By Roger W Byard, School of Medicine, The University of Adelaide, Adelaide, Australia and Florey Institute of Neuroscience and Mental Health, Victoria, Australia
  • Edited by Jodhie R. Duncan, University of Melbourne, Roger W. Byard, University of Adelaide
  • Book:
    SIDS Sudden Infant and Early Childhood Death
    Published by:
    The University of Adelaide Press
    Published online:
    20 July 2018
    Print publication:
    30 April 2018, pp 1-14

  • Summary

    The beginning of wisdom is the definition of terms

    Socrates (470-399 BC)

    Introduction

    Sudden infant death syndrome (SIDS), once known as “cot death”, has been a somewhat controversial term that on one hand has been criticized for not being a proper diagnosis with pathognomonic features, contrasting on the other hand with situations where it has been uncritically and inconsistently applied to all manner of infant deaths. It has been argued that SIDS constitutes a disease with a single cause, an argument which is at odds with those who feel that it is instead a syndrome with common features, and probable heterogeneous and additive risk factors. For this reason it has been called a “diagnosis without a disease” (1). As will be evident from the following chapters, the debate continues.

    The term “SIDS” is used when a sleeping infant, who has apparently been quite well, is found unexpectedly dead. Pathological evaluation, including ancillary testing, is unable to discern a cause of death (2-6). Despite the shortcomings of pathology, however, the SIDS story over the past several decades has been one of the great successes in infant healthcare. After specific environmental risk factors were identified in several large studies, awareness campaigns were initiated and promoted by SIDS organizations worldwide, which resulted in death rates from “SIDS” falling dramatically (7-10).

    In the Australian context the number of SIDS deaths reduced from over 500 per year in 1988 to 134 per year in 1999 (11), which corresponded to a decrease in the average number of SIDS deaths per 100,000 livebirths from 196 in the 1980s to 52 deaths between 1997 and 2002. In California in the United States, the number of SIDS deaths per year fell from 110.5 deaths per 100,000 live births in 1990 to 47.2 deaths per 100,000 live births in 1998 (4). In more recent years SIDS death rates have levelled, although SIDS is still responsible for a large number of infant deaths globally (12-16).

  • 10 - Risk Factors and Theories

    • By Rachel Y Moon, Department of Pediatrics, University of Virginia School of Medicine, Charlottesville, Virginia, USA, Fern R Hauck, Department of Family Medicine, University of Virginia School of Medicine, Charlottesville, Virginia, USA
  • Edited by Jodhie R. Duncan, University of Melbourne, Roger W. Byard, University of Adelaide
  • Book:
    SIDS Sudden Infant and Early Childhood Death
    Published by:
    The University of Adelaide Press
    Published online:
    20 July 2018
    Print publication:
    30 April 2018, pp 169-186

  • Summary

    Introduction

    Identification of factors that increase risk of, or are protective against, sudden infant death syndrome (SIDS) has largely been accomplished through epidemiological case-control studies. Risk factors include side and prone positioning, prenatal and postnatal tobacco smoke exposure, sleeping on soft or cushioned surfaces (particularly sofas, couches, and armchairs), bed sharing, soft bedding, head covering and overheating, and prematurity. Protective factors include breastfeeding, pacifier use, and room sharing. In this chapter, we will discuss the evidence for these risk and protective factors. We will also review the leading theories for SIDS causation including the Triple Risk Hypothesis, rebreathing theory, and deficient arousal and autonomic regulation, and how these theories create a plausible explanation for the risk and protective factors for SIDS identified in casecontrol studies.

    Risk Factors

    Side and prone sleep position

    The prone sleep position was noted in multiple case-control studies to be associated with SIDS (1-6), beginning in 1965 in the United Kingdom (UK) (7). Even before this, in 1944, Abramson reported that prone positioning was found in 68% of young infants who died of accidental mechanical suffocation in New York City (8). Public health campaigns, which first promoted non-prone positioning in the 1980s and then supine placement, only beginning in the 1990s in many Western countries, have all been associated with a decline in SIDS rates. Subsequent studies have confirmed the association of prone sleep positioning and an increased SIDS risk (adjusted odds ratio [aOR] 2.3-13.1) (9-11). Physiologic studies have demonstrated an association of prone positioning with an increased risk of hypercapnia and hypoxia (12-14), overheating (15), diminished cerebral oxygenation (16), altered autonomic control (17), and increased arousal thresholds (18).

    Subsequent studies have identified that the risk of side sleep positioning is similar to that of prone positioning (aOR 2.0 and 2.6 respectively) (10). Side positioning also has a higher population-attributable risk than prone positioning (11), likely because many infants who are placed on their side are found prone (10). Placement in, or rolling to, the prone position, particularly when infants are unaccustomed to that position, places infants at extremely high risk of SIDS (aOR 8.7-45.4) (10, 19). Thus all caregivers, including childcare providers, family members, and friends, should place the infant in the supine position for every sleep.

  • 13 - The Epidemiology of Sudden Infant Death Syndrome and Sudden Unexpected Infant Deaths: Diagnostic Shift and other Temporal Changes

    • By Carrie K Shapiro-Mendoza, Division of Reproductive Health, Centers for Disease Control and Prevention, Atlanta, Georgia, USA, Sharyn Parks, Division of Reproductive Health, Centers for Disease Control and Prevention, Atlanta, Georgia, USA, Alexa Erck Lambert, DB Consulting Group, Inc, Silver, Spring, Maryland, USA, Lena Camperlengo, Division of Reproductive Health, Centers for Disease Control and Prevention, Atlanta, Georgia, USA, Carri Cottengim, Division of Reproductive Health, Centers for Disease Control and Prevention, Atlanta, Georgia, USA, Christine Olson, Division of Reproductive Health, Centers for Disease Control and Prevention, Atlanta, Georgia, USA
  • Edited by Jodhie R. Duncan, University of Melbourne, Roger W. Byard, University of Adelaide
  • Book:
    SIDS Sudden Infant and Early Childhood Death
    Published by:
    The University of Adelaide Press
    Published online:
    20 July 2018
    Print publication:
    30 April 2018, pp 257-282

  • Summary

    Introduction

    To provide a detailed review of the changing epidemiology related to sudden infant death syndrome (SIDS) and sudden unexpected infant deaths (SUID), this chapter begins with an overview of the international system used to code and monitor SIDS trends around the world. Next, we describe the diagnostic shift in reporting and provide possible explanations as to why it occurred. We include a discussion of why using a single code to monitor sudden unexpected and unexplained infant deaths is no longer informative and discuss how new efforts to group codes for surveillance may allow for more consistent monitoring and comparison across jurisdictions and countries. Finally, we provide a description of the epidemiologic profile of SIDS and SUID, including information about current rates and historical trends, and sudden unexpected death in children 1 year old and over.

    Current Practice for Coding Cause of Sudden Infant Deaths

    Vital statistics data, specifically records from live birth and infant death registration, are the typical source of information on population trends in SIDS and SUID. Causes of death are reported on infant death certificates by a death certifier, who, for unexpected infant deaths without an immediately obvious cause, can be a medical examiner, coroner, or forensic pathologist. To facilitate comparisons across jurisdictions and countries, underlying causes of death reported on death certificates are assigned an International Classification of Diseases or ICD code (1).

    The International Classification of Diseases (ICD) coding system was developed by the World Health Organization to catalogue diseases, health conditions, and mortality causes. The coding system is used to monitor death trends and statistics within, and across, jurisdictions and countries (2). The ICD is currently in its 10th Revision (ICD-10). SIDS, first defined in 1969 (3), did not have a unique ICD code assigned until the ICD-9 in 1979. However, in 1973, the US National Center for Health Statistics (NCHS) created a distinct ICD-8 code for SIDS (795.0) for use in the United States (4). SIDS was introduced worldwide in ICD-9 as 798.0. In ICD-10, R95 is the code for SIDS. The SIDS code is indexed in the ICD chapter of nonspecific causes of death.

  • 21 - Neonatal Monitoring: Prediction of Autonomic Regulation at 1 Month from Newborn Assessments

    • By Michael M Myers, Division of Developmental Neuroscience, New York State Psychiatric Institute, New York, USA Department of Pediatrics, Columbia University, New York, USA Department of Psychiatry, Columbia University, New York, USA, Nina Burtchen, Department of Psychosomatic Medicine and Psychotherapy, University of Freiburg, Freiburg, Germany, Maria Ordonez Retamar, Division of Developmental Neuroscience, New York State Psychiatric Institute, New York, USA, Maristella Lucchini, DEIB, Politecnico di Milano, Milano, Italy, William P Fifer, Division of Developmental Neuroscience, New York State Psychiatric Institute, New York, USA Department of Pediatrics, Columbia University, New York, USA Department of Psychiatry, Columbia University, New York, USA
  • Edited by Jodhie R. Duncan, University of Melbourne, Roger W. Byard, University of Adelaide
  • Book:
    SIDS Sudden Infant and Early Childhood Death
    Published by:
    The University of Adelaide Press
    Published online:
    20 July 2018
    Print publication:
    30 April 2018, pp 431-448

  • Summary

    Introduction

    It has been nearly 30 years since the publication of a seminal book that defined the state of knowledge related to the epidemiology of, and mechanisms underlying, sudden infant death syndrome (SIDS) (1). Despite decades of subsequent research, much of which is summarized in other chapters in this book, we must acknowledge that SIDS remains an enigma. Indeed, two longstanding definitions of SIDS (2, 3) are testament to our lack of understanding of why infants die of SIDS — that is, these deaths remain unexplained after thorough investigation. Although infrequent, SIDS remains the most common cause of infant death between 1 month and 1 year of age, and the deaths of 2,000 infants annually in the United States (US) alone are unimaginable tragedies for these 2,000 families. At the heart of the reason why we have such an incomplete understanding of SIDS is, fortunately, its rarity. In the US, the 2014 estimates suggest that SIDS is the cause of death for about 3.9 of every 10,000 infants born each year (4). Over the past few decades, our understanding of the external factors that contribute to why infants die of SIDS has come from numerous, worldwide, epidemiological studies. Associations gleaned from these studies have led to recommendations including strong discouragement for mothers not to smoke during pregnancy paired with specific guidance for safe sleeping practices. Subsequent to these recommendations, the rate of SIDS was reduced in many countries (5). However, the physiological mechanisms that underlie SIDS remain unknown.

    By definition, SIDS deaths are unexpected. While there may be evidence of low-grade infection prior to the time of death (6) in general, there are no overt, chronic signs of the impending demise. These deaths do not seem to be “programmed”, in the sense that they are inevitable; rather, they appear to be due to suboptimal physiological regulatory responses to what may be rather common challenges faced by infants during the first year of life. Nonetheless, these deaths are not random. Some infants are more likely to experience the failure of adequate physiological responses to environmental challenges than others, hence the concept of the vulnerable infant. Infants born prematurely are at greater risk for SIDS (7), as are infants of mothers who smoked or drank during pregnancy (8, 9).

  • 14 - Future Directions in Sudden Unexpected Death in Infancy Research

  • Edited by Jodhie R. Duncan, University of Melbourne, Roger W. Byard, University of Adelaide
  • Book:
    SIDS Sudden Infant and Early Childhood Death
    Published by:
    The University of Adelaide Press
    Published online:
    20 July 2018
    Print publication:
    30 April 2018, pp 283-324

  • Summary

    Introduction

    This chapter on sudden unexpected death in infancy (SUDI) (both explained and unexplained) outlines the background to gaps in practice, advances in our understanding of SUDI, non-compliant aspects of prevention, and needs and education of parents and health providers. From this outline the fourth section on future directions is developed.

    SUDI is defined as the death of an infant aged less than 12 months that is sudden and unexpected “in which there is death (or collapse leading to death), which would not have been reasonably expected to occur 24 hours previously and in whom no preexisting medical cause of death is apparent. It includes those deaths for which a cause is ultimately found (explained SUDI) and those that remain unexplained following investigation” (1).

    Gaps in Practice

    The future of SUDI research remains dependent on accurate investigation and classification of death. This is frequently suboptimal. This section will discuss models of best practice, delineation of a standardized process of investigation, application of standardized percentile charts to SUDI from birth to 1 year, and a proposed simple classification that addresses potential asphyxia.

    Models of best practice

    Various models of SUDI investigation with clear objectives and best practice standards have been defined. Garstang et al. (2015) have categorized the different models of SUDI investigation as coroner- or medical-examiner-led investigation, healthcare-led investigation, police-led investigation, and the joint-agency approach (2). All but policeled investigations have the potential to meet international minimum standards of SUDI investigation. The objectives outlined by Garstang et al. include:

  • • to identify, as far as is possible, any recognizable cause of death including accidental asphyxia, suspicious deaths, medical deaths, and sudden infant death syndrome (SIDS) where diagnostic criteria have been met

  • • to identify any factors contributing to the death, including factors in the physical or social environment, parental care, and service provision or need

  • • to support the family through a sensitive, respectful approach that allows them to grieve and recognizes their need for information

  • • to learn lessons for the prevention of future child deaths

  • • to ensure that all statutory requirements in relation to the death are fulfilled and that the public interest is served through the appropriate administration of justice and protection of children.

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