Kaori Ishida

Evaluation of post-mortem oxymetry with reference to the causes of death.

We examined blood samples of 214 forensic autopsy cases, excluding fire victims, on a CO-oximeter system in order to evaluate post-mortem oxymetric profiles with reference to the causes of death. Oxyhemoglobin (O2-Hb) levels in the left and right heart blood, respectively, ranged from 0 to 97.7% and from 0 to 92.1%, showing no apparent correlation with the post-mortem intervals or rectal temperatures. In nearly 60% of the cases, O2-Hb was lower than 10%. A high O2-Hb level (over 50%) in the left heart blood was most frequently observed in death from cold exposure and occasionally in fatalities from blunt injuries and stab/incised wounds with or without medical care. O2-Hb in the heart blood was usually very low (under 10%) in fatalities from asphyxiation, drowning, poisoning and natural diseases. A greatest oxymetric variation was observed in death from injuries, probably due to varied causal mechanisms of death. In most cases, the differences between blood O2-Hb levels in the heart and iliac vessels were within 15%; whereas O2-Hb in the cerebral venous blood was usually evidently higher than that in the right heart blood. An inverse relation of O2-Hb levels to total hemoglobin contents was observed slightly for the blood in the heart and iliac vessels, and more obviously for the cerebral venous blood. The above post-mortem oxymetric profiles were considered to at least partially reflect the final balance of oxygen uptake and consumption in dying process, possibly also affected by the circulatory status, giving an objective index to the color of cadaveric blood (hypostasis), although it should be assessed in consideration of post-mortem interference and total hemoglobin contents. In any case, however, post-mortem oxymetry seemed to have a limited value owing to severe systemic hypoxia which would be a common final state before death from various fatal traumas and diseases, maybe except for those with extremely short agony.

Methamphetamine-related fatalities in forensic autopsy during 5 years in the southern half of Osaka city and surrounding areas

To outline the recent features of methamphetamine-related fatalities from the medico-legal point of view, a retrospective investigation of forensic autopsy cases involving methamphetamine during a 5-year period (1994-1998) in the southern half of Osaka city and surrounding areas (about 1.57 million population) was undertaken. Among 646 autopsy cases, methamphetamine was detected in 15 victims (nine males, six females; 16-71 years of age; most frequently in males in their thirties). Primary scenes of fatal events were concentrated in the middle of the city. About half of them were transferred from emergency medical centers (survival time, up to 30 h). The cause and manner of death were: methamphetamine poisoning (n=4), homicide (n=4), accidental falls and aspiration from drug abuse (n=4), fire death (n=1), myocardial infarction (n=1), and cerebral hemorrhage (n=1) under drug influence. Usually injection scars and fresh puncture sites were found. Blood methamphetamine concentrations were 2.29-17.05 micromol/dl in the fatal poisoning, 0. 44-3.80 micromol/dl in deaths from other extrinsic causes (trauma), and 1.35-2.17 micromol/dl in cardio- and cerebrovascular strokes. Common complications were cardiomyopathy, cerebral perivasculitis and liver cirrhosis/interstitial hepatitis. Fatal and nonfatal methamphetamine poisonings are separately dealt with by the administrative medical examiners office and in emergency medical centers. Tightly cooperative approaches of clinical and medico-legal experts are required for the effective social and medical management of drug abuse.

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.

Possible postmortem serum markers for differentiation between fresh-, saltwater drowning and acute cardiac death: a preliminary investigation

The aim of the present study was to investigate the differences in postmortem blood biochemistry between fresh-, saltwater drowning and acute myocardial infarction/ischemia (AMI) (n=11, n=15 and n=23, respectively; postmortem interval <48 h). Left and right cardiac blood samples were examined for the serum markers: sodium (Na), chloride (Cl), magnesium (Mg), blood urea nitrogen (BUN), creatinine (Cr), pulmonary surfactant-associated protein A (SP-A) and cardiac troponin T (cTn-T). The most efficient markers were the left-right cardiac BUN ratio for determination of drowning (hemodilution) and the left heart blood Mg level for differentiation between fresh- and saltwater aspiration. A characteristic feature of saltwater drowning was a low left-right BUN ratio and a marked elevation in the serum Cl, Mg and Ca levels of the left heart blood. Serum cTn-T level was usually low in drownings, showing a difference from most cases of AMI. Freshwater drowning showed a significant elevation of serum SP-A, although there was considerable overlapping with saltwater drowning and AMI. These findings suggested the usefulness of serum markers in the investigation of death from drownings.

Intranuclear ubiquitin immunoreactivity of the pigmented neurons of the substantia nigra in fatal acute mechanical asphyxiation and drowning

Abstract To evaluate the significance of immunohistochemical staining of ubiquitin (heat shock protein) in the midbrain for the medico-legal diagnosis of fatal asphyxiation and drowning, we investigated forensic autopsy cases of fatal mechanical asphyxia (n = 18), manual/ligature strangulation (n = 9), hanging (n = 4), aspiration/choking (n = 5) and drowning (n = 16). These were compared to control groups (n = 30) consisting of fatalities from brainstem injury (n = 12) and acute myocardial infarction (n = 18). Ubiquitin was clearly demonstrated in the nuclei of pigmented substantia nigra neurons, showing two intranuclear staining patterns: a type of inclusion (possibly Marinesco bodies) and a diffuse staining. The diffuse staining was significantly more frequently observed in cases of drowning. The percentage of total ubiquitin positive neurons was frequently higher in strangulation (5.1– 28.4%, mean 17.0%), aspiration/choking (5.3–32.0%, mean 17.6%) and drowning (7.0–34.1%, mean 19.8%), but relatively low in hanging (5.1–12.7%, mean 8.6%), brainstem injury (0–10.4%, mean 5.0%) and acute myocardial infarction (1.5–16.9%, mean 8.3%). These observations suggest that intranuclear ubiquitin immunoreactivity of the pigmented substantia nigra neurons in the midbrain was induced by a fatal severe stress on the central nervous system in asphyxiation and drowning.

Serum C-reactive protein levels in postmortem blood—an analysis with special reference to the cause of death and survival time☆

We have investigated postmortem serum CRP levels in 408 forensic autopsy cases consisting of 216 acute and 192 non-acute death cases having postmortem interval of less than 48 h. CRP ranged from 0.03 to 66.13 mg/dl with the median of 0.28 mg/dl. In 362 traumatic death, survival time and the presence of severe infection were the major factors contributing to CRP elevation, while postmortem interval, age, gender, hepatic injury and liver cirrhosis was not. In almost all the immediate deaths (15/16) CRP remained at a low level (<0.5 mg/dl). Acute deaths and subacute deaths within 6 h showed lower CRP levels compared to longer survivors, consistent with the clinical and experimental studies. As for natural diseases, the CRP level reflected the pathological findings. The results suggest a possibility of CRP as a forensic diagnostic marker.

Immunohistochemical investigation of a pulmonary surfactant in fatal mechanical asphyxia

Abstract We evaluated the usefulness of pulmonary surfactant protein A (SP-A) as a practical diagnostic marker of fatal mechanical asphyxia in forensic autopsy cases. ¶A total of 27 cases of asphyxia were examined histologically and immunohistochemically and compared with a control group consisting of 16 cases of poisoning (n = 9) and peracute death (n = 7). Both groups showed histological findings of local atelectasis and local emphysema, congestion, intra-alveolar and interstitial edema in most cases and pulmonary hemorrhages in some cases. The mechanical asphyxia group showed a significantly increased intensity of SP-A staining in the intra-alveolar space accompanied by many massive aggregates in approximately 60% of cases, which was not found in the control group. These structures may be interpreted as aggregates of pulmonary surfactant released from the alveolar wall due to enhanced secretion caused by strong forced breathing or over-excitement of the autonomic nervous system by mechanical asphyxia. The results of our investigation suggest the practical usefulness of the immunohistochemical detection of SP-A in distinguishing mechanical asphyxia from other types of hypoxia.

Pulmonary immunohistochemistry and serum levels of a surfactant-associated protein A in fatal drowning

To evaluate the immunohistochemical distribution and serum levels of a pulmonary surfactant-associated protein A (SP-A) in fatal drowning with regard to the pulmonary alveolar injury, 53 autopsy cases were investigated. SP-A was membranously or linearly demonstrated in varying intensities on the intra-alveolar interior surface and on the interface of the intra-alveolar effusion. A high score of intra-alveolar aggregates of SP-A was significantly more frequently observed in freshwater than saltwater drowning. The left/right ratios of cardiac blood SP-A level were significantly high both in fresh- and saltwater drowning, showing no relationship to aggregated SP-A scores. Immunohistochemical score and serum level of SP-A were independent of the lung weight or pleural effusion. These observations suggest a partial difference of pulmonary pathophysiology depending on the immersion medium in fatal drowning.

Post-mortem urinary myoglobin levels with reference to the causes of death.

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.

A quantitative RT-PCR assay of surfactant-associated protein A1 and A2 mRNA transcripts as a diagnostic tool for acute asphyxial death

Although an immunohistochemical investigation of pulmonary surfactant-associated protein A (SP-A) suggested a characteristic increase in fatal asphyxiation, no particular change was observed in the total amount of SP-A mRNA. SP-A is encoded by two highly similar genes, SP-A1 and SP-A2, which are differentially regulated in the expression. In the present study, to investigate the molecular pathology of SP-A, we established a method for quantitative RT-PCR assay of SP-A1 and SP-A2 mRNA transcripts. Using this method, fatalities from acute mechanical asphyxia (n=12) and drowning (n=9) were examined in comparison with control groups (n=17) of acute myocardial infarction (n=11) and peracute death due to brain lacerations (n=6). The SP-A1/A2 ratio (mean value) was markedly elevated in mechanical asphyxia (6.72) and drowning (5.64), whereas it was low in controls (acute myocardial infarction, 2.80; brain lacerations, 2.56). The analysis of the SP-A1/A2 ratio may assist interpretation of the molecular alterations of SP-A related to acute asphyxial death.