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PubMedDate not supplied

Uncertainty of determining mode and cause of death without autopsy: an autopsy study of medically unattended non-medicolegal deaths.

Eighty-seven cases of medically unattended deaths were autopsied and investigated for alcohol and barbiturate after the general practitioner had certified the death. A detailed survey was made by comparing the mode and cause of death before and after autopsy. After autopsy and chemical analysis, two suicides, one accidental death and two unknown modes of death were found (5%). The high proportion of unknown mode of death was due to the fact that police investigations were not made. The cause of death differed in 30%. It was mostly due to overestimation of ischaemic heart disease, especially acute myocardial infarction, cerebral haemorrhage and because the unknown cause of death could be placed in a definite group after autopsy. Estimated acute myocardial infarciton could only be confirmed in 50% of the cases. Neoplastic disorders as the cause of death was seldom found to be erroneous, but malignancy was undiagnosed in 4% of all cases. It is concluded that doctors should not use acute myocardial infarction as a cause of death unless there is reasonable clinical evidence for the diagnosis, that obscure cases of death should be left to medicolegal investigation, and that the reliability of mortality statistics still has to be improved. The autopsy is still valuable to ensure this extra security.

Adult↗
PubMed2003

Death after injury in rural Norway: high rate of mortality and prehospital death.

BACKGROUND: Finnmark is a rural and remote area in Norway with a sparse population and long distances. Trauma-related mortality has been consistently above the Norwegian national average for the last 20 years. Although the causes of death are well established, very little is known about the time and place of death. This information has implications for the organization of emergency services in rural areas. We examined all trauma deaths over a five-year period in order to inform the debate on how best to reduce our above-average mortality rate. METHODS: A retrospective study of all deaths after trauma (ICD-9 E800-E999) during the years 1991-95 using data obtained from the National Registry of Death. RESULTS: Of the 183 cases found, 130 deaths were due to trauma using definitions comparable to similar studies. The mortality rate was 77 per 100,000 inhabitants per year. Death occurred in the prehospital phase in 85% of cases. Seventy-two per cent of all deaths (regardless of location) occurred within the first h after injury, eight per cent from 1 to 4 h and the remaining 20% occurred after 4 h. CONCLUSION: When planning interventions to reduce the mortality rate from trauma in rural areas, a high proportion of prehospital deaths should be expected. The high number of patients who are found dead (which can only be reduced by injury prevention) must be taken into account. Measures to reduce 'preventable' causes of death by bystanders should be evaluated. Further knowledge of exact mechanisms of death in the prehospital phase is required.

Adolescent↗
PubMed2005

Arsenic trioxide induces autophagic cell death in malignant glioma cells by upregulation of mitochondrial cell death protein BNIP3.

Arsenic trioxide (As(2)O(3)) has shown considerable efficacy in treating hematological malignancies with induction of programmed cell death (PCD) type I, apoptosis. However, the mechanisms underlying the antitumor effect of As(2)O(3) on solid tumors are poorly defined. Previously, we reported that As(2)O(3) induced autophagic cell death (PCD type II) but not apoptosis in human malignant glioma cell lines. The purpose of this study was to elucidate the molecular pathway leading to autophagic cell death. In this study, we demonstrated that the cell death was accompanied by involvement of autophagy-specific marker, microtubule-associated protein light chain 3 (LC3), and damage of mitochondrial membrane integrity, but not by caspase activation. Analysis by cDNA microarray, RT-PCR, and Western blot showed that cell death members of Bcl-2 family, Bcl-2/adenovirus E1B 19-kDa-interacting protein 3 (BNIP3) and its homologue BNIP3-like (BNIP3L), were upregulated in As(2)O(3)-induced autophagic cell death. Exogenous expression of BNIP3, but not BNIP3L, induced autophagic cell death in malignant glioma cells without As(2)O(3) treatment. When upregulation of BNIP3 induced by As(2)O(3) was suppressed by a dominant-negative effect of the transmembrane-deleted BNIP3 (BNIP3 Delta TM), autophagic cell death was inhibited. In contrast, BNIP3 transfection augmented As(2)O(3)-induced autophagic cell death. These results suggest that BNIP3 plays a central role in As(2)O(3)-induced autophagic cell death in malignant glioma cells. This study adds a new concept to characterize the pathways by which As(2)O(3) acts to induce autophagic cell death in malignant glioma cells.

Antineoplastic Agents↗
PubMed2005

[Selective "death programs" or pleiotropic"life programs"? Looking for programmed cell death in the light of evolution].

"Nothing in biology makes sense except in the light of evolution", wrote Theodosius Dobzhansky, one of the founders of the Modern Synthesis that led to the unification of evolutionary theory and genetics in the midst of the 20th century. Programmed cell death is a genetically regulated process of cell suicide that is central to the development, homeostasis and integrity of multicellular organisms. Conversely, the dysregulation of mechanisms controlling cell suicide plays a role in the pathogenesis of a wide range of diseases. While great progress has been achieved in the unveiling of the molecular mechanisms of programmed cell death, a new, and somehow puzzling level of complexity has recently begun to emerge, suggesting i) that several different self destruction pathways may exist and operate in parallel in our cells, and ii) that molecular effectors of cell suicide might also perform other functions unrelated to cell death induction and crucial to cell survival, such as cell differentiation, metabolism, and the regulation of the cell cycle. These new findings, with important physiopathological and therapeutic implications, seem at odds with the paradigm of programmed cell death derived from the studies of Caenorhabditis elegans, which led to the concept of the existence of selective, bona fide death genes that emerged and became selected for their sole capacity to execute or repress cell death. In this review, I will argue that this new level of complexity might only make sense and be understood when considered in a broader evolutionary context than that of our phylogenetic divergence from C. elegans. A new view of the regulated cell death pathways emerges when one attempts to ask the question of when and how they may have become selected during a timeline of 4 billion years, at the level of ancestral single-celled organisms, including the bacteria. I will argue that there may be no such thing as a bona fide genetic cell death program. Rather, in the framework of a model that I have termed the "original sin" hypothesis, I have proposed the existence of an initial pleiotropy of the molecular tools involved in the control and execution of self-destruction--an ancestral involvement in both pro-life and pro-death activities. I will discuss how this hypothesis may be reconciled with the C. elegans paradigm of programmed cell death. Finally I will discuss how an ancestral level of pleiotropic functions of the molecular tools involved in the control of cell death, aging and genetic diversification might have favored their initial selection, their constant availability for de novo selection, and their progressive propagation in most--if not all--species during the course of evolution.

Aging↗
PubMed2005

Tooth loss is associated with increased risk of total death and death from upper gastrointestinal cancer, heart disease, and stroke in a Chinese population-based cohort.

BACKGROUND: Tooth loss has previously been associated with a higher risk of cancer, heart disease, and stroke, but the role of confounding by smoking remains an issue. METHODS: We conducted a cohort study including 29,584 healthy, rural Chinese adults who were participants in a chemoprevention trial from 1986 through 1991 and who have been followed-up through 2001. We categorized tooth loss for each subject as less than or equal to or greater than the median number of teeth lost for other subjects of the same age at baseline. Mortality outcomes were categorized as follows: total death (n = 9362), upper gastrointestinal (GI) cancer death (n = 2625), other cancer death (n = 514), heart disease death (n = 1932), and fatal stroke (n = 2866). RESULTS: Individuals with greater than the age-specific median number of teeth lost had statistically significant 13% increased risk of total death [95% confidence interval (CI) 9-18%], 35% increased risk of upper GI cancer death (95% CI 14-59%), 28% increased risk of heart disease death (95% CI 17-40%), and 12% increased risk of stroke death (95% CI 2-23%), but no significantly increased risk of death from cancer at other sites. These elevated risks were present in male smokers, male non-smokers, and females, nearly all never-smokers. CONCLUSIONS: In this Asian population, tooth loss significantly increased the risk of total death and death from upper GI cancer, heart disease, and stroke. These associations were not limited to tobacco smokers.

Adult↗
PubMed1990

[Narcotic abuse in Jylland. A study based on narcotics and deaths of addicts examined at the Institute of Forensic Medicine, University of Aarhus during the period 1981-1988. 2. Deaths among addicts].

A total of 229 deaths among drug addicts (194 men and 35 women) examined of the Institute of Forensic Medicine, University of Aarhus during the period 1981-1988 is described. In 178 deaths, the cause of death was poisoning with a drug or illegal narcotic. Alcohol was involved in nearly half of these deaths and was, in addition, the cause of death in 4% of the cases. Heroin or morphine were the causes of death in one third of the cases while detropropoxyphene, methadone and ketobemidone were responsible for approximately half of the deaths. Until 1986, dextropropoxyphene was the dominating drug whereas the number of methadone deaths was considerably greater in the latter half of the period investigated than in the first half. Amphetamine alone was rarely the cause of death but the drug was seen in an increasing number of deaths in recent years. Thus, amphetamine was found in one third of the deaths in 1988.

Adolescent↗
PubMed1995

Should coroners be able to recognize unintentional carbon monoxide-related deaths immediately at the death scene?

The aim of this retrospective survey of unintentional carbon monoxide-related deaths in Vienna was to determine whether the cherry-pink coloring of livor mortis is a reliable finding for the coroner to suspect a carbon monoxide-related death immediately at the death scene. In addition, we investigated the recognition pattern of unintentional carbon monoxide-related deaths by Viennese coroners between 1984 and 1993. Therefore, we analyzed autopsy reports of postmortems performed at the Viennese Institute of Forensic Medicine between 1984 and 1993. The study involved 182 unintentional carbon monoxide-related deaths: 92 females and 90 males. We found a strong association between the carboxyhemoglobin level and the cherry-pink coloring of livor mortis. In 98.4% of unintentional carbon monoxide-related deaths livor mortis were clearly cherry-pink. During the 10-year study period Viennese coroners recognized only 61% of unintentional carbon monoxide-related deaths immediately at the death scene. The percentage of unrecognized carbon monoxide fatalities with a clear cherry-pink coloring of livor mortis almost doubled from 1984 to 1993. The older the victim, the worse the coroners recognition. In summary, we have shown that coroners should be able to recognize unintentional carbon monoxide-related deaths immediately at the death-scene, because fresh corpses with carboxyhemoglobin levels greater than 31% show a clear cherry-pink coloring of livor mortis. Therefore, coroners should be encouraged to examine naked corpses thoroughly, especially regarding the color of livor mortis. Thus, a carbon monoxide-related death can be recognized immediately and the source of gas release identified as soon as possible protecting people who otherwise would also be at risk of poisoning.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1998

Validation of death certificate diagnosis of out-of-hospital sudden cardiac death.

The validity of death certificate diagnosis of out-of-hospital sudden cardiac death (OOH-SCD) was studied among 108,676 30- to 74-year-old residents in 5 Minnesota communities using 6-year mortality data (1985 to 1990). Among 4,244 total deaths, location of death was listed on the certificate as out of hospital in 2,035 cases. Of those, 911 were judged not to have OOH-SCD because they had actually been admitted to the hospital or were noncardiovascular deaths. Among the remaining 1,124, 254 were diagnosed as OOH-SCD using a thorough, physician-based procedure that used clinical records, autopsy reports, and an informant (next-of-kin) interview. We used only death certificate information to define OOH-SCD simply and inexpensively as ICD-9 code 427.5 (cardiac arrest) plus location of death listed as out-of-hospital. Compared with the physician diagnosis, sensitivity was only 24%, whereas specificity was 85%. When the definition of OOH-SCD was expanded to include ICD codes 410-414 (acute myocardial infarction and chronic coronary artery disease), sensitivity improved to 87%, whereas specificity became 66%. However, even with this higher sensitivity and specificity, only 27% of the cases labeled OOH-SCD by death certificate agreed with the physician diagnosis. Death certificate diagnosis of OOH-SCD included many erroneous cases, and may not have been suitable for study of etiologic factors, such as cardiac dysrhythmias. Death certificate diagnosis may be useful to assess population time trends in OOH-SCD, provided that misclassification (false-positive rate) remains constant over time.

Adult↗
PubMed1987

Out-of-hospital coronary death in an urban population--validation of death certificate diagnosis. The Minnesota Heart Survey.

To assess the validity of death certificate diagnoses of out-of-hospital coronary heart disease deaths, the authors studied a one-third random sample of out-of-hospital deaths occurring in 1979 in Minneapolis-St. Paul, Minnesota, residents. Death certificates with diagnoses possibly containing coronary heart disease deaths were enumerated, and cause of death was recorded from the certificate in two ways: as the first listed ("immediate") cause and as the "underlying cause" assigned by a trained nosologist. Validation was performed by standardized physician review of information obtained about the death, which included one or more of the following: an interview with a relative or friend, physician report, autopsy report, medical record, and/or nursing home record. Missing information was frequent, but cases with at least an informant interview and/or autopsy report (82%) were representative and could be used for validation. The sensitivity and specificity of the underlying cause of coronary heart disease (International Classification of Diseases, Ninth Revision, codes 410-414, 427) on the death certificate were 90.3% and 82.7%, respectively, compared with the physician-assigned diagnosis. For the immediate cause, sensitivity and specificity were 90.3% and 67.9%, respectively. These findings suggest that the validity of death certificates for out-of-hospital coronary heart disease death is high, as assessed by this method of retrospective physician review.

Coronary Disease↗
PubMed2003

Multiple-cause coding of death from myocardial infarction: population-based study of trends in death certificate data.

BACKGROUND: Data on long-term trends in mortality are generally unavailable for multiple-cause coding of deaths. We wanted to know whether multiple-cause coding of deaths for myocardial infarction contributes much to the interpretation of death certificate data on mortality rates for this condition. METHODS: We analysed all causes of death on death certificates in the former Oxford health service region from 1979 to 1998. RESULTS: Of 69,333 death certificates that included myocardial infarction as a cause of death, it was the underlying cause of death in 93.6 per cent. The ratio of 'mentions' to 'underlying cause' was broadly similar over the study period, during which time there were substantial falls in mortality rates. There were significant changes to the ratios, associated with timing of changes to coding rules; but their effects were small. The ratio of mentions to underlying cause was similar in men and women and in different age groups. CONCLUSION: The underlying cause of death was a robust and almost complete measure of certified deaths for myocardial infarction.

Adult↗
PubMed1983

Instructional units of death education: the impact of amount of classroom time on changes in death attitudes.

The present study sought to provide a better understanding of the impact instructional time devoted to death education had on death attitudes. The study incorporates a three-group experimental research design with repeated measures. Three experimental groups of college students randomly were assigned to one of three short units of death education. The groups varied in terms of the amount of instructional time they were given. One group received three class sessions of death education, while the other two groups received six and nine classes, respectively. Only in the group that received nine class sessions of death education were death attitudes changed significantly. Such changes occurred on one dimension of death attitudes. Results suggest that very brief units of death education are not effective in changing attitudes. When attitude change is deemed important, the most rational length of time to devote to death education is roughly nine class sessions. Even then, attitudes related to death may be affected only partially.

Attitude to Death↗
PubMedDate not supplied

Decline of acute myocardial infarction death rates not due to cause of death coding.

The recent decline in coronary heart disease (CHD) mortality has been attributed to reduction in risk factors, improved management and the possibility of statistical artifacts. The purpose of this study is to assess the impact of geographic and time variation in the coding of cause of death from death certificates into ICD codes upon CHD mortality rates in Canada. Equal samples of death certificates were recoded for Nova Scotia and Saskatchewan for each of the years 1970 and 1984: 1) a first set of 1,600 death certificates originally coded as acute myocardial infarction (AMI) and 2) a second set of 800 death certificates from all causes of death. The coding error rates increased with age and with the number of contributing and underlying causes of death reported on the death certificates. The net effect of false positive and false negative AMI codes on death certificates did not vary significantly by province or year. Thus, variation of death certificate coding over time and geographic regions do not contribute toward the explanation of the AMI mortality rate decline.

Canada↗
PubMed1997

A medical cause of death validation study of adult aboriginal deaths in the Northern Territory of Australia in 1992.

Judged on the criterion of equity, premature adult Aboriginal mortality is the most serious public health problem faced in Australia today. There have been a number of published epidemiological studies that have analysed Aboriginal cause of death data, but this is the first study to formally validate such data. The study sample included all adult Aboriginal people who lived and died in the Northern Territory in 1992, excluding residents of the Alice Springs region. The appropriateness of underlying cause of death codes was assessed by a single reviewer in light of death certificates, medical records, postmortem records and interviews with key health professional informants. Data were collected on 220 deaths. 8% (17 out of 220) of deaths were classified erroneously at the ICD-9 chapter level. Errors in death certification accounted for 64% (11 out of 17) of the chapter errors and diagnostic and coding errors for 18% (3 out of 17) each. The overall impact on mortality statistics was less severe because some cross-chapter classification errors cancelled each other out. Misclassification errors aggregated mainly in chapter VII (circulatory diseases) of the ICD-9 classification which was overcounted by 3.2%, and chapter VIII (respiratory diseases) which was overcounted by 1.3%. Before correction for misclassification error, circulatory diseases were judged to cause the highest proportion of deaths, whereas after correction, respiratory diseases accounted for the highest proportion. Despite this, the overall quality of the medical cause of death statistics was of a sufficiently good standard from a public health perspective to broadly inform health policy. Future attempts to improve the validity of medical cause of death statistics for Australian Aboriginal people should focus on the education of medical practitioners about the purpose and process of death certification.

Adult↗
PubMed1998

[Quality of death certificates in cases of cancer death in France].

International mortality statistics are based on death certificates on which the causes of death are coded using the World Health Organization's International Classification of Diseases. Most of these statistics are based on the underlying cause of death and do not use the contributory causes of death. We studied the validity of death certificates in a sample of 1,194 French patients known to have died of cancer, comparing the cause of death reported on the death certificate with the cause of death found in the medical record. Death certificates correctly identify cancer as the cause of death in 95% of the cases and with the exact site in 86% of the cases.

Cause of Death↗
PubMed2000

Suicide in older people: mode of death, demographic factors, and medical contact before death.

OBJECTIVE: To determine the demographic characteristics, mode of death, and nature and timing of medical contacts in the year before death in a sample of suicides in older people. DESIGN: Descriptive study of a case series of 195 suicides in older people. SETTING: Four counties and one large urban area in central England, UK. SUBJECTS: Individuals 60 years old and over at time of death, who had died between 1 January 1995 and 1 May 1998, and whose deaths has received a coroner's verdict of suicide, or an open or accidental verdict where the circumstances of death indicated probable suicide. MAIN OUTCOME MEASUREMENTS: Demographic details and information on mode of death and medical contact prior to death derived from coroners' inquest notes, General Practitioners' (GP) case-notes and psychiatric records. MAIN RESULTS: 67.7% were male. A higher proportion of men than women were single or divorced. The commonest methods of suicide were hanging in men and drug overdose in women, 49.8% had seen their GP in the month before death, although over half these last consultations were for physical complaints. Only 15.4% were under psychiatric care at the time of death. CONCLUSIONS: Older men are at higher risk of suicide than women. Given the high proportion of drug overdoses in the sample, effective strategies to prevent suicide in older people might include improving the prescribing of analgesics and antidepressants. Although older people at risk of suicide often consult their GP shortly before death, GPs may have difficulty identifying those at risk because of the high proportion of physical complaints.

Age Distribution↗
PubMed1987

When people die. Cause of death versus time of death.

A sample of 4,920 disease-related deaths from New York City for 1979 (8.7 percent of all relevant data from New York City's files) showed a 60 percent rise in death rate beginning at 2 A.M. and reaching a peak at 8 A.M. A smaller peak was also noted at 6 P.M. The rise in human mortality beginning at 2 A.M. and peaking at 8 A.M. might be explained by: artifact of deaths occurring anytime during the night that are discovered after daybreak, effect of less efficient health care between 2 A.M. and 8 A.M., and disease processes that somehow increase risk of death between 2 A.M. and 8 A.M. An attempt was made to differentiate among these possibilities by comparing time of death for various subsamples. The bimodal pattern appeared only in the temporal distribution of deaths of persons over 65 years of age; deaths of persons under 65 did not show significant temporal concentration. There were also prominent differences in the distribution of deaths for different reported causes of death. Ischemic heart disease, which numerically accounted for over 50 percent of the sample, showed peak mortality at 8 A.M. for both males and females. Hypertensive disease showed a significant peak in mortality at 1 A.M. for females only. Cerebrovascular disease peaked significantly at 6 A.M. with a significant peak only for males. The age and disease specificity of the 2 A.M. to 8 A.M. rise in death is consistent with a disease-related explanation for the bimodal circadian pattern in mortality. The quality and efficiency of health care could be improved with more precise information on peak periods of risk for specific morbid conditions.

Aged↗
PubMed1985

In what sense is rheumatoid arthritis the principal cause of death? A study of the National Statistics Office's way of reasoning based on 1224 death certificates.

Physicians' inadequacies in making out death certificates involving rheumatoid arthritis (RA) and the coders' reasons for not registering physicians' stated underlying cause as the underlying cause of death were investigated. The starting point of the study was a disagreement between physicians' reporting of RA on death certificates and the Swedish National Central Bureau of Statistics' (NCBS) registration of this condition, to the effect that the NCBS registered a 3.0-fold increase in mortality for women and a 2.7-fold increase for men attributed to RA between 1971 and 1975, whereas the physicians had reported practically no change at all for women and a slight decrease for men between the years. All Swedish RA death certificates for the years 1971 and 1975 were studied. A total of 1224 such certificates were identified. Four major qualifications for the coders to reject physicians' non-RA underlying cause, and for giving preference to RA in the registration of the underlying cause of death were discerned: RA appeared to have been favoured to the greatest extent by the NCBS (i) when RA was likely to have caused the reported underlying condition; (ii) when there is only one, non-RA, diagnosis reported in Part I of the certificate, and this diagnosis does not completely describe the train of events leading to death; (iii) when the diagnosis for the non-RA underlying condition provides less precise information about the site or nature of the underlying condition, compared with another diagnosis for another condition, RA, stated on the certificate; or (iv) when the reported non-RA underlying condition was unlikely itself to cause death, and was not reported as a cause of a more serious condition. The NCBS' increased registration of RA as the underlying cause of death between 1971 and 1975 could be explained neither by physicians' inadequacies in making out death certificates nor by a strict application of the international coding rules for registration of the underlying cause of death.

Arthritis, Rheumatoid↗
PubMed1998

Predictors of suicide, accidental death, and premature natural death in a general-population birth cohort.

BACKGROUND: Whether putative suicide risk factors, such as conduct and emotional disorders, are specific to suicide or are general associations of a continuum between subintentional and intentional self-destruction is not clear. We undertook an investigation of this issue in a UK population-based birth cohort. METHODS: Using competing-risks analysis, we examined links between prospectively collected childhood and adolescent temperamental and behavioural variables and the risk of natural, accidental, and suicidal death, occurring between the ages of 16 and 50 years. Of the 5362 members of the cohort, full data were available for 3591. A panel of psychiatrists scored deaths on likely suicidal intention. These scores were used in a weighted logistic regression to examine independence of risk factors for (sub)intentional self-destruction. FINDINGS: There were 167 deaths among the risk-set between the 16th and 50th birthdays. 120 were due to natural causes; of the other 47, the panel of psychiatrists judged that 36 were accidental deaths and 11 were suicides (certainty rating > or = 51%). Adolescent emotional instability and conduct problems had different associations with the various causes of premature death, being lowest for natural death (odds ratio 1.0 [95% CI 0.8-1.2] and 1.2 [1.0-1.5]), intermediate for accidental death (1.1 [0.8-1.5] and 1.3 [1.0-1.7]), and highest for suicidal death (2.0 [1.2-3.6] and 1.8 [1.3-2.5]). Emotional instability (boys 1.3 [1.0-1.7], girls 1.4 [1.0-1.9]) increased risk for subintentional or intentional self-destruction, as did low anxiety in adolescence (1.7 [1.3-2.5]) and nocturnal enuresis at age 4 (1.4 [1.2-1.7]) in boys, and conduct problems in girls (1.4 [1.0-2.0]). INTERPRETATION: Suicide shares important risk factors with other causes of premature death. These findings suggest an aetiological continuum of self-destruction from subintentional to intentional. Research on premature mortality associated with psychological disorder should include all causes of death.

Accidents↗