Determination of heavy metals in some human organs, tissue, and fluids under normal conditions

A table has been created, presenting normal levels of heavy metals (Hg, Cd, Cr, Cu, Fe, Mn, Pb, Ni, Zn, Sn, Tl, Ag) in human biological media. In contrast to other handbooks, the authors use the normal values derived on the basis of their own investigations at the spectral laboratory of Bureau of Forensic Medical Expert Evaluations, Public Health Committee of Moscow and published reports. Comparative analysis was carried out for each element in human organs, tissues, and urine, which will facilitate expert work. Every laboratory engaged in expert evaluations and analysis in cases with suspected poisoning with heavy metal salts is to have reference values of these elements' concentrations in human organs and tissues obtained in this very laboratory on available equipment with consideration for specific features of its biogeochemical region.     

Hypophyseal damage in persons with cerebrocranial injuries and who died in the hospital

The pituitary was examined in patients with craniocerebral injuries who died in hospital in various periods after treatment. Control group consisted of victims died at the site of accident. The results indicate the significance of examining the pituitary in craniocerebral injuries for the diagnosis of thanatogenesis, particularly in patients died in hospital. Causes of traumatic changes in the organ were determined, highly incident in the practice of forensic medical experts: directly during injury, as a result of skull bone fractures; during development of dislocation syndrome and in disorders of blood and lymph circulation in the brain matter; resultant from augmenting traumatic edema of the brain.     

Clinico-morphological parameters of heroin abuse and pathology connected with it

Morphological manifestations of narcomania in heroin users are described. Diseases associated with heroin narcomania and causes of death of heroin users are presented. Morphological manifestations at the site of injections and inflammatory reactions in parenchymatous organs are characterized. The authors pay special attention to the productive inflammation which can serve as one of the signs that confirm narcomania in cases with parenteral injections of crude heroin. The authors refer the granulomas to toxic allergic form of granulomatous hypersensitive inflammation.     

GHB. Club drug or confusing artifact?

GHB can be produced either as a pre- or postmortem artifact. The authors describe two cases in which GHB was detected and discuss the problem of determining the role of GHB in each case. In both cases, NaF-preserved blood and urine were analyzed using gas chromatography. The first decedent, a known methamphetamine abuser, had GHB concentrations similar to those observed with subanesthetic doses (femoral blood, 159 microg/ml; urine, 1100 microg/ml). Myocardial fibrosis, in the pattern associated with stimulant abuse, was also evident. The second decedent had a normal heart but higher concentrations of GHB (femoral blood, 1.4 mg/ml; right heart, 1.1 mg/ml; urine, 6.0 mg/ml). Blood cocaine and MDMA levels were 420 and 730 ng/ml, respectively. Both decedents had been drinking and were in a postabsorptive state, with blood to vitreous ratios of less than 0.90. If NaF is not used as a preservative, GHB is produced as an artifact. Therefore, the mere demonstration of GHB does not prove causality or even necessarily that GHB was ingested. Blood and urine GHB concentrations in case 1 can be produced by a therapeutic dose of 100 mg, and myocardial fibrosis may have had more to do with the cause of death than GHB. The history in case 2 is consistent with the substantial GHB ingestion, but other drugs, including ethanol, were also detected. Ethanol interferes with GHB metabolism, preventing GHB breakdown, raising blood concentrations, and making respiratory arrest more likely. Combined investigational, autopsy, and toxicology data suggest that GHB was the cause of death in case 2 but not case 1. Given the recent discovery that postmortem GHB production occurs even in stored antemortem blood samples (provided they were preserved with citrate) and the earlier observations that de novo GHB production in urine does not occur, it is unwise to draw any inferences about causality unless (1) blood and urine are both analyzed and found to be elevated; (2) blood is collected in NaF-containing tubes; and (3) a detailed case history is obtained.     

Blood carbon monoxide and hydrogen cyanide concentrations in the fatalities of fire and non-fire associated civil aviation accidents, 1991-1998

To evaluate pathophysiological significance of post-mortem urinary myoglobin levels in determining the cause of death, we investigated 210 forensic autopsy cases, partially in comparison with serum levels. Post-mortem serum myoglobin levels were extraordinary high in most cases possibly due to post-mortem change. Urinary myoglobin levels did not correlate with the serum levels, showing possible post-mortem elevation in cases of a prolonged post-mortem period over 48h. A high (>1000 ng/ml), moderate (100-1000 ng/ml), slight (50-100 ng/ml) and not significant (<50 ng/ml) elevation of urinary myoglobin were observed in 26, 43, 31 and 110 cases, respectively. Half the highly elevated cases were those with a survival time over 24h. In cases of minor muscle injury such as head trauma, elevation of urinary myoglobin level was closely related to longer survival. In acute/subacute deaths with a post-mortem interval within 48h, a significant difference was observed in relation to the blood carboxyhemoglobin (COHb) levels of fire victims: myoglobinuria over 100 ng/ml was more frequently and markedly observed in cases with COHb below 60% than over 60%, suggesting muscle damage in fatal burns. Similar elevation was observed in heat stroke victims, and also in some cases of acute and subacute death from polytrauma, asphyxiation, drowning, electricity and spontaneous cerebral bleeding, but not in myocardial infarction. Thus, it was suggested that high post-mortem urinary myoglobin levels in acute and subacute death cases may be a possible indicator of antemortem massive skeletal muscle damage as well as exertional muscle hyperactivity or convulsive disorders associated with hypoxia.     

How policy variables influence the timing of applications for Social Security Disability Insurance

This article analyzes the impact of policy variables--employer accommodations, state Social Security Disability Insurance (DI) allowance rates, and DI benefits--on the timing of an application for DI benefits by workers with a work-limiting health condition starting when their health condition first begins to bother them. The analysis uses a rich mixture of personal and employer characteristics from the Health and Retirement Study linked to Social Security administrative records. We find that most workers do not apply immediately for DI benefits when they are first bothered by a health condition. On the contrary, the median working-age man with a work-limiting condition waits 7 years after that time before applying, and the median working-age woman waits 8 years. Although the risk of applying for benefits is greatest in the year following onset, only 16 percent of men and 13 percent of women in our sample apply within the first year, and the risk of application falls thereafter. That finding suggests that institutional factors, in addition to health factors, may play a role in the timing of DI applications. Using kernel density estimates of the distribution of application and nonapplication ordered by state allowance rates (the rate of acceptance per DI determination in each state), we find that both men and women who live in states with high allowance rates are disproportionately more likely to apply for benefits in the first year after their condition begins to bother them than are those in states with low allowance rates. Using life-table analysis, we also find that men and women who are accommodated by their employers are significantly less likely to apply for DI benefits in each of the first few years after their condition begins to bother them than are those who are not accommodated. On the basis of this evidence, we include these policy variables in a model of the timing of DI application that controls for other socioeconomic variables as well as health. Using a hazard model, we find that workers who live in states with higher allowance rates apply for DI benefits significantly sooner than those living in states with lower allowance rates following the onset of a work-limiting health condition. Workers who are accommodated following the onset of a work-limiting health condition, however, are significantly slower to apply for DI benefits. Using the mean values of all explanatory variables, we estimate the relative importance of changes in these policy variables on the speed with which workers apply for benefits after onset. We find that the mean time until application for men is 10.22 years. Universal accommodations following onset would delay application by 4.36 years. In contrast, a 20 percent decrease in state allowance rates would delay application by only 0.88 years. For working-age women, the average expected time until application once a condition begins to bother them is 10.58 years. Universal accommodations would delay that by 3.76 years, and a 20 percent decrease in allowance rates would delay it by 1.47 years. A complication in this analysis is that the policy variables are to some degree endogenous. Accommodation is probably offered more often to workers who want to continue working. Allowance rates are chosen by states on the basis of federal policy and local choices and probably in part on the health condition of workers in the state. Therefore, our estimates are upper bounds of these policy effects. Still, we believe we provide evidence that the social environment faced by workers with work-limiting health conditions can significantly influence their decision to apply for DI benefits, holding their specific health conditions constant.     

Cocaine-associated rhabdomyolysis and excited delirium: different stages of the same syndrome.

Previous case reports indicate that cocaine-associated rhabdomyolysis and excited delirium share many similar features, suggesting that they may be different stages of the same syndrome. We tested this hypothesis by comparing data from 150 cases of cocaine-associated rhabdomyolysis reported in the medical literature with data from an autopsy registry for 58 victims of fatal excited delirium and 125 victims of fatal acute cocaine toxicity. Patients with rhabdomyolysis are similar to victims of fatal excited delirium with regard to age; gender; race; route of cocaine administration; the experiencing of excitement, delirium, and hyperthermia; and the absence of seizures. Compared with victims of fatal acute cocaine toxicity, patients with rhabdomyolysis are different with regard to each of these variables. Compared with victims of fatal acute cocaine toxicity, both victims of rhabdomyolysis and fatal excited delirium are more likely to be black, male, and younger; to have administered cocaine by smoking or injection; and to have experienced excitement, delirium, and hyperthermia; they are also less likely to have had seizures. Because cocaine-associated rhabdomyolysis and excited delirium have similar clinical features and risk factors, occur in similar populations of drug users, and can be explained by the same pathophysiologic processes, we conclude that they are different stages of the same syndrome. It appears that this syndrome is caused by changes in dopamine processing induced by chronic and intense use of cocaine rather than by the acute toxic effects of the drug.