[Cause of death determined at autopsy in the University Hospital of Liège. Developments from 1878 to 1986].
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Aged↗
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Results for “Causes Of Death--determinants”
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[Cause of death determination and identity of an unknown man].
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Aged↗
Influence of cause-of-death assignment on time-to-tumor analyses in animal carcinogenesis studies.
The importance of cause-of-death determination in an animal carcinogenesis study with respect to estimation of time-to-tumor distributions of internally occurring (occult) tumors is discussed. A nontechnical description of time-to-tumor estimation is presented. The information obtained from time-to-tumor estimation when cause-of-death designation was used is illustrated for liver tumors in female mice of the inbred strain BALB/cStCrlfC3Hf/Nctr from the ED01 study with N-2-fluorenylacetamide done at the National Center for Toxicological Research. A time-to-tumor analysis of reticulum cell sarcoma data from the same study has provided insight into some difficulties involved in routine case-by-case determination of cause of death. A more flexible system for assigning of cause of death to dead animals and cause of morbidity to moribund animals is described as a way to improve cause-of-death assignment.
2-Acetylaminofluorene↗
United States mortality from ill-defined causes, 1968-1988: potential effects on heart disease mortality trends.
BACKGROUND: Deaths are coded to the International Classification of Diseases (ICD) category, 'Symptoms, Signs, and ill-defined Conditions' when there is insufficient information for cause of death determination. Due to difficulties of diagnosis of coronary heart disease (CHD) death and since CHD is the leading cause of death among US adults, CHD is the most likely cause of ill-defined deaths. METHODS: Vital statistics and census data were used to create annual age-adjusted ill-defined rates, unrevised CHD rates, and CHD rates revised to include ill-defined deaths for US African Americans and whites, ages 35-74 years, during 1968-1988. Ill-defined and CHD mortality trend analyses were conducted. RESULTS: In 1968, African American/white ratios of ill-defined mortality were 5 among men and 7 among women; following steep declines in ill-defined mortality among African Americans, ratios were 3 among men and 2 among women in 1988. In 1968, approximately 3% and 1% of all deaths among African Americans and whites, respectively, were certified to ill-defined causes; in 1988, approximately 1.5% of deaths among African Americans were coded ill-defined, with no change among whites. Revised CHD rates showed substantially higher excess CHD mortality among African Americans than whites compared to unrevised CHD rates. Declines in revised CHD mortality steepened throughout the study period among men, and among women began to decelerate after 1978. CONCLUSIONS: Ill-defined mortality was of sufficient magnitude to potentially contribute to substantial underestimation of racial disparities in CHD mortality. Also, temporal changes in ill-defined mortality may have affected CHD trends which are used to evaluate the efficacy of public health interventions.
Adult↗
Risk of gastric cancer in pneumoconiotic coal miners and the effect of respiratory impairment.
OBJECTIVES: This study was carried out to investigate the mortality patterns in a group of 3790 coal miners. The study population had abnormal chest x ray films at a routine medical examination that was performed in the 1950s. METHODS: The total group of 3790 coal miners were followed up for mortality up to 1 January 1992. Causes of death, determined and coded at time of death, were traced with help from the Central Bureau of Statistics. RESULTS: Total mortality in this group of coal miners with abnormal chest x ray films was significantly higher than expected (SMR 127.1, 95% CI 122.5-131.6), mainly a reflection of the increase in mortality from non-malignant respiratory disease (SMR 411.0, 95% CI 382.3-441.3). Mortality from gastric cancer was also significantly increased (SMR 147.5, 95% CI 122.3-176.3). This risk of mortality from gastric cancer was confined to workers with no pneumoconiosis or only a mild form. Despite the strong relation to duration of employment and pneumoconiosis the group of workers with more severe manifestations of pneumoconiosis did not experience an excess in mortality from gastric cancer. CONCLUSION: This study confirms the earlier reported risk of gastric cancer in coal miners. Also it confirms the hypothesis that this risk of gastric cancer is limited to workers with a mild degree of pneumoconiosis or none. In workers with severe forms of pneumoconiosis the pulmonary clearance system is impaired in such a way that the inhaled coal dust does not reach the digestive tract.
Adult↗
Mechanisms and timing of deaths from cerebral infarction.
Clinicopathologic correlations were reviewed in 100 cases of recent cerebral infarctions in the internal carotid artery distribution. The most frequent cause of death was transtentorial herniation, followed in frequency by pneumonia, cardiac causes, and pulmonary embolism. Thirty-six percent of all patients and 47% of those with transtentorial herniation died within 48 hours of cerebral infarction. Of the treatable extracerebral causes of death determined at autopsy, only 34% were recorded premortem in the clinician's death summary.
Brain Edema↗
Statistical support of the proposed National Toxicology Program protocol.
Statistical issues related to the design, analysis and interpretation of carcinogenicity studies are considered. A proposed modification of the "standard" National Cancer Institute (NCI) design of carcinogenicity studies in rodents is discussed. The primary objective was to obtain a design that maintained the power of the NCI design for detecting carcinogenic effects, while increasing the precision with which the underlying dose-response model could be estimated. "Optimum" three-dose designs are presented and discussed. Data analysis issues are also considered. Comparisons of tumor incidence should include adjustments for survival differences, and, if possible, cause of death determinations should be made for each individual animal. In some instances historical control data can aid an investigator in the overall evaluation of experimental results. Several important problems are discussed that must be overcome before historical control data can be used in a meaningful way. One critical issue in the interpretation of tumor incidence data is the issue of false positives. Data from 25 recent long term feeding studies are used to derive a statistical decision rule that closely approximates the scientific judgment process used in these studies. The overall false positive rate associated with this decision rule was found to be no more than 7-8%.
Animals↗
Reported causes of death of captive killer whales (Orcinus orca).
Inquiries were made to all oceanaria that maintain killer whales in North America. Causes of death determined at necropsy included mediastinal abscesses, pyometra, pneumonia, influenza, salmonellosis, nephritis, Chediak-Higashi syndrome, fungus infection, ruptured aorta, cerebral hemorrhage and a perforated post-pyloric ulcer. Captive females appear to have a higher rate of mortality than males. Growth rates for whales that died were greater than for those that survived.
Abscess↗
[The cardiomyopathy of idiopathic hemochromatosis].
A retrospective study of the case histories of 216 patients with idiopathic haemochromatosis has highlighted the frequency of cardiac involvement in this condition (53%). Two forms can be distinguished: a latent one (65%), in which the changes are predominantly electrocardiographic, and a clinical form (35%) with the features of congestive cardiomyopathy, notable for the rapidity of onset after right heart failure, the degree of cardiomegaly, the constant finding of abnormalities of ventricular repolarisation, the relative frequency of latent disorders of supra-His atrio-ventricular conduction, and the finding of elongation of the isovolumic contraction time on the phonomechanocardiogram. A haemodynamic profile is the same as for non-obstructive hypotonic cardiomyopathies, and is usually associated with a slow rise in left ventricular pressure. The cardiomyopathy, which is the most frequent cause of death, determines the prognosis in this condition. It may be found in association with diabetes and gonad failure. The finding of cardiomyopathy indicates basic treatment by veresection, which may be the only means of establishing a favourable outcome.
Adult↗
Comparative study on the underlying cause and mode of death established prior to and after medicolegal autopsy.
A comparative study was made on the underlying cause and mode of death determined in 600 consecutive cases by forensic physicians before and after medicolegal autopsy. All available information including police records, medical documents of decedents and the results of the external medicolegal examination of the corpse were utilized to determine the cause and mode of death before autopsy. The mode of death would have been defined erroneously in 10% of cases and the underlying cause of death in 29.5% of cases if medicolegal autopsy had not been performed. The present results are consistent with previous studies which indicate that the determination of the underlying cause of death is significantly more accurate when an autopsy is performed. They also suggest that in a large number of routine medicolegal cases a similar trend, but at a lower rate, is associated with the determination of the mode of death.
Accidents↗
Histopathologic correlates of inducible ventricular tachycardia in two experimental canine models of myocardial infarction.
Ventricular tachyarrhythmias are the leading cause of sudden cardiac death. Determination of the substrates conducive to the initiation of ventricular tachyarrhythmias remains an important clinical goal. The purpose of this study was to correlate electrophysiologic and histopathologic parameters conducive to the initiation of sustained ventricular tachycardia using programmed electrical stimulation in two canine models of myocardial infarction. Histopathologic correlates included: infarct pattern (heterogeneous vs. homogeneous morphology), distribution (viable epicardial or endocardial rim), and size. Twenty-one adult dogs were randomly divided into two groups: (1) 12 dogs underwent two-stage, 2-hour occlusion of the proximal left anterior descending coronary artery (LAD); and (2) nine animals had permanent, complete occlusion of the LAD with latex embolization. Using programmed ventricular pacing with two premature ventricular extrastimuli, initiation of ventricular tachycardia was attempted at both 1 and 2 weeks after infarction with the chest closed and opened each time. Electrophysiologic evaluation of the infarct type correlated significantly with the histologic morphology of the infarction (p less than 0.001), the presence of a viable epicardial rim was an extremely important discriminating variable for ability to induce sustained ventricular tachycardia (p = 0.04). The presence of an endocardial rim was not significant (p = 1.0). Infarct size alone was only marginally related to ventricular tachycardia inducibility (p = 0.08). Non-uniform infarcts were more conducive to the initiation of sustained ventricular tachycardia than homogeneous infarcts (p = 0.025). The presence of a large, non-uniform infarct was the best overall discrimination variable for inducibility (p = 0.0002). Thus, in these experimental models, specific infarct morphologies correlate significantly with susceptibility to inducible sustained ventricular tachyarrhythmias.
Animals↗
Histopathologic factors conducive to experimental ventricular tachycardia.
Ventricular tachyarrhythmia is the leading cause of sudden cardiac death. Determination of the substrates conducive to the initiation of this arrhythmia remains an important clinical goal. The purpose of this study was to correlate histopathologic findings, specifically: pattern (heterogeneous versus homogeneous infarct morphology), distribution (viable epicardial and/or endocardial rim), and infarct size, with susceptibility to the initiation of sustained ventricular tachycardia employing programmed electrical stimulation in two canine models of experimental myocardial infarction. Twenty-one adult dogs were randomly divided into two groups: 12 dogs underwent two-stage, 2-hour occlusion of the proximal left anterior descending coronary artery and nine animals underwent permanent, complete occlusion of the left anterior descending coronary artery with latex embolization. With programmed ventricular pacing with two premature ventricular extrastimuli, initiation of ventricular tachycardia was attempted, open chest, two weeks after infarction. Electrophysiologic evaluation of the infarct type correlated significantly with the histologic morphology of the infarction (p less than 0.001). The presence of a viable epicardial rim was an extremely important variable for ability to induce sustained ventricular tachycardia (p = 0.04). The presence of an endocardial rim was not significant (p = 1.0). Infarct size alone was only marginally related to ventricular tachycardia inducibility (p = 0.08). Nonuniform infarcts were more conducive to the initiation of sustained ventricular tachycardia than were homogeneous infarcts (p = 0.025). The presence of a large, nonuniform infarct correlated best with inducibility (p = 0.0002). Thus in these experimental models, specific infarct morphologies correlate significantly with susceptibility to inducible sustained ventricular tachyarrhythmias.
Animals↗
Nitric oxide in retina: relation to excitatory amino acids and excitotoxicity.
This study was undertaken to determine whether nitric oxide pathways exist in the retina and are linked to excitatory amino acid (EAA)-induced increases in cyclic guanosine monophosphate (cGMP). Exposure of embryonic day 15 chick retina for 5 min to either 1 mM glutamate, 100 microM NMDA or 100 microM kainate (KA) increased cGMP content 2-3-fold. The putative environmental neurotoxins, domoic acid (DO, 20 microM), and beta-oxalyl-amino-L-alanine (BOAA, 200 microM), but not beta-methyl-amino-L-alanine (BMAA, 3 mM), also increased cGMP. The nitric oxide synthase inhibitor N-nitro-L-arginine (NNA) and nitric oxide scavenger, hemoglobin, completely blocked the increases in cGMP induced by the above glutamate-agonists. These glutamate agonist induced increases in cGMP were receptor mediated. MK-801, a NMDA receptor antagonist, blocked NMDA, and partially blocked glutamate-stimulated, cGMP formation. CNQX, a KA/AMPA receptor antagonist blocked cGMP increases produced by KA, BOAA and partially blocked those evoked by DO and glutamate. In order to examine the involvement of nitric oxide pathways in NMDA-mediated toxicity, the ability of NNA to protect against delayed excitotoxic damage caused by a 60 min exposure to NMDA was assessed. Delayed cell death, determined by LDH release and histology, following a 24 hr recovery period after NMDA treatment, was unchanged by the presence of NNA. NNA did not interfere with acute NMDA-stimulated GABA release indicating that NNA did not effect NMDA receptor interactions.(ABSTRACT TRUNCATED AT 250 WORDS)
Amino Acid Oxidoreductases↗
Systemic atropine administration during cardiac arrest does not cause fixed and dilated pupils.
OBJECTIVES: Systemic administration of atropine during CPR may postpone brain death determination because of its reputed ability to produce fixed and dilated pupils. We studied the effect of atropine administered in the usual doses as an adjunct to endotracheal intubation and for cardiac arrest to determine if it would interfere with neurological assessment. DESIGN: Two groups of children were studied. Group 1 consisted of 28 patients who received atropine (0.03 +/- 0.003 mg/kg) prior to endotracheal intubation. Group 2 consisted of 21 patients previously without evidence of brainstem disease who suffered a witnessed arrest and had prompt return of spontaneous circulation and received an atropine dose of 0.03 +/- 0.01 mg/kg. RESULTS: In group 1, pupillary size averaged 4.02 +/- 0.78 mm before and 4.75 mm +/- .84 mm after atropine (P less than .001). In group 2, the pupillary examination was conducted 30 minutes after return of spontaneous circulation. The pupillary diameter was 4.80 +/- 0.91 mm. All pupils were reactive to light in both groups. CONCLUSION: Atropine administration in conventional dose causes slight pupillary dilation but does not abolish pupillary light reactivity.
Adolescent↗
Survival after brain injury. Cause of death, length of survival, and prognostic variables in a cohort of brain-injured people.
Injuries are the leading cause of death in the United States for those between 1 and 44 years of age and brain injuries are a major component of trauma. This report examines survival in a cohort of San Diego County, California, residents who incurred a brain injury in 1981. Cumulative risk of death over time, using the Cox Proportional Hazards Model, and predictors of death (determined by logistic regression) are used to evaluate survival. The results showed that about half of all brain-injured people who died, died in less than 2 h. Severe overall body damage and severe brain injury are the greatest causes of prehospital death. Even if they survived to the hospital, most people who die have brain injury as their underlying cause of death. Age as well as nature and severity of brain injury are the important predictors of in-hospital death. People who are discharged alive from the hospital have survival comparable to that of the population they came from. However, more die from trauma-related causes than would be expected.
Adolescent↗
Medical examiners and manner of death.
An experimental study of medical examiners in Alberta, Canada, produced manner of death determinations from simulated cases (vignettes) in order to examine interexaminer variation in certification judgments. Characteristics of medical examiners such as experience, residence, and religious background were investigated. The influence of victim characteristics was also examined, including race, age, gender, marital status, cause of death, and the presence of alcohol. Experience, residence, and religion of examiner were found to be related to judgments as were gender, medical cause of death, and the presence of alcohol.
Accidents↗
Cancer mortality of Chinese in Canada.
Cancer deaths determined from national vital statistics in Canadian ('Chinese') immigrants who were born in mainland China, Hong Kong or Taiwan were compared with those in the Canadian-born population. Standardized mortality ratios (SMR) based on 1981 census data and on 755 deaths among 81,740 Chinese males and 586 deaths among 83,965 females during 1980-1984, showed that the overall cancer mortality in Chinese males (SMR 141), and females (SMR 116), was significantly higher than in the Canadian-born. Moreover, SMR varied by cancer site and showed a pattern of risks similar to those reported for foreign-born Chinese in the USA: strikingly high SMR for nasopharynx and liver or gallbladder in males and females; high ratios for stomach, intestines or colon, rectum, and lung, but a low ratio for prostate in males; and high ratios for lung and cervix uteri but low ratios for breast and ovary in females. These findings indicate that useful studies on cancer mortality could be carried out in Canadian Chinese.
Adolescent↗
Causes and factors affecting perinatal mortality at Princess Basma Teaching Hospital in North Jordan.
This is the first study about the perinatal mortality in North Jordan. Between 1st June 1991 and 31st May 1992, 8,146 deliveries took place at Princess Basma Teaching Hospital. There were 250 perinatal deaths comprised of 124 stillbirths and 126 early neonatal deaths. The perinatal mortality rate was 30.6 per 1,000. The factors which might have affected this rate were mainly prematurity, low birth weight, unexplained intrauterine fetal death, and congenital malformations. The possible ways of improving the results are discussed.
Congenital Abnormalities↗