SIDS Sudden infant and early childhood death

This volume covers aspects of sudden infant and early childhood death, ranging from issues with parental grief, to the most recent theories of brainstem neurotransmitters. It also deals with the changes that have occurred over time with the definitions of SIDS (sudden infant death syndrome), SUDI (sudden unexpected death in infancy) and SUDIC (sudden unexpected death in childhood). The text will be indispensable for SIDS researchers, SIDS organisations, paediatric pathologists, forensic pathologists, paediatricians and families, in addition to residents in training programs that involve paediatrics. It will also be of use to other physicians, lawyers and law enforcement officials who deal with these cases, and should be a useful addition to all medical examiner/forensic, paediatric and pathology departments, hospital and university libraries on a global scale. Given the marked changes that have occurred in the epidemiology and understanding of SIDS and sudden death in the very young over the past decade, a text such as this is very timely and is also urgently needed

SIDS Sudden infant and early childhood death

This volume covers aspects of sudden infant and early childhood death, ranging from issues with parental grief, to the most recent theories of brainstem neurotransmitters. It also deals with the changes that have occurred over time with the definitions of SIDS (sudden infant death syndrome), SUDI (sudden unexpected death in infancy) and SUDIC (sudden unexpected death in childhood). The text will be indispensable for SIDS researchers, SIDS organisations, paediatric pathologists, forensic pathologists, paediatricians and families, in addition to residents in training programs that involve paediatrics. It will also be of use to other physicians, lawyers and law enforcement officials who deal with these cases, and should be a useful addition to all medical examiner/forensic, paediatric and pathology departments, hospital and university libraries on a global scale. Given the marked changes that have occurred in the epidemiology and understanding of SIDS and sudden death in the very young over the past decade, a text such as this is very timely and is also urgently needed

Adolescent inhalant abuse leads to other drug use and impaired growth; implications for diagnosis

Abstract Objective: Abuse of inhalants containing the volatile solvent toluene is a significant public health issue, especially for adolescent and Indigenous communities. Adolescent inhalant abuse can lead to chronic health issues and may initiate a trajectory towards further drug use. Identification of at‐risk individuals is difficult and diagnostic tools are limited primarily to measurement of serum toluene. Our objective was to identify the effects of adolescent inhalant abuse on subsequent drug use and growth parameters, and to test the predictive power of growth parameters as a diagnostic measure for inhalant abuse. Methods: We retrospectively analysed drug use and growth data from 118 Indigenous males; 86 chronically sniffed petrol as adolescents. Results: Petrol sniffing was the earliest drug used (mean 13 years) and increased the likelihood and earlier use of other drugs. Petrol sniffing significantly impaired height and weight and was associated with meeting ‘failure to thrive’ criteria; growth diagnostically out‐performed serum toluene. Conclusions: Adolescent inhalant abuse increases the risk for subsequent and earlier drug use. It also impairs growth such that individuals meet ‘failure to thrive’ criteria, representing an improved diagnostic model for inhalant abuse. Implications for Public Health: Improved diagnosis of adolescent inhalant abuse may lead to earlier detection and enhanced health outcomes

The Anti-Inflammatory Agent N-Acetyl Cysteine Exacerbates Endotoxin-Induced Hypoxemia and Hypotension and Induces Polycythemia in the Ovine Fetus

Background: Lipopolysaccharide (LPS) delivered acutely to the ovine fetus induces cerebral white matter injury and brain inflammation. N-acetyl cysteine (NAC) is potentially neuroprotective as it blocks the production of inflammatory cytokines and increases glutathione levels; however, it is unknown whether NAC affects the physiological status of the fetus already exposed to an inflammatory environment. Objectives: Our objective was to determine whether NAC influences the physiological effects of LPS exposure in the ovine fetus. Methods: Catheterized fetal sheep underwent one of four treatments (saline, n = 6; LPS, n = 6; LPS + NAC, n = 6; NAC, n = 3) on 5 consecutive days from 95 days of gestation (term similar to 147 days). Fetal arterial pressure and heart rate were recorded and blood samples collected. Results: LPS administration resulted in fetal hypoxemia and hypotension; simultaneous treatment with NAC exacerbated these effects and induced polycythemia. NAC treatment alone had no effect on the fetus. Conclusion: In the presence of LPS, NAC compromises fetal physiological status, suggesting that it may not be a suitable antenatal treatment for a fetus with evidence of inflammation. Copyright (C) 2010 S. Karger AG, Base

Cardiovascular and renal disease in the adolescent guinea pig after chronic placental insufficiency

OBJECTIVE:The aim of this study was to determine the long-term effects of chronic placental insufficiency on the metabolic state and organ structure in the fetal and adolescent guinea pig. STUDY DESIGN: The maternal uterine artery was ligated at day 28–30 to reduce placental function and restrict fetal growth. Whole body and tissue weights and plasma metabolites were determined at 60 days of gestation and 8 weeks of age; tissue structure was determined at the latter age in restricted and control offspring. RESULTS: Fetal growth restriction increased fibrosis in the heart and kidneys (P < .05), increased aortic wall thickening (P < .01), reduced the number of glomeruli in the kidneys (P < .05), and increased the plasma urea and chloride in adolescent offspring. CONCLUSION: This study demonstrates that diseases in the heart, aorta, and kidneys that result from an adverse prenatal environment are evident at adolescence and may contribute to subsequent adult disease.Todd A. Briscoe, Alexandra E. Rehn, Sandra Dieni, Jhodie R. Duncan, Mary E. Wlodek, Julie A. Owens and Sandra M. Ree

Clinicopathological data.

<p>Clinicopathological data.</p

Normative distribution and density of mean total NK1R binding (fmol/mg) in the human infant medulla of non-SIDS controls.

<p>Normative distribution and density of mean total NK1R binding (fmol/mg) in the human infant medulla of non-SIDS controls.</p