NSIDRC Journal Article Alert — June 5, 2009
Prepared by the National Sudden and Unexpected Infant/Child Death and Pregnancy Loss Resource Center at Georgetown University.
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Sudden Infant Death
1. Randall BB, Wadee SA, Sens MA, Kinney HC, Folkerth RD, Odendaal HJ, Dempers JJ
A practical classification schema incorporating consideration of possible asphyxia in cases of sudden unexpected infant death
Forensic Sci Med Pathol. 2009 May 31. [Epub ahead of print]
University of South Dakota Sanford School of Medicine, 2441 Stanton Drive, Sioux Falls, SD, 57103, USA, fornix@aol.com.
Although the rate of the sudden infant death syndrome (SIDS) has decreased over the last two decades, medical examiners and coroners are increasingly unwilling to use the SIDS diagnosis, particularly when there is an unsafe sleeping environment that might pose a risk for asphyxia. In order to reliably classify the infant deaths studied in a research setting in the mixed ancestory population in Cape Town, South Africa, we tested a classification system devised by us that incorporates the uncertainty of asphyxial risks at an infant death scene. We classified sudden infant deaths as: A) SIDS (where only a trivial potential for an overt asphyxial event existed); B) Unclassified-Possibly Asphyxial-Related (when any potential for an asphyxial death existed); C) Unclassified-Non-Asphyxial-Related (e.g., hyperthermia); D) Unclassified-No autopsy and/or death scene investigation; and E) Known Cause of Death. Ten infant deaths were classified according to the proposed schema as: SIDS, n = 2; Unclassified-Possibly Asphyxial-Related, n = 4; and Known Cause, n = 4. A conventional schema categorized the deaths as 6 cases, SIDS, and 4 cases, Known Cause, indicating that 4/6 (67%) of deaths previously classified as SIDS are considered related importantly to asphyxia and warrant their own subgroup. This new classification schema applies a simpler, more qualitative approach to asphyxial risk in infant deaths. It also allows us to test hypotheses about the role of asphyxia in sudden infant deaths, such as in brainstem defects in a range of asphyxial challenges.
2. Paterson DS, Hilaire G, Weese-Mayer DE
Medullary Serotonin Defects and Respiratory Dysfunction in Sudden Infant Death Syndrome
Respir Physiol Neurobiol. 2009 May 26. [Epub ahead of print]
Department of Pathology, Children's Hospital Boston, 300 Longwood Avenue, Boston, MA 02115, USA.
Sudden infant death syndrome (SIDS) is defined as the sudden and unexpected death of an infant less than 12 months of age that occurs during sleep and remains unexplained after a complete autopsy, death scene investigation, and review of the clinical history. It is the leading cause of postneonatal mortality in the developed world. The cause of SIDS is unknown, but is postulated to involve impairment of brainstem-mediated homeostatic control. Extensive evidence from animal studies indicates that serotonin (5-HT) neurons in the medulla oblongata play a role in the regulation of multiple aspects of respiratory and autonomic function. A subset of SIDS infants have several abnormalities in medullary markers of 5-HT function and genetic polymorphisms impacting the 5-HT system, informing the hypothesis that SIDS results from a defect in 5-HT brainstem-mediated control of respiratory (and autonomic) regulation. Here we review the evidence from postmortem human studies and animal studies to support this hypothesis and discuss how the pathogenesis of SIDS is likely to originate in utero during fetal development.
3. Campos M, Bravo E, Eugenín J
Respiratory dysfunctions induced by prenatal nicotine exposure
Clin Exp Pharmacol Physiol. 2009 May 19. [Epub ahead of print]
Laboratory of Neural Systems, Department of Biology, Universidad de Santiago, USACH, Santiago, Chile.
Maternal tobacco smoking is the principal risk factor associated to the Sudden Infant Death Syndrome (SIDS), a leading cause of death of infants under 1 year old. Victims of SIDS show a higher incidence of respiratory control abnormalities including central apnoeas, delayed arousal responses, and diminished ventilatory chemoreflexes. 2. Nicotine is likely the link between maternal tobacco smoking and SIDS. Prenatal nicotine exposure can alter the breathing pattern and can reduce hypoxia- and hypercarbia-induced ventilatory chemoreflexes. In vitro approaches have revealed that prenatal nicotine exposure impairs central chemosensitivity, switching the cholinergic contribution from a muscarinic to a nicotinic receptor based drive. In addition, serotonergic, noradrenergic, GABAergic, glycinergic, and glutamatergic, among other systems, are affected by prenatal nicotine. 3. Here we propose that prenatal nicotine affects the respiratory network through two main processes: reorganization of neurotransmitter systems and remodelling of neural circuits. These changes make breathing more vulnerable to fail in the early postnatal life, which could be related to the pathogenesis of SIDS.
Other Infant Death
1. Pulver LS, Guest-Warnick G, Stoddard GJ, Byington CL, Young PC
Weight for gestational age affects the mortality of late preterm infants
Pediatrics. 2009 Jun;123(6):e1072-7
Department of Pediatrics, University of Utah, Salt Lake City, UT 84158, USA. laurie.pulver@hsc.utah.edu
BACKGROUND: Late preterm infant mortality is higher than that for term newborns. The association between weight for gestational age (WGA) category and late preterm mortality has not been well described. OBJECTIVES: Our objectives for this research were as follows: (1) to compare neonatal and infant mortality rates of SGA, AGA, and LGA late preterm, early term, and term newborns; (2) to determine the relative risk of neonatal and infant death for each WGA category; and (3) to examine causes of neonatal and infant death. METHODS: We reviewed linked birth and death certificate data for all infants from Utah born between 1999 and 2005 with a GA > or =34 weeks. We calculated neonatal and infant mortality rates for each GA/birth weight stratum and estimated mortality rate ratios using AGA term infants as the reference. International Classification of Diseases, Ninth Revision, codes were used to classify cause of death. RESULTS: There were 343322 newborns with GA > or =34 weeks from 1999 to 2005. Late preterm SGA infants were approximately 44 times more likely than term AGA newborns to die in their first month and 22 times more likely to die in their first year. When infants dying from congenital conditions were excluded, the differences in mortality rate ratios persisted for SGA infants, especially those born in the late preterm period. CONCLUSIONS: Being SGA substantially increases the already higher mortality of late preterm and early term newborns. This increased risk cannot be fully explained by an increased prevalence of lethal congenital conditions among SGA late preterm newborns. Clinicians caring for late preterm and early term newborns should be cognizant of their WGA category.
2. Zuppan CW, Wells LM, Kerstetter JC, Johnston JK, Bailey LL, Chinnock RE
Cause of death in pediatric and infant heart transplant recipients: review of a 20-year, single-institution cohort
J Heart Lung Transplant. 2009 Jun;28(6):579-84. Epub 2009 May 5.
Departments of Pathology, Pediatrics and Surgery, Loma Linda University and Children's Hospital, 11234 Anderson Street, Loma Linda, CA 92354, USA. czuppan@llu.edu
BACKGROUND: As infant and pediatric heart transplantation becomes more common, there is a growing need to better understand the causes of failure or death, if we are to continue to improve the outcome in these children. METHODS: A multidisciplinary team reviewed all deaths occurring in the cohort of infants and children transplanted during the first 20 years of the Loma Linda Pediatric Heart Transplant program, with 2 additional years of follow-up beyond the 20-year accrual period, and classified them as to cause. RESULTS: There were 169 deaths among 421 recipients, with a median follow-up of 9.7 years. Autopsy was performed in 128 cases. The causes of death, in decreasing order of frequency, included acute rejection (26.0%), infection (16.0%), cardiac allograft vasculopathy (CAV) (14.2%), technical issues (8.3%), acute graft dysfunction (6.5%), neoplasm (7.1%), chronic graft dysfunction (4.7%) and miscellaneous factors (10.1%), and in twelve deaths (7.1%) the cause was unclassified. Acute graft dysfunction and technical issues accounted for nearly two-thirds of the deaths in the first 30 days after transplant, while acute rejection resulted in the largest number of deaths after the first year (30.4%), with CAV a close second (23.5%). CONCLUSIONS: Acute graft dysfunction and technical issues were the most frequent cause of early death. Late deaths were most often due to acute rejection and CAV, which differs somewhat from the experience reported in adults. Acute rejection was the single most important cause of late mortality, and resulted in a significant number of late sudden and unexpected deaths.
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