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The author, a philosopher, suggests that the concept of death should be left as it is 'in its present indeterminate state', and that we ought to reject attempts to define death in terms of whole-brain death or any other type of brain death, including cerebral death and 'irreversible coma'. Instead of 'fiddling with the definition of death' clear rules should be established specifying 'what can be appropriately done to whom when'.
OBJECTIVE: To describe causes of death and other characteristics of "avoidable" deaths in patients admitted to hospital after trauma, and estimate and analyse changes in the avoidable death rate during the years studied. DESIGN: Retrospective analysis of medico legal autopsy material. SETTING: One northern and one western area in Sweden 1988-1996. SUBJECTS: 335 cases who died in hospital after trauma. MAIN OUTCOME MEASURES: Avoidable death, defined as an Injury Severity Score (ISS) of 35 or less and Abbreviated Injury Scale (AIS) head of 4 or less and cause of death. RESULTS: We found 70 avoidable deaths (21%). Among these, 15 (21%) died of head injuries, 17 (24%) of thoracic, abdominal, or pelvic injuries, and 38 (54%) of medical complications. The number of deaths after trauma decreased considerably from 1988-90 to 1994-96, but the proportion who died in hospital remained almost constant. The proportion of avoidable deaths decreased from 22% to 17%, mainly because the proportion of deaths from medical complications was halved. CONCLUSION: The standard of Swedish in-hospital trauma care has improved, particularly with a reduction in post-traumatic complications. However, there is still room for improvement in the treatment of complications among elderly people.
Sudden death is defined as a death that occurs suddenly, develops during an unpredictable course, and is due to natural or unnatural causes. Although there is no universally standardized definition on how "sudden" a sudden death is, WHO defines sudden death as a death that occurs within 24 hours after the onset of symptoms. The aim of this study is to present 2 rarely reported autopsy cases and to emphasize the importance of systemic autopsy at sudden death. On macroscopic examination, crescent-shaped, thick, fibrous membranes, located 5 mm and 3 mm away from the aortic valves, were detected. Fibrous membranes extended from the ventricular septum to the left ventricular outflow tract, thus apparently narrowing this region. Left ventricular wall and septum were slightly thickened, and there were scattered grayish-white areas of a small diameter. These became more intense in the septum and myocardium of the left ventricle on the anterior plane of the myocardial sections. In both cases, the aortic valves of were thickened and also markedly narrowed on one of them. In this case, the fibrous membrane adhered to the aortic valve and extended to the anterior leaflet of the mitral valve at one side. Both aortic valves comprised 3 leaflets. Other valves and coronary arteries showed no macroscopic pathologic findings. Microscopic examination of both cases demonstrated that the fibrous membrane comprising abundant collagen fibers was situated on the ventricular septum. Hypertrophy, moderate to severe interstitial fibrosis, and focal areas of scarring were observed in the specimens taken from the septal and ventricular myocardium. No abnormality was found on the conduction system examinations. Toxicologic analysis results in blood were negative. Based on the findings, membranous-type (discrete type) subvalvular aortic stenosis, diagnosed during the autopsy, was considered as the cause of sudden death in both cases.
OBJECTIVE: This retrospective study was undertaken to evaluate the accuracy of risk-adjusted EuroSCORE models in predicting mortality in individual patients who are undergoing coronary artery bypass grafting. MATERIAL AND METHODS: The study population is a consecutive series of 1698 isolated primary and repeat coronary artery bypass grafting patients, inclusive patients in cardiogenic shock or resuscitation, operated in Kaunas Heart Center from January 1997 to December 2001. The pre-operative risk of death was calculated with EuroSCORE models and then compared with the actual outcome. The accuracy score was used to evaluate the reliability of each score to predict the individual outcome. The studied event was in-hospital death, defined as mortality during hospital stay, which was unlimited in time and included a stay in a secondary hospital without discharge home. RESULTS: Eighty deaths (4.7%) were observed. The age of this patients was 66.0+/-9.5 years, 73.7% were male and 3.7% were repeat procedures. In most patients who died the mean predictive scores were high. The EuroSCORE average was 11.0+/-4.3, with a range from 3 to 21. CONCLUSIONS: The EuroSCORE presurgical predictive models were highly accurate to predict overall mortality, but were inaccurate to predict mortality in individual patients.
Over one-half of death certificates from elderly people contain ill-defined causes of death. Usually, signs and symptoms rather than causes of death are registered. Electrolyte imbalance, decubitus ulcer, atherosclerosis, diabetes, etc are some of the most frequently quoted conditions. Adequate preventive programs are jeopardized by lack of more precise information regarding the cause of death and relevant associated conditions in the elderly.
OBJECTIVES: Intra- and interdepartmental benchmarking require scoring systems with excellent performance on several properties: discrimination (resolution), reliability (calibration) and stability over the complete spectrum of peri-procedural risk. This single centre, single domain study validates the European system for cardiac operative risk evaluation (EuroSCORE) on an independent sample of primary and repeat coronary artery bypass grafting (CABG) patients and will evaluate these different properties. METHODS: The study population is a consecutive series of 2051 isolated primary and repeat CABG patients, inclusive of patients in cardiogenic shock or resuscitation, operated on in a single institution from January 1997 to July 2000. The age of the patients was 66+/-9 years, 77% were males and 7% were repeat procedures. The EuroSCORE was 5.0+/-3%, with a range from 0 to 22. The studied event was in-hospital death, defined as mortality during hospital stay, which was unlimited in time and included a stay in a secondary hospital without discharge home. RESULTS: The EuroSCORE predicted 102 deaths versus 81 deaths observed (P=0.14, Fisher exact test). The EuroSCORE described only 20% of the variance of in-hospital mortality. The EuroSCORE created an area under the receiver operating characteristic curve of 0.83+/-0.03. The highest discriminative accuracy was obtained with 8% EuroSCORE risk (only 64% sensitivity and 87% specificity). Further exploration identified an over score in the EuroSCORE range 0-8 (57%, P<0.0001). There was an equal score (-2%, P=1) in the range 9-11, but an under score in the range 12-22 (-133%, P=0.003). CONCLUSIONS: On the condition that these single centre results could be extended to any European cardiac surgery centre, it can be concluded that the overall acceptable performance of the EuroSCORE is the result of an over score in the lower risk and insufficient correction in the higher risk spectrum. The EuroSCORE is probably refined enough for improved informed consent versus aggregated results but should only be used for inter-institutional benchmarking with great caution, preferably below the 12% risk pivot.
The concept of death has evolved medically, legally and culturally since the introduction of life support technologies in the middle of the 20th century. The traditional cardiopulmonary and the new neurologically based brain death criterions of death are examined. We conclude that brain death, defined as total and irreversible loss of function of the whole brain, fulfills better "the permanent cessation of functioning of the organism as a whole" definition of death. Brain death diagnosis, based on standard neurologic clinical examination performed accurately, is unequivocal. Transplantation medicine, mostly based on organ donation of brain dead people, has become a routine and universally accepted therapeutic intervention nowadays, which benefits many people. Ethics foundations of organ transplantation are reviewed. Even though brain death and organ donation are widely accepted in medical, legal, religious and public opinion today, the whole society and medical community need to be further educated about these matters, so that unavoidable changes of traditional concepts might be better understood. Permanent education should be the best way to dissipate social fears and distrust towards organ donation and brain death.
CD40 is known as an important T-B cell interaction molecule which rescues B lymphocytes from undergoing apoptosis. Like other receptors of the tumor necrosis factor (TNF) receptor gene family, CD40 is expressed on cells of different tissue origins including some transformed cells. In contrast to its well-studied effects on B cells, the biological functions of CD40 in non-immune cells remain largely unknown. Here we show that CD40 ligation induces apoptotic cell death in transformed cells of mesenchymal and epithelial origin. This CD40-mediated cell death seems to use a preformed signaling pathway since it occurs even when protein synthesis is blocked. Notably, the CD40 cytoplasmic domain shares a structural homology with the recently defined "death domains" of the 55-kD TNF receptor (p55TNFR) and Fas. Despite these structural similarities, differences are seen in the way phorbol myristate acetate, interleukin 1, TNF, and various metabolic inhibitors influence the cellular responsiveness to CD40, p55TNFR, and Fas-mediated killing. Our study indicates that CD40 induces cell death by a distinct mechanism.
Until 1968, when an ad hoc Harvard Medical School Committee published a landmark paper calling for determination of death using neurological rather than cardiovascular criteria, death was considered to have occurred when the heart irreversibly ceased beating. Since that time, every jurisdiction in the country has come to accept through law or court decision neurological criteria to define death. The authors review the issue of death by neurological criteria in light of current guidelines and recent advances.
If in the case of brain death breathing and circulation are continued artificially we deceive ourselves emotionally not to except death of the so treated organism. But on scientific medical grounds brain death defines the end of the organism as a whole beyond doubt. No rational reasons can be seen, why organs should not be taken from the brain dead provided that diagnosis of brain death and the organ retrieval are done by independent teams of doctors and an opposing will of the dead person is not known. Honour should be payed to the remains of the dead organ donor. Donation of living donors should be seen more critically because of the ethical problems involved for the managing doctors.
Consistent with the constitutive activation of Rel/NF-kappaB in human hematopoietic tumors, the v-Rel oncoprotein induces aggressive leukemia/lymphomas in animal models. v-Rel is thus a valuable tool to characterize the role of Rel/NF-kappaB in cancer and the mechanisms involved. Prior studies by our group identified a serine-rich domain in v-Rel that was required for biological activity. Here, we investigated the molecular basis for the transformation defect of specific serine mutants. We show that the transforming efficiency of these mutants in primary lymphoid cells is correlated with their ability to mediate kappaB site-dependent transactivation and with specific changes in phosphorylation profiles. Interestingly, coexpression of the death antagonists Bcl-xL and Bcl-2 significantly increased their oncogenicity, whereas other NF-kappaB-regulated death inhibitors showed little or no effect. The fact that a subset of apoptosis inhibitors could rescue v-Rel transactivation mutants suggests that their reduced transcriptional activity may critically affect expression of defined death antagonists essential for oncogenesis. Consistent with this hypothesis, we observed selection for high endogenous expression of Bcl-2-related death antagonists in cells transformed by weakly transforming v-Rel mutants. These results emphasize the need for Rel/NF-kappaB to efficiently activate expression of a subset of antiapoptotic genes from the Bcl-2 family to manifest its oncogenic phenotype.
Many reports have described the amounts of atherosclerotic plaque in victims of sudden coronary death, defining the number of coronary arteries narrowed at some point greater than 75% in cross-sectional area (XSA). In order to quantitate more precisely the amount and distribution of plaque, 70 victims of sudden coronary death aged 22-81 years (mean 50) were studied. The four major epicardial coronary arteries (left main, left anterior descending, left circumflex, and right) from each of 70 victims were cut into 5-mm segments (average 50 per patient) and a histologic section prepared from each segment. The amount of luminal narrowing by plaque was categorized into five groups (0-25%, 26-50%, 51-75%, 76-95%, 96-100%). Of 3,484 five-mm segments, 950 (27%) were narrowed 76-100% in XSA. Comparison of 31 previously symptomatic victims (angina pectoris and/or myocardial infarction) to 39 victims who had been asymptomatic disclosed a higher mean percent of severely narrowed segments (30% vs. 25%, p = less than 0.005) and a lower mean percent of minimally narrowed segments in the symptomatic group. Comparison of the 31 patients with a healed myocardial infarction at necropsy with 39 patients with no left ventricular scar disclosed a higher mean percent of segments severely narrowed (33% vs. 24%, p = less than 0.001) and a lower mean percent of segments narrowed minimally in those with a left ventricular scar (13% vs. 26%, p = less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
The endotoxic shock syndrome is characterized by systemic inflammation, multiple organ damage, circulatory collapse and death. Systemic release of tumor necrosis factor (TNF)-alpha and other cytokines purportedly mediates this process. However, the primary tissue target remains unidentified. The present studies provide evidence that endotoxic shock results from disseminated endothelial apoptosis. Injection of lipopolysaccharide (LPS), and its putative effector TNF-alpha, into C57BL/6 mice induced apoptosis in endothelium of intestine, lung, fat and thymus after 6 h, preceding nonendothelial tissue damage. LPS or TNF-alpha injection was followed within 1 h by tissue generation of the pro-apoptotic lipid ceramide. TNF-binding protein, which protects against LPS-induced death, blocked LPS-induced ceramide generation and endothelial apoptosis, suggesting systemic TNF is required for both responses. Acid sphingomyelinase knockout mice displayed a normal increase in serum TNF-alpha in response to LPS, yet were protected against endothelial apoptosis and animal death, defining a role for ceramide in mediating the endotoxic response. Furthermore, intravenous injection of basic fibroblast growth factor, which acts as an intravascular survival factor for endothelial cells, blocked LPS-induced ceramide elevation, endothelial apoptosis and animal death, but did not affect LPS-induced elevation of serum TNF-alpha. These investigations demonstrate that LPS induces a disseminated form of endothelial apoptosis, mediated sequentially by TNF and ceramide generation, and suggest that this cascade is mandatory for evolution of the endotoxic syndrome.
We retrospectively review our results of 96 stent placements in 64 patients identified from our data base who received stents acutely and within 48 hr of acute myocardial infarction. The average age was 60 years; 77% were male. The average length of stay was 6.75 days. Three patients needed coronary artery bypass grafting (CABG) before discharge: 2 for stent occlusion and 1 for papillary muscle rupture. Need for CABG, further percutaneous transluminal coronary angioplasty (PTCA), myocardial infarction, and death defined outcome. Mean patient follow-up was 10.3 (+/-5.3) months. Seventy-two percent of patients were free of outcome events at 1 year, 17% needed CABG, and 11% required further PTCA. There were 2 myocardial infarctions and 1 death. Presence of left bundle branch block on admission electrocardiogram and angina in hospital after stent placement predicted worse outcome (P < 0.01).
OBJECTIVE: To test the hypothesis that stress generated by the Newcastle earthquake led to increased risk of heart attack and coronary death. DESIGN: A natural experiment. SUBJECTS: People living in the Newcastle and Lake Macquarie local government areas of New South Wales, Australia. INTERVENTION: At 10.27 a.m. on 28 December 1989 Newcastle was struck by an earthquake measuring 5.6 on the Richter scale. OUTCOME MEASURES: Myocardial infarction and coronary death defined by the criteria of the WHO MONICA Project and hospital admissions for coronary disease before and after the earthquake and in corresponding periods in previous years. Well established, concurrent data collection systems were used. RESULTS: There were six fatal myocardial infarctions and coronary deaths among people aged under 70 years after the earthquake in the period 28-31 December 1989. Compared with the average number of deaths at this time of year this was unusually high (P = 0.016). Relative risks for this four-day period were: fatal myocardial infarction and coronary death, 1.67 (95% confidence interval [Cl]: 0.72, 3.17); non-fatal definite myocardial infarction, 1.05 (95% Cl: 0.05, 2.22); non-fatal possible myocardial infarction, 1.34 (95% Cl: 0.67, 1.91); hospital admissions for myocardial infarction or other ischaemic heart disease, 1.27 (95% Cl: 0.83, 1.66). There was no evidence of increased risk during the following four months. CONCLUSION: The magnitude of increased risk of death was slightly less than that previously reported after earthquakes in Greece. The data provide weak evidence that acute emotional and physical stress may trigger myocardial infarction and coronary death.
The paper reports on the study of 1457 patients with acute myocardial infarct (Ami) admitted in the word of the cardiac intensive care of the clinic for 10.5 years. The general mortality was of 21.2% and the sudden death (defined as such when appeared suddenly within less than 1 hour from the onset of the acute symptoms, but after 24 hours from the onset of AMI in a patient apparently equilibrated) appeared in 114 patients who were examined postmortem (43.3% of the total of the deaths). The main causes of the SD was rupture of the myocardium (28.8% of the general mortality), primary ventricular fibrillation (22.0%) and thromboembolic phenomena (17.8%). The sudden death by rupture of the myocardium appeared in a first AMI, usually large and was not helped by the anticoagulant treatment or by other therapy. Primary ventricular fibrillation appeared during the first week from the onset and was favoured by the ventricular hyperexcitability and active myocardial ischemia (which were not specific). Xyline (only more than 2 mg/min) and amiodarone gave a good protection. The sudden death by systemic thromboembolization appeared almost only in the antero-lateral myocardial infarcts, 5-8 days after the onset. The appearance of a small flow syndrome "sine materia" with or without association of some recurrent arrhythmias was suggested. Efficient anticoagulation prevented systemic thromboembolization and, to a smaller extent to pulmonary thromboembolization.
OBJECTIVE: (1) To compare mortality estimates based on clinicopathological diagnoses of death from acute coronary heart disease with official estimates of coronary heart disease mortality; (2) to compare present day mortality figures with those from earlier reports. DESIGN: Prospective community study over the two years 1994 and 1995. SETTING: The health districts of Brighton, South Glamorgan, and York. SUBJECTS: 1589 men and women under 75 years of age who, based on our study criteria, died from acute coronary events were compared with certified cases of coronary death in the same age group. MAIN OUTCOME MEASURES: (1) Comparison of the underlying cause recorded on death certificates with the diagnosis of acute coronary death defined by our study criteria; (2) comparison of age specific mortality figures of the present with earlier studies. RESULTS: Up to age 65, age specific mortality for coronary heart disease, using study criteria, was similar to official estimates. However, at ages 65-74 years there was a shortfall in study deaths of about 20% compared with official figures. One reason for this was that many death certificates in elderly people attributed death to coronary disease in the absence of confirmatory evidence. Despite this, deaths in the under 65 age group in the 1990s appear to be occurring in people who are about 10 years older than was the case during the 1970s. CONCLUSIONS: There are differences, most noticeable in elderly subjects, between estimates of coronary mortality made according to strict clinical and pathological definitions and official rates based on death certification. Recognition of these differences will be important for future epidemiological studies.
Accurate criteria for death are increasingly important as it becomes more difficult for the public to distinguish between patients who are still alive from those who, through the aid of medical technology, merely look like they are alive even though they are dead. Patients and their families need to know that a clear line can be drawn between life and death, and that patients who are alive will not be unintentionally treated as though they are dead. For the public to trust the pronouncements of medical doctors as to whether a patient is dead or alive, the criteria must be unambiguous, understandable, and infallible. It is equally important to physicians that accurate, infallible criteria define death. Physicians need to know that a clear line can be drawn between life and death so that patients who are dead are not treated as though they are alive. Such criteria enable us to terminate expensive medical care to corpses. Clear criteria for death also allow us to ethically request the gift of vital organs. Clear, infallible criteria allow us to assure families and society that one living person will not be intentionally or unintentionally killed for the sake of another. The pressure of organ scarcity must not lead physicians to allow the criteria for life and death to become blurred because of the irreparable harm this would cause to the patient-physician relationship and the devastating impact it could have on organ transplantation. As the cases presented here illustrate, anesthesiologists have an important responsibility in the process of assuring that some living patients are not sacrificed to benefit others. Criteria for declaring death should be familiar to every anesthesiologist participating in organ retrieval. Before accepting the responsibility of maintaining a donor for vital organ collection, the anesthesiologist should review data supplied in the chart supporting the diagnosis of brain death and seriously question inconsistencies and inadequate testing conditions. Knowledge of brain death criteria and proper application of these criteria could have changed the course of each of the cases presented.