“…These findings led to the conclusion that decompositional changes were not associated with 3HB production and that blood 3HB levels in decomposed bodies could be considered an appropriate biochemical parameter in the estimation of 3HB concentrations at the time of death. Similar results were obtained in two former studies, in which we investigated blood 3HB levels in a series of medicolegal autopsies that included bodies with decompositional changes [40,47]. Kadiš et al [39] had already postulated that 3HB does not increase after death but, at most, may decrease due to spontaneous molecule degradation.…”
The concentrations of 3-beta-hydroxybutyrate (3HB) in blood and two liver samples were retrospectively examined in a series of medicolegal autopsies. These cases included diabetic ketoacidosis, nondiabetic individuals presenting moderate to severe decompositional changes and nondiabetic medicolegal cases privy of decompositional changes. 3HB concentrations in liver sample homogenates correlate well with blood values in all examined groups. Additionally, decompositional changes were not associated with increases in blood and liver 3HB levels. These results suggest that 3HB can be reliably measured in liver homogenates when blood is not available at autopsy. Furthermore, they suggest that metabolic disturbances potentially leading or contributing to death may be objectified through liver 3HB determination even in decomposed bodies.
“…These findings led to the conclusion that decompositional changes were not associated with 3HB production and that blood 3HB levels in decomposed bodies could be considered an appropriate biochemical parameter in the estimation of 3HB concentrations at the time of death. Similar results were obtained in two former studies, in which we investigated blood 3HB levels in a series of medicolegal autopsies that included bodies with decompositional changes [40,47]. Kadiš et al [39] had already postulated that 3HB does not increase after death but, at most, may decrease due to spontaneous molecule degradation.…”
The concentrations of 3-beta-hydroxybutyrate (3HB) in blood and two liver samples were retrospectively examined in a series of medicolegal autopsies. These cases included diabetic ketoacidosis, nondiabetic individuals presenting moderate to severe decompositional changes and nondiabetic medicolegal cases privy of decompositional changes. 3HB concentrations in liver sample homogenates correlate well with blood values in all examined groups. Additionally, decompositional changes were not associated with increases in blood and liver 3HB levels. These results suggest that 3HB can be reliably measured in liver homogenates when blood is not available at autopsy. Furthermore, they suggest that metabolic disturbances potentially leading or contributing to death may be objectified through liver 3HB determination even in decomposed bodies.
“…While microscopic examination is also noncontributive in these cases, postmortem chemistry is of uttermost importance. Studies have shown that vitreous sodium and chloride are relatively stable after death and correlate well with antemortem serum sodium and chloride levels . In this here described case, the vitreous sodium and chloride levels were extremely elevated.…”
In the forensic literature, fatal dehydration predominantly concerns young children or incapacitated elderly persons. The postmortem diagnosis of fatal dehydration can be challenging to confirm, especially if the preceding circumstances are unknown. Here presented is a case of a 23‐year‐old man who died while held in an isolation cell during police custody for 18 days. Autopsy findings were unspecific, but vitreous fluid analysis showed 192 mmol/L sodium, 179 mmol/L chloride, 16 mmol/L potassium, 352 μmol/L (3.98 mg/dL) creatinine, and 81 mmol/L (226.9 mg/dL) urea nitrogen. Based on the findings and circumstances, the cause of death was determined as severe dehydration and manner of death accident. This case illustrates the importance of performing postmortem biochemistry.
“…Also, PM glucose analysis is not feasible due to rapid glucose metabolization (glycolysis) into lactate [21]. However, using the recently developed biochemical analyses, and alternative matrices (such as vitreous humor and urine), fatal DM-related ketoacidosis is readily diagnosed, even in cases of no medical history of DM or cadavers with advanced postmortem changes [22,29,30]. Recently Palmiere discussed the caveats on using a single measurement as a definitive indication of dysregulation of glucose metabolism [31]; single measurement of glucose metabolism from any PM sample is likely unreliable.…”
Section: Discussionmentioning
confidence: 99%
“…Practically, any trace of glucose in the vitreous fluid is likely an indication of antermortem hyperglycemia [20]. For urine PM glucose measurements, specifying cutoff values for evaluating AM glucose balance from PM urine samples is challenging, and the urine glucose measurement should primarily be used to confirm vitreous findings [21][22][23].…”
Diabetes mellitus (DM) could cause pilot incapacitation and result in aviation fatalities. The mechanisms could be directly as a consequence of acute hypoglycemia/subacute diabetic ketoacidosis (DKA) or indirectly as an acute cardiovascular event by contributing to the development of atherosclerosis in coronary or carotid and cerebral arteries. In this study, DM-related fatal flight accidents in the US National Transport Bureau's database between years 2011-2016 were analyzed with special emphasis on postmortem (PM) glucose levels and correlation of toxicological reports with anamnestic information on DM. Additionally, autopsy results on coronary arteries were reviewed. In 43 out of 1491 (~ 3%) fatal accidents pilots had DM. Postmortem glucose or glycated hemoglobin percentage (Hb1Ac) was measured in 12 of the 43 cases; while antidiabetic medication was found in 14 of the cases (only two of the cases had both glucose measurements and medication). With the increasing prevalence of DM, a possibility of pilot incapacitation due to DM or complications of DM should be actively studied, even if no anamnestic information of DM was available. While PM hypoglycemia is difficult to assess, we propose a systematic investigation based on measurement of glucose, Hb1Ac%, and ketone bodies, and documentation of atherosclerotic lesions in major arteries to identify or rule out DM as a cause of pilot incapacitation.
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