Postmortem blood sampling-Comparison of drug concentrations at different sample sites.

Drug concentrations in postmortem blood samples can differ considerably, depending on the sample site - a phenomenon named postmortem redistribution. In this study, blood samples from 48 cases of suspected intoxications were collected during autopsy at the Department of Forensic Medicine in Stockholm, Sweden. Samples were collected from the right and left heart, the carotid artery, jugular vein, external iliac artery and external iliac vein. The mean ratio of right heart/iliac vein was 1.3, which confirms the results from previous studies that drug concentrations in central blood are generally higher than in peripheral blood. The mean ratio of the ext iliac artery/ext iliac vein and the ratio of the carotid artery/jugular vein were 1.3 and 1.4, respectively, suggesting that drug concentrations are higher in arterial than in venous blood. Drugs with a low volume of distribution had a lower ratio of central/peripheral blood than drugs with a high volume of distribution (1.2 vs 1.4) and also a lower ratio of arterial/venous blood (1.3 vs 1.4). In cases with a short postmortem interval (PMI) there were no significant concentration differences in central and peripheral blood, but in cases with medium and long PMI, the ratios increased (1.2 and 1.4). Cases with a long PMI had an arterial/venous concentration ratio of 2.0. The results suggest that postmortem blood sampling should be performed as soon as possible after death and that peripheral venous blood, if available, should be used for analysis.

Interpretation of postmortem vitreous concentrations of sodium and chloride.

Vitreous fluid can be used to analyze sodium and chloride levels in deceased persons, but it remains unclear to what extent such results can be used to diagnose antemortem sodium or chloride imbalances. In this study we present vitreous sodium and chloride levels from more than 3000 cases. We show that vitreous sodium and chloride levels both decrease with approximately 2.2mmol/L per day after death. Since potassium is a well-established marker for postmortem interval (PMI) and easily can be analyzed along with sodium and chloride, we have correlated sodium and chloride levels with the potassium levels and present postmortem reference ranges relative the potassium levels. We found that virtually all cases outside the reference range show signs of antemortem hypo- or hypernatremia. Vitreous sodium or chloride levels can be the only means to diagnose cases of water or salt intoxication, beer potomania or dehydration. We further show that postmortem vitreous sodium and chloride strongly correlate and in practice can be used interchangeably if analysis of one of the ions fails. It has been suggested that vitreous sodium and chloride levels can be used to diagnose drowning or to distinguish saltwater from freshwater drowning. Our results show that in cases of freshwater drowning, vitreous sodium levels are decreased, but that this mainly is an effect of postmortem diffusion between the eye and surrounding water rather than due to the drowning process, since the decrease in sodium levels correlates with immersion time.

A new model for the estimation of time of death from vitreous potassium levels corrected for age and temperature.

Analysis of potassium concentration in the vitreous fluid of the eye is frequently used by forensic pathologists to estimate the postmortem interval (PMI), particularly when other methods commonly used in the early phase of an investigation can no longer be applied. The postmortem rise in vitreous potassium has been recognized for several decades and is readily explained by a diffusion of potassium from surrounding cells into the vitreous fluid. However, there is no consensus regarding the mathematical equation that best describes this increase. The existing models assume a linear increase, but different slopes and starting points have been proposed. In this study, vitreous potassium levels, and a number of factors that may influence these levels, were examined in 462 cases with known postmortem intervals that ranged from 2h to 17 days. We found that the postmortem rise in potassium followed a non-linear curve and that decedent age and ambient temperature influenced the variability by 16% and 5%, respectively. A long duration of agony and a high alcohol level at the time of death contributed less than 1% variability, and evaluation of additional possible factors revealed no detectable impact on the rise of vitreous potassium. Two equations were subsequently generated, one that represents the best fit of the potassium concentrations alone, and a second that represents potassium concentrations with correction for decedent age and/or ambient temperature. The former was associated with narrow confidence intervals in the early postmortem phase, but the intervals gradually increased with longer PMIs. For the latter equation, the confidence intervals were reduced at all PMIs. Therefore, the model that best describes the observed postmortem rise in vitreous potassium levels includes potassium concentration, decedent age, and ambient temperature. Furthermore, the precision of these equations, particularly for long PMIs, is expected to gradually improve by adjusting the constants as more reference data are added over time. A web application that facilitates this calculation process and allows for such future modifications has been developed.

Postmortem identification of hyperglycemia.

The detection of diabetic coma postmortem requires accurate biochemical analysis. Due to continuous consumption of glucose by surviving cells postmortem, blood glucose levels decrease rapidly. Therefore, vitreous fluid has been used as a substitute in forensic practice, since it has a very low cell count. It has been repeatedly reported that the sum value of vitreous glucose and lactate should be used to estimate the original antemortem blood glucose level, based on the assumption that pre-existing glucose is gradually converted to lactate under anaerobic conditions during agonal phase and the early postmortem period. In this study, we applied a strategy including consistent sampling of vitreous fluid from the centre of both eyes of deceased subjects as soon as possible after arrival at the morgue, and immediate bedside analysis using a blood gas instrument. In total, 3076 cases were included during 2004-2006. We found that, after an initial drop of vitreous glucose during the very early postmortem period, the levels stayed stable for appreciable time postmortem. Analysis of a second sample collected at autopsy 1-3 days later gave similar results (R(2)=0.90). In contrast, the vitreous lactate levels showed a steady increase. This implies that the sum value of glucose and lactate increases with postmortem time, as reflected by vitreous potassium level. In fact, a statistically significant difference in the sum value was seen between subjects with potassium below 10 mmol/L (n=1086) and above 20 mmol/L (n=531), p<.001. In addition, in this large material, we did not identify a single case with circumstantial indication of hyperglycemia that only showed high vitreous lactate. We therefore suggest that vitreous glucose alone should be used to diagnose hyperglycemia postmortem and that the limit of 10 mmol/L should have a good specificity for diabetic coma, which theoretically would equal an original blood glucose value of about 26 mmol/L. As to the methodology, we found that sonication, centrifugation and addition of fluoride to the samples are unnecessary procedures when using a blood gas instrument. The strategy resulted in a doubling of the number of diabetic coma identified at our department compared to preceding period when analysis only was performed on selected cases.