Evaluation of postmortem serum calcium and magnesium levels in relation to the causes of death in forensic autopsy

There appears to be very poor investigation of postmortem serum calcium (Ca) and magnesium (Mg) for diagnostic evidence to determine the cause of death. The aim of the present study was a comprehensive analysis of the serum levels in relation to the causes of death in routine casework. Autopsy cases (total, n=360; 5-48 h postmortem), including blunt injury (n=76), sharp injury (n=29), asphyxiation (n=42), drownings (n=28: freshwater, n=11; saltwater, n=17), fire fatalities (n=79), methamphetamine (MA) poisoning (n=8), delayed death from traumas (n=37), and acute myocardial infarction/ischemia (AMI, n=61), were examined. In total cases, there was no significant postmortem time-dependent rise in serum Ca and Mg. Both Ca and Mg levels in the heart and peripheral blood were significantly higher in saltwater drowning compared with those of the other groups. In addition, a significant elevation in the Ca level was observed in freshwater drowning and fire fatalities, and in the Mg level in fatal MA intoxication and asphyxiation. Topographic analyses suggested a rise in serum Ca and Mg due to aspirated saltwater in drowning, that in serum Ca in freshwater drowning and fire fatalities of peripheral skeletal muscle origin and that in serum Mg in MA fatality and asphyxiation of myocardial and/or peripheral origin. These markers may be useful especially for diagnosis and differentiation of salt- and freshwater drownings and may be also helpful to determine the causes of death involving skeletal muscle damage, including burns and MA intoxication.     

Disappearance of ethyl glucuronide during heavy putrefaction

Adrenocorticotropic hormone (ACTH) is involved in systemic reactions to stress. The aim of the present study was a comprehensive analysis of serum and cerebrospinal fluid (CSF) levels of ACTH, and the pituitary immunohistochemistry with special regard to fatal hypothermia in routine forensic autopsy cases (n=162: 5-97 years of age; 114 males and 48 females; 4 h to 3 days postmortem, median, 19.2 h). The ACTH concentrations were independent of the postmortem time, gender, or age of the subjects. The serum ACTH level was similar to the clinical reference value for sharp instrument injury, fire fatality, and hypothermia, but was lower in other groups including hyperthermia, in particular for asphyxia and poisoning. The CSF level was usually much higher than the serum level, but was significantly lower for hypothermia and hyperthermia than in other groups (p<0.01). The rate of ACTH-immunopositivity in the anterior pituitary was low in cases of fatal hypothermia and hyperthermia, while it was high in cases of blunt injury, fire fatality, and acute ischemic heart disease. These observations showed that ACTH levels in the serum and CSF depended on the cause of death. The serum level was maintained despite a low CSF level and pituitary immunopositivity for fatal hypothermia, while the serum and CSF levels as well as pituitary immunopositivity were decreased for hyperthermia.     

Postmortem serum uric acid and creatinine levels in relation to the causes of death

Serum uric acid (UA) and creatinine (Cr) mainly derive from skeletal muscle tissues. Although, remarkable postmortem stability of the serum levels has been reported, there appears to be very poor knowledge of the diagnostic value in investigation of death, except for uremia. The aim of the present study was to evaluate postmortem serum UA and Cr levels using 395 forensic autopsy cases, in comparison with blood urea nitrogen (BUN), for investigation of the pathophysiology of death with special regard to the causes of death involving possible skeletal muscle damage, e.g. due to hypoxia, heat or agonal convulsions. Cr and BUN showed relatively good topographic stability in the cadaveric blood, whereas, UA was often much higher in the right heart blood than in the left heart and peripheral blood, independent of postmortem intervals. Moderate to marked elevation of Cr and BUN accompanied with hyperuricemia was observed in delayed death. In the acute death cases (survival time <30 min), UA, especially in the right heart blood, showed a considerable elevation in mechanical asphyxiation and drowning. The Cr level in fire victims with a lower carboxyhemoglobin (COHb) level (<60%) was significantly higher than in those with the possible fatal level (>60%). A similar elevation of Cr was observed in fatalities from heat stroke and methamphetamine (MA) poisoning. The observations suggested that hyperuricemia in acute death may be indicative of advanced hypoxia and that elevated Cr level may reflect the skeletal muscle damage, especially due to thermal influence.     

Immunohistochemical investigation of ubiquitin and myoglobin in the kidney in medicolegal autopsy cases

We examined the immunohistochemical distributions of ubiquitin (Ub) and myoglobin (Mb) in human kidney tissues to assist the pathological assessment of death due to trauma. Medicolegal autopsy cases at our institute (n=138: 0-96 years of age, 105 males and 33 females) were examined. Causes of death were blunt injury (n=31), sharp injury (n=15), poisoning (n=11), drowning (n=10), fire fatalities (n=25), hypothermia (n=7), asphyxiation (n=14), hyperthermia (n=3), and natural diseases (n=22) for controls. Immunostaining of Ub and Mb was performed on the formalin-fixed paraffin-embedded kidney tissue sections. Quantitative analyses by estimating the proportion of Ub- and Mb-positive cells (%positivity) of renal tubule epithelial cells showed that the positivities for Ub and Mb were higher in subjects who died due to fire, blunt injury, sharp injury and fatal hypothermia than in other groups. The Ub-positivity correlated with the severity of airway thermal injury in fire deaths, survival time in blunt injury, and serum markers for renal failure in deaths due to sharp injury. Concomitant increases in the tubular Mb- and Ub-positivities were characteristic to deaths from injury and hypothermia. These findings suggest that Ub may serve as a sensitive indicator of the fatal influence of traumas.     

Postmortem Diagnosis of Fatal Hypothermia by Fourier Transform Infrared Spectroscopic Analysis of Edema Fluid in Formalin-Fixed,Paraffin-Embedded Lung Tissues

The goal of this study was to investigate whether pulmonary edema could become a specific diagnostic marker for fatal hypothermia using Fourier transform infrared (FTIR) spectroscopy in combination with chemometrics. The spectral profile analysis indicated that hypothermia fatalities associated with pulmonary edema fluid contained more β-sheet protein conformational structures than the control causes of death, which included sudden cardiac death, brain injury, cerebrovascular disease, mechanical asphyxiation, intoxication, and drowning. Subsequently, the results of principal component analysis (PCA) further revealed that the content of β-sheet protein conformational structures in the pulmonary edema fluid was the main discriminatory marker between fatal hypothermia and the other causes of death. Ultimately, a robust postmortem diagnostic model for fatal hypothermia using a partial least-squares discriminant analysis (PLS-DA) algorithm was constructed. Pulmonary edema fluid spectra collected from eight new forensic autopsy cases that did not participate in the construction of the diagnostic model were predicted using the model. The results showed the causes of death of all these eight cases were correctly classified. In conclusion, this preliminary study demonstrates that FTIR spectroscopy in combination with chemometrics could be a promising approach for the postmortem diagnosis of fatal hypothermia.     

A Fatal Case of Poisoning with Fentanyl Transdermal Patches in Japan

Fentanyl transdermal patches have been used to treat cancer‐ and noncancer‐related chronic pain. However, its inappropriate or illegal application may cause fatal poisoning. We herein present the case of a Japanese woman in her 40s who was found dead with seven 25‐μg/h fentanyl transdermal patches on her body. We established a detailed toxicological analysis procedure to quantify fentanyl, and its metabolite norfentanyl, and other drugs (acetaminophen, allylisopropylacetylurea, celecoxib, estazolam, promethazine, and sertraline) in human whole blood by ultra‐high‐performance liquid chromatography–tandem mass spectrometry. The measured fentanyl and norfentanyl concentrations in the femoral and cardiac blood were 0.051 and 0.072 μg/mL and 0.033 and 0.076 μg/mL, respectively. The decedent's fentanyl concentrations were consistent with previously reported postmortem blood levels for fatal cases of poisoning by fentanyl transdermal patches. Based on the decedent's case history, autopsy findings, and toxicological analyses, the cause of death was identified as intoxication with transdermal fentanyl.     

Serum concentrations of cardiac troponin T in sudden death

Ischemic heart disease is the most common cause of sudden death of natural causes in most western countries. By autopsy, there may be no gross or histologic evidence of acute myocardial damage unless the patient survived for several hours following the event. Cardiac troponin in serum has become the recommended biochemical marker for myocardial injury in the clinical setting. We performed a prospective study on 102 autopsied subjects at the Central Hospital of Rogaland, Stavanger, Norway. Femoral blood was sampled for subsequent analysis of cardiac troponin T (cTnT). In the subjects with morphologic evidence of recent myocardial injury (n = 34), the mean serum cTnT level was 1.95 microg/L compared with 0.16 microg/L in the subjects with a noncardiac cause of death (n = 35) and 0.61 microg/L in the group with probable sudden cardiac death without morphologic signs of acute myocardial injury (n = 33). The observed differences in mean serum cTnT levels between the groups were statistically significant (P < 0.0001). These data suggest that elevated postmortem serum concentration of cTnT reflects ongoing myocardial damage and may support a diagnosis of cardiac-related death in cases associated with sparse or inconclusive morphologic findings postmortem.     

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.     

Intrapulmonary aquaporin-5 expression as a possible biomarker for discriminating smothering and choking from sudden cardiac death: a pilot study

The diagnosis of mechanical asphyxia as a cause of death, especially smothering and choking lacking evident injury, is one of the most difficult tasks in forensic pathology. The present study investigated the intrapulmonary expressions of aquaporins (AQPs; AQP-1 and AQP-5), as markers of water homeostasis, in forensic autopsy cases (total n=64, within 48 h postmortem) of mechanical asphyxiation due to neck compression (strangulation, n=24), including manual/ligature strangulation (n=12) and atypical hanging (n=12), smothering (n=7) and choking (n=8), compared with sudden cardiac death (n=14) and acute brain injury (n=11). Quantification of mRNA using a Taqman real-time PCR assay system demonstrated suppressed expression of AQP-5, but not AQP-1, in smothering and choking, compared with that in strangulation as well as sudden cardiac death and acute brain injury death. Immunostaining of AQP-5 was weakly detected in a linear pattern in the type I alveolar epithelial cells in smothering and choking cases, while cardiac and brain injury death showed marked positivity, and most strangulation cases had AQP-5-positive granular aggregates and fragments in intra-alveolar spaces. These observations indicate a partial difference in pulmonary molecular pathology among these causes of death, suggesting a procedure for possible discrimination of smothering and choking from sudden cardiac death.     

Single-stranded DNA as an immunohistochemical marker of neuronal damage in human brain: an analysis of autopsy material with regard to the cause of death

Single-stranded DNA (ssDNA) is a marker of apoptosis and programmed cell death, which appears prior to DNA fragmentation during delayed neuronal death. The present study investigated the immunohistochemical distribution of ssDNA in the brain to investigate apoptotic neuronal damage with regard to the cause of death in medicolegal autopsy cases (n=305). Neuronal immunopositivity for ssDNA was globally detected in the brain, independent of the age, gender of subjects and postmortem interval, and depended on the cause of death. Higher positivity was typically found in the pallidum for delayed brain injury death and fatal carbon monoxide intoxication, and in the cerebral cortex, pallidum and substantia nigra for drug intoxication. For mechanical asphyxiation, a high positivity was detected in the cerebral cortex and pallidum, while the positivity was low in the substantia nigra. The neuronal ssDNA increased during the survival period within about 24h at each site, depending on the type of brain injury, and in the substantia nigra for other blunt injuries. The neuronal positivity was usually lower for drowning and acute ischemic disease. Topographical analysis of ssDNA-positive neurons may contribute to investigating the cause of brain damage and survival period after a fatal insult.     

Comparative evaluation of postmortem serum concentrations of neopterin and C-reactive protein

The cellular immune response is accompanied by the release of neopterin. The level of neopterin in serum is increased in patients suffering from viral infections, autoimmune diseases, systemic inflammation, allograft rejection and malignant diseases, while that of C-reactive protein (CRP) is known to rise during inflammatory diseases and traumas. To investigate postmortem neopterin and CRP concentrations with regard to the cause of death, we examined cardiac and peripheral blood samples in 474 autopsy cases without advanced decomposition (0-96 years of age, 343 males and 131 females), 2.8 h to 3 days (median, 18.0 h) after death. Survival time was 0.1 h to 5 months (median, 3.0 h) for traumatic death, and 0.1-1, 440 h (median, 2.5 h) for natural death. In autopsied subjects, neopterin concentrations were higher than the clinical reference, independent of the time after death, and depended on the survival time. In cases of acute and subacute death due to trauma, the neopterin level in right heart blood was mildly to moderately elevated (about 50-200 nmol/l) except for sharp instrument injury, whereas the CRP concentration usually remained low (<1 mg/dl). However, a moderate rise in the CRP level (around 1-10 mg/dl) was observed in fatal cases of hypothermia (cold exposure). Markedly elevated serum CRP and neopterin levels (>10 mg/dl and >500 nmol/l, respectively) were detected in cases of delayed death due to trauma involving systemic inflammatory response syndrome (SIRS) and of fatal bacterial infections. For sepsis, the serum CRP level was markedly elevated but the neopterin level was low in some cases. Fatal viral infections usually resulted in a marked elevation in the serum neopterin level (>500 nmol/l) with a mild to moderate rise in the CRP level. Combined analyses of neopterin and CRP may be useful to investigate viral infections and delayed traumatic death involving SIRS to support pathological findings.     

Investigation of cardiac troponins in postmortem subjects: comparing antemortem and postmortem levels

The limitations of autopsy in the diagnosis of death due to ischemic heart disease are well known. In the living, a simple reliable biochemical assay for cardiac troponins is used in the diagnosis of acute myocardial ischemia. Several studies have investigated the use of biochemical assays for cardiac troponins in postmortem subjects as a means to distinguish between a cardiac and anoncardiac cause of death. All of these studies, however, rely upon assigning subjects to "cardiac" or "noncardiac" death on the basis of a postmortem examination. As postmortem examination does not always accurately distinguish between these two groups, this approach is intrinsically flawed.Our study compares antemortem and postmortem cardiac troponin levels in five subjects. The antemortem samples were retrieved from the hospital biochemistry laboratory after each subject's death. The postmortem samples for each subject were taken from different sites and at different times during the early postmortem period.Erratic results bearing little or no relation to the antemortem cardiac troponin level were obtained for all subjects. Four of the five subjects had raised antemortem troponin levels, although only one had a cardiac cause of death.From this, we conclude that postmortem blood is not a suitable substrate for standard biochemical assays of cardiac troponins, which are designed for use on serum taken from living patients. In addition, the results of our study support the view that elevated cardiac troponins are a marker of serious morbidity and are not specific for cardiac injury as the primary cause of morbidity or mortality.     

Postmortem citalopram concentrations: alone or along with other compounds

Citalopram, an antidepressant whose use has become more widespread in Spain in recent years participates directly and indirectly in the lethal mechanism in voluntary and involuntary poisonings. There were 30 cases of autopsies in the Madrid region where citalopram and other psychoactive substances (psychotropic drugs, alcohol, opiates) were detected in the corpses. The postmortem citalopram levels in relation to the manner and mechanism of death were evaluated, and a significant difference between the toxic and nontoxic cases (p < 0.01) was found. We studied the citalopram blood levels alone and along with other psychoactive products, and these cases were then further divided into those where the compounds were at deadly levels and those which were not. We found a range of citalopram levels between 0.37 and 0.83 microg/mL in which some cases were associated with citalopram toxicity and others were not. Citalopram blood levels of less than 0.35 microg/mL did not lead to fatal poisoning when it was the sole substance detected.     

溴敌隆及其代谢物-苄叉丙酮在犬体内的死后分布

目的研究溴敌隆及其代谢物-苄叉丙酮在中毒致死犬体内死后分布规律,为溴敌隆中毒检材的采取提供实验依据。方法分别经口给予犬2倍和4倍LD_(50)溴敌隆,待其死亡后迅速解剖取材,气相色谱-质谱联用法测定心血、外周血、尿、胆汁、心、肝、脾、肺、肾、脑、左下肢肌、膀胱、胃、胃内容、胰等脏器和体液中溴敌隆和代谢物-苄叉丙酮的含量。结果犬经2倍和4倍LD_(50)溴敌隆灌胃染毒后3d开始出现出血症状,(178.40±20.94)h后死亡。溴敌隆和代谢物-苄叉丙酮在各组织脏器及体液中的死后分布为:溴敌隆2LD_(50)组溴敌隆:胆汁尿、肝、心、肾心血、外周血、脾、肺等;苄叉丙酮:胆汁、尿、心血、外周血、肺、胃内容中含量高于其他脏器。溴敌隆4LD_(50)组溴敌隆:胆汁、尿肝、外周血心血、胃内容物等脏器。苄叉丙酮:胆汁、尿、肺浓度高于其他脏器。结论溴敌隆及其代谢物-苄叉丙酮在中毒致死犬体内死后分布不均匀,溴敌隆在胆汁、尿、肝脏、心血和外周血含量较高,代谢物-苄叉丙酮在胆汁、尿、肺较高。胆汁、尿、肝脏、心血、外周血可作为疑似溴敌隆中毒毒物分析的检材。     

Fatal methanol intoxication with different survival times--morphological findings and postmortem methanol distribution

Three corresponding cases of fatal methanol intoxication with different survival times were investigated ante-mortem and postmortem. Ante-mortem serum methanol concentrations were determined during treatment in hospital for 4 days. Furthermore, postmortem distribution of methanol in various tissues and fluids was measured after autopsy. Morphological and toxicological findings are discussed based on the literature. The morphological findings correlated with the different survival times. The results of the toxicological analyses were partly in keeping with previously published data. Interestingly, very high methanol levels were determined in brain with very low concentrations in femoral venous blood. These results may have implications for postmortem toxicological analysis, brain death diagnosis and organ explanation for transplantation.     

Interleukin-6 and C-reactive protein serum levels in sepsis-related fatalities during the early postmortem period

Postmortem interleukin-6 (IL-6) and C-reactive protein (CRP) serum levels were investigated prospectively in sepsis-related fatalities and non-septic fatalities by using a linear regression model. At least three blood samples were collected between 0.3 and 139 h postmortem from sepsis-related fatalities (n=8) and non-septic fatalities (n=16). In addition, one antemortem blood sample was collected shortly before death from the septic patients. Antemortem and postmortem IL-6 and CRP levels were highly elevated in all individuals included in the sepsis group. An excessive postmortem increase of IL-6 serum levels associated with progressive time after death was observed in five out of the eight septic patients. Both, IL-6 and CRP serum concentrations seem to be suitable biochemical postmortem markers of sepsis. The determination of IL-6 serum levels above 1500 pg/ml in peripheral venous blood obtained in the early postmortem interval can be considered as a diagnostic hint towards an underlying septic condition. A more precise postmortem discrimination between sepsis and non-septic underlying causes of death is provided by the postmortem measurement of serum CRP in peripheral venous blood: on condition that at least two postmortem CRP values have been determined at different time points postmortem, the CRP level of a deceased at the time of death can be calculated by using linear regression analysis. When assessing postmortem IL-6 and CRP concentrations as biochemical postmortem markers of sepsis, various clinical conditions, such as a preceding trauma or burn injury going along with elevated IL-6 and/or CRP levels prior to death as a result of the systemic inflammatory response syndrome (SIRS) should be taken into consideration, thus adding relevant information for the practical interpretation of the results.     

Biochemical measurements of glucose metabolism in relation to cause of death and postmortem effects

This study was performed to examine the relationship between postmortem biochemical values and cause of death. The follow samples were taken from 399 corpses: cerebrospinal fluid (CSF; n = 376, suboccipital), blood (n = 158, femoral vein), and urine (n = 101, at autopsy). (See Table 1 for causes of death) All samples were stored at -80 degrees C. A further 100 samples of blood were later taken and stored at +4 degrees C before testing. Biochemical determinations made were: glucose in CSF, blood, and urine (hexokinase method); lactate (LDH/GPT) and free acetone (HS-gas chromatography) in CSF; hemoglobin A1 in blood (microcolumn technique). In 34 cases fatal diabetic coma was considered verified by morphological and chemical findings. One hundred cases of sudden cardiac death were chosen as the main control group. In 32 of the 34 cases defined above, the value of the formula of Traub (glucose + lactate in CSF) exceeded 415 mg/dl. It is not influenced significantly by hyperglycemia or hyperlactatemia due to factors other than diabetes (i.e., carbon monoxide, asphyxia). After death the value rose till the 30th hpm, then remained stable for at least 1 week. Fatal coma was defined as the ketoacidotic form if free acetone in CSF ranged above 21 mg/l. In these cases, CSF glucose and free acetone correlated positively. Hemoglobin A1 remained stable after death. Its amount was independent from postmortem blood glucose, postmortem interval and total hemoglobin. Furthermore, the manner of storage (-80 degrees or +4 degrees C) had no significant influence on its values. In 29 of 34 cases of fatal coma, Hb A1 exceeded 12.1%. Analysis of urine glucose showed elevated levels (over 500 mg/dl) in diabetic comas. On conclusion, fatal diabetic coma seems indicated as the cause of death if measured values of postmortem biochemistry exceed the following limits: CSF-Traub 415 mg/dl, free acetone (CSF) 21 mg/l; Hb A1 12.1%; urine glucose 500 mg/dl. Most important are the Traub formula and hemoglobin A1. Usually, in fatal coma both values are elevated. If both of them are normal, diabetic coma can nearly be excluded. Combined evaluation of all values is absolutely necessary. Morphology must also always be taken into account. Consequently, a diagnosis of fatal coma can be obtained by a process of elimination.     

Fatal cyclobenzaprine overdose with postmortem values

There are only two published cases of overdose with postmortem blood cyclobenzaprine concentrations, both with confounding factors. We report two additional cases of fatal cyclobenzaprine overdose with postmortem values. Case 1: a 56-year-old female was found in full cardiopulmonary arrest after a verbal suicide threat to a friend. Postmortem blood concentrations were cyclobenzaprine 0.96 mg/L and diazepam 0.3 mg/L. Case 2: a 37-year-old male was found in full arrest by a family member after an intentional ingestion of cyclobenzaprine. Postmortem blood concentrations were cyclobenzaprine 0.8 mg/L and ethanol 0.174 gm/dL. The concentrations of diazepam and ethanol reported in these two patients were not found in quantities usually associated with a fatal outcome, suggesting that the cyclobenzaprine was the primary cause of the fatality. Additionally, the blood was drawn from a femoral site, so that postmortem redistribution is not a likely factor. Blood concentration of > or = 0.8 mg/L cyclobenzaprine may be associated with a fatal outcome.     

Evaluation of human brain damage in fire fatality by quantification of basic fibroblast growth factor (bFGF), glial fibrillary acidic protein (GFAP) and single-stranded DNA (ssDNA) immunoreactivities

Burns and inhalation of toxic gases, including carbon monoxide (CO) and cyanide, which are produced by combustion, are major factors involved in fire death. The present study immunohistochemically investigated basic fibroblast growth factor (bFGF), glial fibrillary acidic protein (GFAP) and single-stranded DNA (ssDNA) in the brains of fire fatalities (n=49) to examine the differences between fatal burns and CO intoxication, compared with those in cardiac deaths (n=24) and mechanical asphyxiation cases (n=23). In acute fire fatality, neuronal ssDNA immunopositivity in the cerebral cortex of the parietal lobe was high in both fatal burns and fatal CO intoxication, but that of the pallidum was higher for CO intoxication than for burns. The number of neurons was decreased in prolonged fire deaths, irrespective of the severity of burns or CO intoxication, but glias were increased in cases of fatal burns. Prolonged deaths due to burns had a higher glial bFGF immunopositivity in the cortex and white matter, higher and lower glial GFAP immunopositivity in the cortex and white matter, respectively, and a low neuronal ssDNA immunopositivity in the cerebral cortex and hippocampus. In prolonged deaths due to CO intoxication, however, glial bFGF and GFAP immunopositivities were low at each site, but neuronal ssDNA immunopositivity showed a higher value. These observations suggest increased cerebral neuronal ssDNA immunopositivity to be a finding of vitality in acute fire death, and a neuronal loss accompanied by active glial responses after severe burns, and a neuronal loss and progressive apoptosis without glial responses after CO intoxication to be characteristic in prolonged death.     

Fatal poisoning with alcohol and drugs in the Greater Amman County

A study of fatal poisoning due to alcohol and drugs was carried out, to examine the mortality resulting from alcohol and drugs in the Greater Amman County, Jordan. A retrospective review of all autopsy records and certified deaths issued by the Department of Forensic Medicine at Jordan University Hospital in the greater Amman county was undertaken. During the 18 years (1978-1996) 6109 postmortem cases were performed in our department. A total of 60 cases were identified and analyzed according to age, race, sex, manner of death of the victims along with blood alcohol concentration, the drug detected at autopsies, the scene circumstances, and the geographic location of the accident and death.