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Unexpected Death (unexpected + death)
Kinds of Unexpected Death Selected AbstractsProlactin Levels in Sudden Unexpected Death in EpilepsyEPILEPSIA, Issue 1 2000K. Opeskin Summary: Purpose: To assess serum prolactin levels in sudden unexpected death in epilepsy (SUDEP) and control groups to test the hypothesis that if seizures occur routinely as a terminal event in SUDEP, then raised prolactin levels may be an indicator of terminal seizure. Methods: Blood was taken for measurement of prolactin levels from subjects with SUDEP and three control groups. The control groups were those with epilepsy dying from causes other than epilepsy (e.g., ischemic heart disease or injuries), physiologically stressed individuals without epilepsy (they were admitted to the hospital after an acute illness and died after several hours to 3 days), and nonepileptic rapid deaths (these people collapsed suddenly and died at the scene). In the SUDEP group, evidence for terminal seizure was considered to be at least one of the following: body found half on, half off the bed, or urinary incontinence at the scene, or bitten lips or tongue at autopsy. Results: There was evidence for terminal seizure at the scene or at autopsy in four of the 10 SUDEP cases. Serum prolactin levels were not significantly increased in the SUDEP group compared with the controls. None of the SUDEP subjects, including those with clinical evidence of a terminal seizure, had high prolactin levels characteristic of those observed after seizures in living subjects. Conclusions: Prolactin levels are not raised in SUDEP, even if there is evidence of terminal seizure. As prolactin takes 15,20 min to peak after a seizure in life, there may be insufficient time for a prolactin increase to occur in SUDEP. Thus prolactin levels cannot be used to determine if a deceased individual with epilepsy had a seizure or to answer the broad question whether SUDEP is always associated with a terminal seizure. [source] The Role of Environmental Factors in the Causation of Sudden Death in Infants: Two Cases of Sudden Unexpected Death in Two Unrelated Infants Who Were Cared for by the Same BabysitterJOURNAL OF FORENSIC SCIENCES, Issue 6 2007Bennet I. Omalu M.D., M.P.H. Abstract:, We report two cases of sudden unexpected death in two unrelated African American female infants, 2 months and 4 months old. Both infants were attended to by the same babysitter in the same apartment and died 39 days apart in the same bed and in the same bedroom. The autopsy of the first infant revealed sudden unexplained death in an infant. Toxicologic analysis for carbon monoxide (CO) was not performed because it was not suspected. When the second infant died, investigation into the ambient air quality within the apartment revealed high levels of CO emanating from a poorly ventilated and defective hot water heater, which was located across a hallway from the bedroom where the two babies died. CO saturation levels in the postmortem blood samples of the two babies were elevated and were similar (13% and 14%). Nicotine and cotinine were not detected in the blood sample of the two infants. Cherry-red livor mortis was absent. Acute CO intoxication was determined to be the underlying cause of these two unexpected deaths. These two cases underscore the need to integrate ambient air analysis and postmortem CO analysis as routine components of the comprehensive death investigation of infants who die suddenly and unexpectedly. [source] Esophageal Causes of Sudden and Unexpected DeathJOURNAL OF FORENSIC SCIENCES, Issue 2 2006Roger W. Byard M.D. ABSTRACT: Gastrointestinal conditions are uncommon causes of sudden and/or unexpected death as compared to cardiovascular diseases, motor vehicle trauma, or suicide, and may involve an array of fatal mechanisms. Lethal esophageal conditions are encountered even less often, the manifestations of which include acute upper airway occlusion from tumors or foreign material, intraluminal hemorrhage from vascular abnormalities, or perforation with fistula formation resulting in hemorrhage and sepsis. When encountered at autopsy, a particular condition may also be a manifestation of a disease that does not primarily involve the esophagus. For this reason, a detailed autopsy investigation is required for evidence of systemic or remote disease when lesions are found within the esophagus. In this report, possible life-threatening esophageal conditions are reviewed with a description of lethal mechanisms, mention of rare associated diseases, and comment on difficulties that may arise at autopsy in the evaluation of such cases. [source] Epidemiological investigation of Sudden Infant Death Syndrome infants , recommendations for future studiesCHILD: CARE, HEALTH AND DEVELOPMENT, Issue 2002P. Blair Abstract In recent years the study of infant care practices within the sleeping environment has proved to be the single most important set of observations for reducing the risk of Sudden Infant Death Syndrome (SIDS). To further reduce the number of deaths and resolve the debate on safe infant care practice, a closer scrutiny of this environment is required. However, anecdotal observation from uncontrolled death-scene investigations and a reluctance to diagnose SIDS because of adverse social conditions or circumstantial evidence at the time of death is undermining future research. To investigate SIDS now means investigating the wider umbrella of all Sudden Unexpected Deaths in Infancy (SUDI) because of the potential for misdiagnosis. In trying to find out why SIDS infants die we have increasingly been forced to search for why infants survive in the first few months of life and it is this comparative component of epidemiological observation that has saved so many lives. A death-scene investigation is vital to any planned future investigation of SIDS but equally essential is a sleep-scene investigation of surviving infants to put any findings into context. SIDS infants are no longer scattered across the social strata and the cot is not the only environment in which they are found, social deprivation and use of the parental bed are now more discernable. Future studies should therefore reflect these changes with a second control group of surviving infants more closely matched to the type of environment in which SIDS infants might be found. [source] Sudden unexpected death in epilepsyDEVELOPMENTAL MEDICINE & CHILD NEUROLOGY, Issue 5 2001Neil Gordon MD FRCP Hon FRCPCH First page of article [source] Circadian Variation in Heart-Rate Variability in Localization-related EpilepsyEPILEPSIA, Issue 5 2007Håkan Persson Summary:,Purpose: Case,control studies of sudden unexpected death in epilepsy (SUDEP) have reported that SUDEP is more likely to occur during sleep and thus presumably during night hours. The circadian variation of heart-rate variability (HRV) might be of relevance to this risk. We examined night versus daytime HRV in patients with newly diagnosed and refractory localization-related epilepsy, assessing the effects of drug treatment and epilepsy surgery on the night/daytime HRV ratio. Methods: We used spectral analysis to assess HRV and calculated the night-time (00.00,05.00)/daytime (07.30,21.30) ratio of HRV in 14 patients with newly diagnosed localization-related epilepsy before and during carbamazepine (CBZ) treatment and in 21 patients with temporal lobe epilepsy before and after epilepsy surgery. Both groups were compared with age- and sex-matched controls. Results: No significant differences were found from controls in the night/daytime ratios of HRV whether compared before or after initiation of treatment with CBZ in newly diagnosed epilepsy patients. When patients were used as their own controls, night/daytime ratios of standard deviation of RR intervals (p = 0.04) and total power (p = 0.04) were significantly lower during treatment than before. Compared with those of controls, the night/daytime ratios were lower in epilepsy surgery patients before surgery [low-frequency power (p = 0.04); high-frequency power (p = 0.04)]. Night/daytime ratios did not change significantly after surgery. Conclusions: The HRV of the patients was more affected during night-time when the risk of SUDEP seems to be highest in such patients. [source] Cardiac Dysrhythmia Associated with the Immediate Postictal State after Maximal Electroshock in Freely Moving RatEPILEPSIA, Issue 4 2002Olivier Darbin Summary: ,Purpose: Cardiac autonomic changes accompany complex partial seizures and generalized tonic,clonic seizures, and participate, at least partially, in the sudden and unexpected death in epilepsy (SUDEP). The analysis of the heart rate variability (HRV) is one of the simplest ways of providing insight into autonomic functions. The entropy quantifies the repetition of complex patterns in a signal and refers to systems randomness, regularity, and predictability. Clinical investigations have reported that entropy decreases in patients with a high risk of sudden cardiac death. The goal of this study was to evaluate the effects of the maximal electroshock (MES) on the entropy of HRV, monitored in the immediate postictal stage in the model of the freely moving rat. Methods: Entropy changes were correlated with the high and low frequencies of spectral analysis, which reflect the participation of the sympathetic and parasympathetic activities. Results: MES-induced arrhythmia is characterized by an HRV increase, an imbalance in favor of the parasympathetic activity, and a decrease in the entropy. Entropy decrease was restricted to the duration of the arrhythmia, suggesting that the postictal arrhythmia may be associated with a higher risk of lethal cardiac complications. Nevertheless, entropy changes did not correlate with spectral changes. Conclusions: The results suggest that the imbalance demonstrated in the spectral domain explains only partially the contribution of each autonomic system in the complexity of the heart rate during the postictal state. [source] Prolactin Levels in Sudden Unexpected Death in EpilepsyEPILEPSIA, Issue 1 2000K. Opeskin Summary: Purpose: To assess serum prolactin levels in sudden unexpected death in epilepsy (SUDEP) and control groups to test the hypothesis that if seizures occur routinely as a terminal event in SUDEP, then raised prolactin levels may be an indicator of terminal seizure. Methods: Blood was taken for measurement of prolactin levels from subjects with SUDEP and three control groups. The control groups were those with epilepsy dying from causes other than epilepsy (e.g., ischemic heart disease or injuries), physiologically stressed individuals without epilepsy (they were admitted to the hospital after an acute illness and died after several hours to 3 days), and nonepileptic rapid deaths (these people collapsed suddenly and died at the scene). In the SUDEP group, evidence for terminal seizure was considered to be at least one of the following: body found half on, half off the bed, or urinary incontinence at the scene, or bitten lips or tongue at autopsy. Results: There was evidence for terminal seizure at the scene or at autopsy in four of the 10 SUDEP cases. Serum prolactin levels were not significantly increased in the SUDEP group compared with the controls. None of the SUDEP subjects, including those with clinical evidence of a terminal seizure, had high prolactin levels characteristic of those observed after seizures in living subjects. Conclusions: Prolactin levels are not raised in SUDEP, even if there is evidence of terminal seizure. As prolactin takes 15,20 min to peak after a seizure in life, there may be insufficient time for a prolactin increase to occur in SUDEP. Thus prolactin levels cannot be used to determine if a deceased individual with epilepsy had a seizure or to answer the broad question whether SUDEP is always associated with a terminal seizure. [source] Sotalol and a Broken HeartJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 2 2010F.H.R.S., PETER L. FRIEDMAN M.D., Ph.D. Sotalol and a Broken Heart., An 82-year-old woman with persistent atrial fibrillation underwent successful electrical cardioversion and was begun on sotalol. After 3 days of in-hospital observation she had only mild lengthening of the QT interval. Two weeks later in clinic, the day after her husband's unexpected death, she was noted to have profound QT interval prolongation. Although she was asymptomatic and echocardiography did not disclose regional wall motion abnormalities consistent with takotsubo cardiomyopathy, she probably had a forme fruste of stress cardiomyopathy. Following emotional trauma, a period of heightened vigilance for ventricular proarrhythmia is probably warranted in women treated with antiarrhythmic drugs that lengthen repolarization. (J Cardiovasc Electrophysiol, Vol. 21, pp. 207-210, February 2010) [source] Sickle Cell Trait Mimicking Multiple Inflicted Injuries in a 5-Year-Old BoyJOURNAL OF FORENSIC SCIENCES, Issue 5 2009Charis Kepron M.D. Abstract:, Sickle cell disease (SCD) and sickle cell trait (SCT) can be associated with sudden unexpected death in the pediatric population, usually due to pulmonary complications occurring within the acute chest syndrome (ACS). Musculoskeletal complications can occur and are classically limited to bone infarcts. The occurrence of bone pathology centered upon the epiphyseal growth plate in SCD/SCT is extremely rare, and multiple such injuries in a single patient have not been previously reported. Herein, we describe a case of sudden unexpected death in a 5-year-old child with undiagnosed SCT due to the ACS, with widespread epiphyseal and periosteal bone lesions mimicking multiple inflicted injuries at autopsy. This case highlights the importance of clinicopathological correlation and is the first to describe SCT pathology as a mimic of nonaccidental injury. [source] The Role of Environmental Factors in the Causation of Sudden Death in Infants: Two Cases of Sudden Unexpected Death in Two Unrelated Infants Who Were Cared for by the Same BabysitterJOURNAL OF FORENSIC SCIENCES, Issue 6 2007Bennet I. Omalu M.D., M.P.H. Abstract:, We report two cases of sudden unexpected death in two unrelated African American female infants, 2 months and 4 months old. Both infants were attended to by the same babysitter in the same apartment and died 39 days apart in the same bed and in the same bedroom. The autopsy of the first infant revealed sudden unexplained death in an infant. Toxicologic analysis for carbon monoxide (CO) was not performed because it was not suspected. When the second infant died, investigation into the ambient air quality within the apartment revealed high levels of CO emanating from a poorly ventilated and defective hot water heater, which was located across a hallway from the bedroom where the two babies died. CO saturation levels in the postmortem blood samples of the two babies were elevated and were similar (13% and 14%). Nicotine and cotinine were not detected in the blood sample of the two infants. Cherry-red livor mortis was absent. Acute CO intoxication was determined to be the underlying cause of these two unexpected deaths. These two cases underscore the need to integrate ambient air analysis and postmortem CO analysis as routine components of the comprehensive death investigation of infants who die suddenly and unexpectedly. [source] Esophageal Causes of Sudden and Unexpected DeathJOURNAL OF FORENSIC SCIENCES, Issue 2 2006Roger W. Byard M.D. ABSTRACT: Gastrointestinal conditions are uncommon causes of sudden and/or unexpected death as compared to cardiovascular diseases, motor vehicle trauma, or suicide, and may involve an array of fatal mechanisms. Lethal esophageal conditions are encountered even less often, the manifestations of which include acute upper airway occlusion from tumors or foreign material, intraluminal hemorrhage from vascular abnormalities, or perforation with fistula formation resulting in hemorrhage and sepsis. When encountered at autopsy, a particular condition may also be a manifestation of a disease that does not primarily involve the esophagus. For this reason, a detailed autopsy investigation is required for evidence of systemic or remote disease when lesions are found within the esophagus. In this report, possible life-threatening esophageal conditions are reviewed with a description of lethal mechanisms, mention of rare associated diseases, and comment on difficulties that may arise at autopsy in the evaluation of such cases. [source] Mortality in epilepsy in the first 11 to 14 years after diagnosis: Multivariate analysis of a long-term, prospective, population-based cohortANNALS OF NEUROLOGY, Issue 3 2001Samden D. Lhatoo MRCP The United Kingdom National General Practice Study of Epilepsy is a prospective, population-based study of newly diagnosed epilepsy. A cohort of 792 patients has now been followed for up to 14 years (median follow-up [25th, 75th percentiles] 11.8 years, range 10.6,11.7 years), a total of 11,400 person-years. These data are sufficient for a detailed analysis of mortality in this early phase of epilepsy. Over 70% of patients in this cohort have developed lasting remission from seizures, although the mortality rate in the long term was still twice that of the general population. The standardized mortality ratio (SMR), the number of observed deaths per number of expected deaths, was 2.1 (95% confidence interval [CI] = 1.8, 2.4). Patients with acute symptomatic epilepsy (SMR 3.0; 95% CI = 2.0, 4.3), remote symptomatic epilepsy (SMR 3.7; 95% CI = 2.9, 4.6), and epilepsy due to congenital neurological deficits (SMR 25; 95% CI = 5.1, 73.1) had significantly increased long-term mortality rates, whereas patients with idiopathic epilepsy did not (SMR 1.3; 95% CI = 0.9, 1.9). This increase in mortality rate was noted particularly in the first few years after diagnosis. Multivariate Cox regression and time-dependent co-variate analyses were utilized for the first time in a prospective study of mortality in epilepsy. The former showed that patients with generalized tonic-clonic seizures had an increased risk of mortality. The hazard ratio (HR), or risk of mortality in a particular group with a particular risk factor compared to another group without that particular risk factor, was 6.2 (95% CI = 1.4, 27.7; p = 0.049). Cerebrovascular disease (HR 2.4; 95% CI = 1.7, 3.4; p < 0.0001), central nervous system tumor (HR 12.0; 95% CI = 7.9, 18.2; p < 0.0001), alcohol (HR 2.9; 95% CI = 1.5, 5.7; p = 0.004), and congenital neurological deficits (HR 10.9; 95% CI = 3.2, 36.1; p = 0.003) as causes for epilepsy and older age at index seizure (HR 1.9; 95% CI = 1.7,2.0; p < 0.0001) were also associated with significantly increased mortality rates. These hazard ratios suggest that epilepsy due to congenital neurological deficits may carry almost the same risk of mortality as epilepsy due to central nervous system tumors and that epileptic seizures subsequent to alcohol abuse may carry almost the same risk of mortality as epilepsy due to cerebrovascular disease. The occurrence of one or more seizures before the index seizure (the seizure that led to the diagnosis of epilepsy and enrolment in the study) was associated with a significantly reduced mortality rate (HR 0.57; 95% CI = 0.42, 0.76; p = 0.00001). Time-dependent co-variate analysis was used to examine the influence of ongoing factors, such as seizure recurrence, remission, and antiepileptic drug use, on mortality rates in the cohort. Seizure recurrence (HR 1.30; 95% CI = 0.84, 2.01) and antiepileptic drug treatment (HR 0.97; 95% CI = 0.67, 1.38) did not influence mortality rate. There were only 5 epilepsy-related deaths (1 each of sudden unexpected death in epilepsy, status epilepticus, burns, drowning, and cervical fracture), suggesting that death directly due to epileptic seizures is uncommon in a population-based cohort with epilepsy. Ann Neurol 2001;49:336,344 [source] Acidosis and Catecholamine Evaluation Following Simulated Law Enforcement "Use of Force" EncountersACADEMIC EMERGENCY MEDICINE, Issue 7 2010Jeffrey D. Ho MD ACADEMIC EMERGENCY MEDICINE 2010; 17:E60,E68 © 2010 by the Society for Academic Emergency Medicine Abstract Objectives:, Law enforcement authorities are often charged with controlling resisting suspects. These encounters sometimes result in the sudden and unexpected death of the suspect. Drug intoxication, excited delirium syndrome, or excessive uses of force are factors that are often blamed, but sometimes the mechanism of these deaths is not fully understood. It is possible that worsening acidosis or excessive catecholamine release play a part. The objective of this study was to determine the effect on markers of acidosis and catecholamines of various tasks intended to simulate common arrest-related situations. Methods:, Subjects were assigned to one of five task groups: 1) a 150-meter sprint and wall hurdle (simulated flight from arrest); 2) 45 seconds of striking a heavy bag (simulated physical resistance); 3) a 10-second TASER X26 electronic control device exposure; 4) a fleeing and resistance exercise involving a law enforcement dog (K-9); or 5) an oleoresin capsicum (OC) exposure to the face and neck. Baseline serum pH, lactate, potassium, troponin I, catecholamines, and creatine kinase (CK) were evaluated. Serum catecholamines, pH, lactate, and potassium were sampled immediately after the task and every 2 minutes for 10 minutes posttask. Vital signs were repeated immediately after the task. Serum CK and troponin I were evaluated again at 24 hours posttask. Results:, Sixty-six subjects were enrolled; four did not complete their assigned task. One subject lost the intravenous (IV) access after completing the task and did not have data collected, and one subject only received a 5-second TASER device exposure and was excluded from the study, leaving 12 subjects in each task group. The greatest changes in acidosis markers occurred in the sprint and heavy bag groups. Catecholamines increased the most in the heavy bag group and the sprint group and increased to a lesser degree in the TASER, OC, and K-9 groups. Only the sprint group showed an increase in CK at 24 hours. There were no elevations in troponin I in any group, nor any clinically important changes in potassium. Conclusions:, The simulations of physical resistance and fleeing on foot led to the greatest changes in markers of acidosis and catecholamines. These changes may be contributing or causal mechanisms in sudden custodial arrest-related deaths (ARDs). This initial work may have implications in guiding applications of force for law enforcement authorities (LEAs) when apprehending resisting subjects. [source] Lamotrigine does not prolong QTc in a thorough QT/QTc study in healthy subjectsBRITISH JOURNAL OF CLINICAL PHARMACOLOGY, Issue 3 2008Ruth Dixon WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT , Drugs that inhibit the human cardiac delayed rectifier potassium current may lead to prolongation of the cardiac QT interval and are associated with a fatal, polymorphic, ventricular tachycardia known as torsades de pointes. , Lamotrigine is indicated in the treatment of epilepsy and the prevention of mood episodes in patients with bipolar disorder. , Lamotrigine inhibits the human cardiac delayed rectifier potassium current in vitro, and it has been hypothesized that QT prolongation may contribute to the risk of sudden unexpected death in epilepsy patients. WHAT THIS STUDY ADDS , This is the first reported thorough QT/QTc study with lamotrigine conducted to International Conference on Harmonization guidelines. , The mean QTc interval was not prolonged by lamotrigine in healthy subjects, as assessed by the standard heart rate correction methods (Fridericia's and Bazett's). , The in vitro inhibition of the delayed rectifier potassium current does not translate into an effect on QT in man. AIM To characterize the effects of lamotrigine on QT interval in healthy subjects. METHODS Healthy subjects received a single oral dose of moxifloxacin (400 mg) or placebo in crossover design, followed by a dose-escalating regimen of lamotrigine (n = 76) over a 77-day period, or matched placebo (n = 76). Blood samples were taken for determination of moxifloxacin and lamotrigine concentrations and digital 12-lead ECGs were recorded. The relationships between individual QT values and respective individual moxifloxacin or lamotrigine concentrations were explored using population pharmacokinetic,pharmacodynamic (PK,PD) modelling. RESULTS Moxifloxacin was associated with a maximum mean increase from baseline in QTcF of 14.81 ms [90% confidence interval (CI) 13.50, 16.11] 2.5 h after dosing. Steady-state exposure to lamotrigine (50, 150 or 200 mg b.d.) was not associated with an increase in QTc interval. Small reductions in QTcF (maximum mean difference from placebo ,7.48 ms, 90% CI ,10.49, ,4.46) and small increases in heart rate (maximum mean difference from placebo 5.94 bpm, 90% CI 3.81, 8.06) were observed with lamotrigine 200 mg b.d. vs. placebo. No effect of lamotrigine on QRS duration or blood pressure was observed. No outliers with QTcF > 450 ms, or with an increase from baseline of >60 ms were observed in the lamotrigine group. PK,PD modelling indicated statistically significant decreases in individually corrected QT intervals for lamotrigine and statistically significant increases in individually corrected QT intervals for moxifloxacin over the concentration ranges studied. CONCLUSIONS Therapeutic doses of lamotrigine (50,200 mg b.d.) were not associated with QT prolongation in healthy subjects. [source] Relation between ictal asystole and cardiac sympathetic dysfunction shown by MIBG-SPECTACTA NEUROLOGICA SCANDINAVICA, Issue 2 2009F. Kerling Objective,,, Tachyarrhythmias are common during epileptic seizures while bradyarrhythmias or asystoles are less frequent. Ictal asystole might be related to epilepsy-induced cardiac sympathetic denervation. Methods,,, To evaluate cardiac post-ganglionic denervation in epilepsy patients with ictal asystoles we assessed I123 -meta-iodobenzylguanidine (MIBG) as a marker of post-ganglionic cardiac norepinephrine-uptake, using single photon emission computed tomography (MIBG-SPECT). Results,,, In five of 844 patients with presurgical video-electroencephalography-monitoring, we recorded ictal asystoles during nine of 37 seizures. Asystole patients underwent cardiologic examination (Holter-electrocardiogram, echocardiogram) and cardiac MIBG-SPECT. We compared cardiac MIBG uptake in the asystole patients to the uptake in 18 temporal lobe epilepsy (TLE) patients without bradyarrhythmias and in 14 controls without cardiac or neurological disease. As the cardiological examinations were unremarkable in all subjects, the heart/mediastinum-MIBG-uptake ratios (H/M-ratios) differed significantly between the three groups (P = 0.004). H/M-ratios were lower in asystole TLE patients (mean ± SD: 1.58 ± 0.3) than in patients without asystole (1.81 ± 0.18; P = 0.037) or controls (1.96 ± 0.16). Conclusions,,, Pronounced reduction in cardiac MIBG uptake of asystole patients indicates post-ganglionic cardiac catecholamine disturbance. Impaired sympathetic cardiac innervation limits adjustment and heart rate modulation, and may increase the risk of asystole and ultimately sudden unexpected death in epilepsy (SUDEP). [source] Cholinergic and oxidative stress mechanisms in sudden infant death syndromeACTA PAEDIATRICA, Issue 11 2009Anne Dick Abstract Aim:, To determine whether biochemical parameters of cholinergic and oxidative stress function including red cell acetylcholinesterase (AChE), serum/plasma thyroglobulin, selenium, iron, ferritin, vitamins C, E, and A affect risk in apparent life-threatening event (ALTE), sudden infant death syndrome (SIDS), and sudden unexpected death in infancy (SUDI). To assess these biochemical parameters as a function of age; and for influence of pharmacology and epidemiology, including infant health, care, and feeding practices. Methods:, A multicentre, case,control study with blood samples from 34 ALTE and 67 non-ALTE (control) infants matched for age, and 30 SIDS/SUDI and four non-SIDS/non-SUDI (post-mortem control) infants. Results:, Levels/activity of the biochemical parameters were not significantly different in ALTE vs. control infants, with the exception of higher vitamin C levels in the ALTE group (p = 0.009). In ALTE and control groups, AChE and thyroglobulin levels increased and decreased respectively from birth to attain normal adult levels from 6 months. Levels of iron and ferritin were higher in the first 6 month period for all infant groups studied, intersecting with vitamin C levels peaking around 4 months of age. Conclusion:, Lower AChE levels and higher combined levels of iron and vitamin C in the first 6 months of life may augment cholinergic and oxidative stress effect, particularly at the age when SIDS is most prevalent. This may contribute to risk of ALTE and SIDS/SUDI events during infancy. [source] Post-Traumatic Stress Disorder in CanadaCNS: NEUROSCIENCE AND THERAPEUTICS, Issue 3 2008Michael Van Ameringen Post-traumatic stress disorder (PTSD) has become a global health issue, with prevalence rates ranging from 1.3% to 37.4%. As there is little current data on PTSD in Canada, an epidemiological study was conducted examining PTSD and related comorbid conditions. Modified versions of the Composite International Diagnostic Interview (CIDI) PTSD module, the depression, alcohol and substance abuse sections of the Mini International Neuropsychiatric Interview (MINI), as well as portions of the Childhood Trauma Questionnaire (CTQ) were combined, and administered via telephone interview in English or French. Random digit dialing was used to obtain a nationally representative sample of 2991, aged 18 years and above from across Canada. The prevalence rate of lifetime PTSD in Canada was estimated to be 9.2%, with a rate of current (1-month) PTSD of 2.4%. Traumatic exposure to at least one event sufficient to cause PTSD was reported by 76.1% of respondents. The most common forms of trauma resulting in PTSD included unexpected death of a loved one, sexual assault, and seeing someone badly injured or killed. In respondents meeting criteria for PTSD, the symptoms were chronic in nature, and associated with significant impairment and high rates of comorbidity. PTSD is a common psychiatric disorder in Canada. The results are surprising, given the comparably low rates of violent crime, a small military and few natural disasters. Potential implications of these findings are discussed. [source] What Is the mechanism of SIDS?DEVELOPMENTAL PSYCHOBIOLOGY, Issue 3 2009Clues from epidemiology Abstract The cause of sudden infant death syndrome (SIDS) is unknown. Many mechanisms have been postulated, although thermal stress, rebreathing of expired gases and infection/inflammation seem the most viable hypotheses for the causation of SIDS. Deaths from SIDS have reduced dramatically following the recommendation not to place infants to sleep prone. Epidemiological data have shown that prone sleeping position is more risky in winter, colder latitudes, higher altitudes, if the infant is unwell or has excessive bedding or clothing. This suggests prone sleeping position involves either directly or indirectly a thermal mechanism. SIDS caused by an infective/inflammatory mechanism might be associated with deaths occurring during the night. Rebreathing of expired gases, airway obstruction, long QT syndrome and other genetic conditions may explain a small number of sudden unexpected deaths in infancy. © 2009 Wiley Periodicals, Inc. Dev Psychobiol 51: 215,222, 2009 [source] The Role of Environmental Factors in the Causation of Sudden Death in Infants: Two Cases of Sudden Unexpected Death in Two Unrelated Infants Who Were Cared for by the Same BabysitterJOURNAL OF FORENSIC SCIENCES, Issue 6 2007Bennet I. Omalu M.D., M.P.H. Abstract:, We report two cases of sudden unexpected death in two unrelated African American female infants, 2 months and 4 months old. Both infants were attended to by the same babysitter in the same apartment and died 39 days apart in the same bed and in the same bedroom. The autopsy of the first infant revealed sudden unexplained death in an infant. Toxicologic analysis for carbon monoxide (CO) was not performed because it was not suspected. When the second infant died, investigation into the ambient air quality within the apartment revealed high levels of CO emanating from a poorly ventilated and defective hot water heater, which was located across a hallway from the bedroom where the two babies died. CO saturation levels in the postmortem blood samples of the two babies were elevated and were similar (13% and 14%). Nicotine and cotinine were not detected in the blood sample of the two infants. Cherry-red livor mortis was absent. Acute CO intoxication was determined to be the underlying cause of these two unexpected deaths. These two cases underscore the need to integrate ambient air analysis and postmortem CO analysis as routine components of the comprehensive death investigation of infants who die suddenly and unexpectedly. [source] Sudden death caused by chronic Chagas disease in a non-endemic country: Autopsy reportPATHOLOGY INTERNATIONAL, Issue 3 2010Fumiko Satoh Chagas disease is a tropical disease that is prevalent in Latin America. Described herein is an autopsy case of the sudden death of a 48-year-old Brazilian man who had stayed in Japan for 7 years. The man, who had a history of Chagas disease, collapsed unexpectedly at work. Because the cause of death was unknown, forensic autopsy examination was performed. As gross findings, the heart was dilated and rounded with an increase in size and weight. The esophagus and large intestine were dilated moderately, with extensive interstitial inflammatory infiltration in the cardiac muscle, but no apparent parasite nest was observed in various tissues. On post-mortem laboratory examinations, indirect immunofluorescence antibody test indicated the presence of IgG antibody specific to Trypanosoma cruzi in the serum. Subsequent polymerase chain reaction amplification using DNA extracted from blood yielded the specific product derived from T. cruzi genomic DNA. These examinations indicate that the infection had resulted from the Tripanosoma parasite. The cause of death was judged to be chronic cardiomyopathy caused by Chagas disease. It is important for pathologists to know the possible involvement of chronic Chagas disease in sudden unexpected deaths in the current globalized society of Japan. [source] Radiofrequency fields and teratogenesis,BIOELECTROMAGNETICS, Issue S6 2003Louis N. Heynick Abstract Experimental studies that sought teratologic effects or developmental abnormalities from exposure to radiofrequency electromagnetic fields (RFEMF) in the range 3 kHz,300 GHz are critically reviewed for their possible consequences on human health. Those studies were conducted on beetles, birds, rodents, and nonhuman primates. Collectively, those experimental studies indicate that teratologic effects can occur only from exposure levels that cause biologically detrimental increases in body temperature. No reliable experimental evidence was found for nonthermal teratologic effects; rodents, mouse fetuses, and perinatal mice are more susceptible to such effects than rats. The primary confirmed effect in rats at high RFEMF levels was initial weight deficits in fetuses and neonates that decreased with infant growth. More generally from findings with pregnant mammals, exposures at RFEMF levels far higher than those permitted under the IEEE human exposure guidelines are necessary to reach or exceed cited experimental thresholds for maternal temperature increases. Some results indicated that the levels necessary to cause such effects in pregnant mammals could exceed those lethal to the dams. In a behavioral study of squirrel monkeys, no effects were observed on usual dam-offspring interactions or EEGs, but unexpected deaths of a number of offspring had occurred. However, this finding was not confirmed in a study solely on infant death using a larger number of subjects for greater statistical validity. Also reviewed were epidemiologic studies of various human populations considered to have been chronically exposed to environmental levels of RFEMF. Early studies on the incidence of congenital anomalies yielded no credible evidence that chronic exposure of pregnant women or of fathers exposed to RFEMF from nearby sources at levels below those guidelines would cause any anomalies in their offspring. The findings of studies on pregnancy outcomes of female physiotherapists occupationally exposed while treating patients with RFEMF were mixed, but taken collectively, the findings were negative. Bioelectromagnetics Supplement 6:S174,S186, 2003. Published 2003 Wiley-Liss, Inc. [source] Rib fractures identified at post-mortem examination in sudden unexpected deaths in infancy (SUDI)CHILD: CARE, HEALTH AND DEVELOPMENT, Issue 3 2010Richard Reading No abstract is available for this article. [source] Medical students' first clinical experiences of deathMEDICAL EDUCATION, Issue 4 2010Emily Kelly Medical Education 2010: 44: 421,428 Objectives, Many medical students feel inadequately prepared to address end-of-life issues, including patient death. This study aimed to examine medical students' first experiences of the deaths of patients in their care. Methods, Final-year medical students at the Schulich School of Medicine & Dentistry, University of Western Ontario were invited to share their first experience of the death of a patient in their care. The students could choose to participate through telephone interviews, focus groups or e-mail. All responses were audiotaped, transcribed verbatim and analysed using a grounded theory approach. Results, Twenty-nine students reported experiencing the death of a patient in their care. Of these, 20 chose to participate in an interview, five in a focus group and four through e-mail. The issues that emerged were organised under the overlying themes of ,young', ,old' or ,unexpected' deaths and covered seven major themes: (i) preparation; (ii) the death event; (iii) feelings; (iv) the role of the clinical clerk; (v) differential factors between deaths; (vi) closure, and (vii) relationships. These themes generated a five-stage cyclical model of students' experiences of death, consisting of: (i) preparation; (ii) the event itself; (iii) the crisis; (iv) the resolution, and (v) the lessons learned. ,Preparation' touches on personal experience and pre-clinical instruction. ,The event itself' could be categorised as referring to a ,young' patient, an ,old' patient or a patient in whom death was ,unexpected'. In the ,resolution' phase, coping mechanisms included rationalisation, contemplation and learning. The ,lessons learned' shape medical students' experiences of future patient deaths and their professional identity. Conclusions, A tension between emotional concern and professional detachment was pervasive among medical students undergoing their first experience of the death of a patient in their care. How this tension was negotiated depended on the patient's clinical circumstances, supervisor role-modelling and, most importantly, the support of supervisors and peers, including debriefing opportunities. Faculty members and residents should be made aware of the complexities of a medical student's first experience of patient death and be educated regarding sympathetic debriefing. [source] | ||||||||||||||||