Sudden cardiac death in children and adolescents between 1 and 19 years of age.

Background: Understanding pediatric sudden cardiac death (SCD) may inform age-specific prevention strategies.

Objective: To characterize potential underlying causes of SCD in children and adolescents

Methods: We performed a retrospective population-based study in Ontario, Canada, of all SCD cases in a 5-year period (2005-2009) involving persons aged 1-19 years identified from the comprehensive database of the Office of the Chief Coroner. Of 1204 coroner's cases, 351 potential SCD cases were reviewed.

Characteristics of opioid-users whose death was related to opioid-toxicity: a population-based study in Ontario, Canada.

Background: The impact of the prescription opioid public health crisis has been illustrated by the dramatic increase in opioid-related deaths in North America. We aimed to identify patterns and characteristics amongst opioid-users whose cause of death was related to opioid toxicity.

Methods: This was a population-based study of Ontarians between the years 2006 and 2008.

Scope and nature of sudden cardiac death before age 40 in Ontario: a report from the cardiac death advisory committee of the office of the chief coroner.

Background: Understanding sudden cardiac death in the young may inform prevention strategies.

Objective: To determine the scope and nature of sudden death in a geographically defined population.

Methods: We performed a retrospective population-based cohort study in Ontario, Canada, of all sudden cardiac death cases involving persons aged 2-40 years identified from the 2008 comprehensive Coroner database.

Fatal hydrocodone overdose in a child: pharmacogenetics and drug interactions.

Fatal opioid toxicity occurred in a developmentally delayed child aged 5 years 9 months who was inadvertently administered high doses of hydrocodone for a respiratory tract infection. The concentration of hydrocodone in postmortem blood was in the range associated with fatality; however, hydromorphone, a major metabolite catalyzed by cytochrome P450 2D6 (CYP2D6), was not detected when using mass spectrometry. Genetic analysis revealed that the child had a reduced capability to metabolize the drug via the CYP2D6 pathway (CYP2D6*2A/*41).