Evaluation of the severity of harm to health by gastrointestinal injury caused by blunt trauma

A total of 226 forensic medical conclusions in traumas of the gastrointestinal tract with blunt objects, 111 of these with lethal outcomes, are analyzed. The types of injuries, clinical course, medical care, complications, flaws in medical care and their consequences, and pathomorphology of the injury were analyzed. Criteria of harm inflicted to health are determined and a table of qualifying signs is suggested for cases with blunt injuries of the gastrointestinal system, with consideration for the type of injury.     

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.