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Aims: Clinical and medico-legal decisions often requite knowledge of alcohol impairnienl that is not necessarily revealed by an individual's appearance, and in turn, may not necessarily refitet level of blood alcohol. This study computes clinical signs and symptoms with measured and estimated blood alcohol concentrations (BACs). Method: Individuals (n = 384) perceived to be under the influence of alcohol at presentation 10 an emergency department were assessed by physicians and nurses for clinical features of alcohol intoxication (alcohol symptom checklist, ASC), who were asked to estimate the patienl's BAC. Relation to measured BACs was assessed by correlation. Results: BACs ranged from 0 to 418 mg/lOb ml. The correlation between the estimated BAC and measured BAC was r = 0.513. Measured BAC correlated with ASC r = 0.250. In subjects without a history of chronic drinking (n = 134) there was a better (P <0.05) correlation with the ASC score (r = 0.363) versus measured BAC compared with that for chronic drinkers (r = 0.154). The positive predictive value of estimating BAC at or above a particular BAC cut-off decreased from 93.2% at 100 mg/I 00 ml to 37.7% at 300 mg/100 ml (P<0.05). Conclusions: Measured BAC does not correlate well with the outward physical signs of intoxication, especially for chronic drinkers. There is a need for further educaticn on how tolerance masks clinical signs of intoxication for the chronic drinker. BACs should be measured especially in the obtunded where no history (symptoms) can be given by the patient. [ABSTRACT FROM AUTHOR]

Background: Identifying persons at risk for sudden cardiac death (SCD) is challenging. A comprehensive evaluation may reveal clues about the clinical, anatomical, genetic, and metabolic risk factors for SCD., Methods: Seventy-one patients who had SCD (25-60 years old) without an initially apparent cause of death were evaluated at the Hennepin County Medical Examiner's office (Minneapolis, MN) from August 2001 to July 2004. We reviewed their clinic records conducted next-of-kin interviews and performed autopsy, laboratory testing, and genetic analysis for mutations in genes associated with the long QT syndrome., Results: Mean age was 49.5 +/- 7 years, 86% were male, and 2 subjects had history of coronary heart disease (CHD). Coronary risk factors were highly prevalent in comparison to individuals of the same age group in this community (eg, smoking 61%, hypertension 27%, hyperlipidemia 25%) but inadequately treated. On autopsy, 80% of the subjects had high-grade coronary stenoses. Acute coronary lesions and previous silent myocardial infarction (MI) were found in 27% and 34%, respectively. Furthermore, 32% of the subjects had recently smoked cigarettes, and 50% had ingested analgesics. Possible deleterious mutations of the ion channel genes were detected in 5 subjects (7%). Of these, 4 were in the sodium channel gene SCN5A., Conclusions: Most of the persons who had SCD in the community had severe subclinical CHD, including undetected previous MI. Traditional coronary risk factors were prevalent and undertreated. Mutations in the long QT syndrome genes were detected in a few subjects. These findings imply that improvements in the detection and treatment of subclinical CHD in the community are needed to prevent SCD., (Copyright 2010 Mosby, Inc. All rights reserved.)

The purpose of this study was to compare blood fentanyl concentrations in fentanyl-related deaths with fentanyl concentrations found incidentally at autopsy, as well as with fentanyl concentrations found in hospitalized patients receiving fentanyl. Between the years 1997 to 2005, 23 fentanyl-positive postmortem cases were identified. Nineteen of 23 (82.6%) cases were deemed to be drug overdoses. Fentanyl alone was responsible for 8 of the 19 (42.1%) overdose deaths. Mean and median fentanyl concentrations were 36 (SD 38) microg/L and 22 microg/L, respectively, range 5-120 microg/L. Seven of the cases were accidental, one undetermined. The remaining 11 of the 19 (57.9%) cases were mixed drug overdoses. Fentanyl concentrations in these cases were 31 (SD 46) microg/L, range 5-152 microg/L. All of the mixed drug overdoses were determined to be accidental. Four cases where fentanyl was considered an incidental postmortem finding were determined to be natural deaths. In hospitalized inpatients (n = 11) receiving fentanyl 2 of the patients receiving fentanyl for chronic pain for more than 3 months had concentrations of 8.5 microg/L and 9.9 microg/L. The other nine inpatient concentrations were less than 4 microg/L. In conclusion, blood fentanyl concentrations found in cases where fentanyl alone was determined to be the cause of death were similar to cases where fentanyl was part of a mixed drug overdose. There was also considerable overlap between fentanyl concentrations in fentanyl-related overdose deaths compared to hospitalized patients being treated for chronic pain. Fentanyl concentrations in postmortem cases must be interpreted in the context of the deceased's past medical history and autopsy findings.

Patients with symptoms suggestive of, but at low risk for, acute coronary syndrome (ACS), who have a negative electrocardiogram (EKG) and a single normal troponin I at 6-9 h after symptom onset are frequently discharged from our Emergency Department (ED). We sought to determine their rate of adverse cardiac events at 30 days (ACE-30), defined as cardiac death or myocardial infarction (MI), by chart review, telephone interview, or county death records. Of 663 patients, data were available for 588 (89%). Mean age was 48 years; 59% were male. There were 390 patients (66%) who complained of chest pain. Previous coronary artery disease (CAD) was reported in 145 patients (25%). Two patients (0.34%) had ACE-30, both with non-ST elevation MI. There were no cases of cardiac death. None of the patients died in Hennepin County within 30 days. At our institution, low-risk patients with symptoms suggestive of ACS who are discharged home after a normal cTnI drawn 6-9 h after symptom onset have a very low incidence of cardiac events at 30 days.

Context: Increasing numbers of patients are presenting to emergency departments with symptoms suggestive of an acute myocardial infarction., Objective: To demonstrate the comparative performance of the Ortho Vitros Troponin I and Beckman Access AccuTnI assays used to detect myocardial infarction and to develop risk stratification schemes for all-cause death in patients who presented with myocardial ischemia symptoms that were suggestive of acute coronary syndrome (ACS)., Design: The prospective enrollment of patients with ACS and the measurement of serial plasma samples by 2 commercial cardiac troponin I (cTnI) assays., Setting: A metropolitan medical center that admitted patients with ACS during a 2-month period., Patients: The study population consisted of 200 consecutively admitted patients who presented with symptoms that were suggestive of ACS., Results: Correlation scatterplots showed no significant bias between cTnI assays based on 659 specimens across the dynamic range of each assay. Only minor differences in slopes and intercepts were observed between assays when correlations were based across selected concentration ranges. The receiver operating characteristic curve areas for the detection of myocardial infarction were not significantly different (Ortho,.991; Beckman,.995). At the 99th percentile (Beckman, 0.04 microg/L; Ortho, 0.08 microg/L), each assay demonstrated 100% sensitivity with 78% and 80% specificity, respectively. Kaplan-Meier survival curves and the log-rank test were used to compare time-to-event data. Patients with increased baseline cTnI values had higher odds ratios of death than did those with normal concentrations. For Ortho, the 99th percentile cutoff was 5.9, and the 10% coefficient of variation cutoff was 10.3; for Beckman, the 99th percentile cutoff was 31.4, and the 10% coefficient of variation cutoff was 15.3., Conclusions: Comparable diagnostic and risk stratification abilities were demonstrated in patients with ACS by the Ortho Vitros and Beckman Access cTnI assays, with no significant analytic bias between cTnI assays.

Methadone maintenance therapy (MMT) is the only currently established medical therapy for heroin addiction. However, MMT still remains controversial. In Hennepin County, Minnesota, methadone is one of the top ten drugs reported in medical examiner investigated deaths and one of the most commonly diverted pharmaceuticals. This report reviews the role of methadone in medical examiner deaths over a 10-year period, 1992-2002. We compare cause and manner of death (accidental, natural, suicide) and methadone blood concentrations for decedents who were members of MMT programs with illicit users and those prescribed methadone for chronic pain. Findings reveal that 65% of decedents with measurable blood methadone concentrations were not participating in MMT programs. A total of 96 cases were identified, with the majority white (90.5%) and male (76.8%). MMTP program members were the minority (34.7%) of the methadone positive deaths and 39% were illicit users. Fifteen percent were chronic pain patients with almost half of this group dying from overdose. Methadone concentrations of drug caused/related deaths (0.18-3.99 mg/L) overlapped with those of deaths not attributable to methadone (0.18-3.03 mg/L) with no definable lethal level. Interpretation of methadone blood concentrations must be done in the context of the clinical history for determining cause of death, and may be confounded by postmortem redistribution.

Background: This study determined the prevalence of increased cardiac troponin I (cTnI) and T (cTnT) in end-stage renal disease (ESRD) patients and whether an increased troponin was predictive of death., Methods and Results: Serum was obtained from 733 ESRD patients and measured for cTnI and cTnT. Relative risks were estimated using Cox proportional hazards regressions univariately and adjusted for age, time on dialysis, and coronary artery disease. Kaplan-Meier curves compared time to event data between groups. Greater percentages of patients had an increased cTnT versus cTnI at each cutoff, as follows: 99th percentile, 82% versus 6%; 10% coefficient of variation, 53% versus 1.0%; and receiver operator characteristic, 20% versus 0.4%. Increased versus normal cTnT was predictive of increased mortality using all cutoffs and only above the 99th percentile for cTnI. Two-year cumulative mortality rates increased (P<0.001) with changes in cTnT from normal (<0.01 microg/L, 8.4%) to small (> or =0.01 to <0.04 microg/L, 26%), moderate (> or =0.04 to <0.1 microg/L, 39%), and large (> or =0.1 microg/L, 47%) increases. Two-year mortalities were 30% for cTnI <0.1 microg/L and 52% if > or =0.1 microg/L. Univariate and adjusted relative risks of death associated with elevated (>99th percentile) cTnT were 5.0 (CI, 2.5 to 10; P<0.001) and 3.9 (CI, 1.9 to7.9; P<0.001) and cTnI were 2.0 (CI, 1.3 to 3.3; P=0.008) and 2.1 (CI, 1.3 to 3.3; P=0.007). Age, coronary artery disease, and time on dialysis were also independent predictors of mortality., Conclusions: Increases in cTnT and cTnI in ESRD patients show a 2- to 5-fold increase in mortality, with a greater number of patients having an increased cTnT.