Diabetic ketoacidosis (DKA) is a lethal acute hyperglycemic complication of diabetes mellitus (DM) and it represents the initial manifestation of DM in about 15–20% of cases in adults and about 30–40% of cases in children. Postmortem diagnosis of DKA can only be made by applying thanatochemistry. Biochemistry applied postmortem is viewed with skepticism by many practitioners in the forensic field, completely lacking in many forensic services around the world, and especially in the national ones. This article aims to underline the importance of the postmortem application of biochemistry by reviewing the case of a person in the third decade of life who died suddenly at home due to diabetic ketoacidosis (DKA), whose autopsy was performed at an early PMI of approximately 24 h. Routine postmortem examinations (macroscopic, anatomopathological, and toxicological) could not establish a clear cause of death. When attention was turned to biochemical determinations (i.e., determination of glycated hemoglobin, glucose and ketone bodies (acetone, beta-hydroxybutyrate) in the blood, vitreous humor, and cerebrospinal fluid), the identified values clarified the thanatogenic mechanisms by establishing the diagnosis of DKA.

Particularities of Medical Education in the Field of Forensic Toxicology. Studying Dangerous Chemical Agents in Forensic Research

Introduction: Forensic identification practice requires a multitude of methods for positive identification, among which the facial reconstruction occupies a high place. For this to be done in the best way possible, it is mandatory that each population have their own database regarding soft tissue thickness. Objective: The present research is focused on creating such a database for the Romanian adult population and on exploring the statistical distribution and correlation of craniometric landmarks, overall, and in groups defined according to sex and weight categories. This might provide support in estimating the values of missing landmarks or other variables (e.g., age, sex) for unidentified bodies. Methods: Twelve craniometric landmarks were measured on 100 cadavers less than 24 h after death. Results and discussions: Of the 12 anatomical landmarks, only one appears to manifest statistically significant differences between sexes, and seven landmarks appear to vary significantly among the weight categories. Additionally, some evidence of interpopulation differences in the average soft tissue thicknesses were observed by the comparison of these data with similar studies from Caucasian groups with different geographic origin. Additionally, correlations between facial landmarks were examined, overall and between sexes.

Background and objectives. In forensic medicine, the postmortem determination of glycated hemoglobin (HbA1c) helps identify undiagnosed cases of diabetes or cases with uncontrolled glycemic status. In order to contribute to the solidification of thanatochemistry, both globally and especially nationally, we aimed to determine this biomarker postmortem, for the first time in our institution, in order to identify undiagnosed pre-mortem diabetics, as well as those with inadequate glycemic control. Materials and Methods. Our research consisted of analyzing a total number of 180 HbA1c values, 90 determinations from the peripheral blood and 90 from the central blood. The determination of HbA1c was performed by means of a fully automatic analyzer (HemoCue HbA1c 501), certified by the National Glycohemoglobin Standardization Program (NGSP)/Diabetes Control and Complications Trial (DCCT) and calibrated according to the standards developed by the International Federation of Clinical Chemistry (IFCC). According to ADA criteria, HbA1c values can provide us with the following information about the diagnosis of diabetes: normal 4.8–5.6%; prediabetes 5.7–6.4%; diabetes ≥ 6.5%. Results. A considerable number of cases with an altered glycemic status (cases that had HbA1c values equal to or greater than 5.7%) were identified—51% demonstrable by peripheral blood determinations and 41% by central blood determinations. Notably, 23 people with diabetes (25%) were identified by analyzing the peripheral blood; 18 other people with diabetes (20%) were identified by analyzing the central blood. Conclusions. Our study managed to confirm the antemortem diagnosis of DM using a simple point-of-care analyzer and applying standardized and certified criteria on HbA1c levels measured postmortem. We also identified a considerable number of cases with DM in patients with no antemortem history of glucose imbalance—at least 20% more cases. Although the two different sites used for blood collection showed a strong statistical correlation, it seems that the peripheral site could have a higher sensibility in detecting postmortem altered glycemic status.

Cranio cerebral trauma is the most common cause of death and post-traumatic disability in people under 45 years of age. In Romania, the annual incidence shows, that for every 100,000 inhabitants, there are 300 cases of craniocerebral trauma that require specialized medical assistance. Craniocerebral traumas are the most common types of traumas encountered in current forensic practice. Research on the mechanisms of injury, the timing of head trauma and the establishment of causes of death remain relevant. Establishing the traumatic moment implies both the distinction between pre-mortem and post-mortem injuries but also considerations regarding the post-traumatic survival interval. Regarding the elucidation of the moment of occurrence of the craniocerebral trauma from the forensic point of view, a satisfactory result has not been reached so far. The classic hypothesis regarding the development of traumatic brain injuries shows that they are the result of primary traumatic injuries due to cell necrosis combined with the inflammatory brain response that causes secondary brain injuries. It was considered that post-traumatic neuronal losses are strictly due to necrosis and inflammation, and cellular apoptosis being a physiological process, does not play a role in this process. Due to recent experimental data, brain cell apoptosis has begun to be reevaluated. The pathophysiology of traumatic brain injury is far from being fully understood, with the idea that apoptosis would play an even more important role than originally thought. Specifically, damaged brain cells release neuromodulatory substances that can lead to late-onset neuronal damage long after necrotic and inflammatory brain phenomena have ceased to act. These neuronal cell losses are responsible for the development of various neurological deficits and post-traumatic sequelae.

Traumatic brain injury (TBI) is one of the leading causes of death worldwide, particularly in young people. Diffuse axonal injuries (DAI) are the result of strong rotational and translational forces on the brain parenchyma, leading to cerebral oedema and neuronal death. DAI is typically characterized by coma without focal lesions at presentation and is defined by localized axonal damage in multiple regions of the brain parenchyma, often causing impairment of cognitive and neuro-vegetative function. Following TBI, axonal degeneration has been identified as a progressive process that begins with the disruption of axonal transport, leading subsequently to axonal swelling, axonal ballooning, axonal retraction bulges, secondary disconnection and Wallerian degeneration. The objective of this paper is to report on a series of patients who have suffered fatal traumatic brain injury, in order to verify neurological outcomes in dynamics, relative to the time of injury, using antibodies for neurofilament (NFL), spectrin II, beta-amyloid (β-APP), glial fibrillary acidic protein (GFAP) and cluster of differentiation 68 (CD68). From the studied cases, a total of 50 cases were chosen, which formed two study groups. The first study group comprises 30 cases divided according to survival interval. The control group comprises 20 cases with no history of traumatic brain injury. Cardiovascular disease and history of stroke, cases suffering from loss of vital functions, a post-traumatic survival time of less than 15 min, autolysis and putrefaction were established as criteria for exclusion. Based on their expression, we tested for diagnosis and degree of DAI as a strong predictor of mortality. Immunoreactivity was significantly increased in the DAI group compared to the control group. The earliest changes were recorded for GFAP and CD68 immunolabeling, followed by β-APP, spectrin II and NFM. The most intense changes in immunostaining were recorded for spectrin II. Comparative analysis of brain apoptosis, reactive astrocytosis and inflammatory reaction using specific immunohistochemical markers can provide important information on diagnosis of DAI and prognosis, and may elucidate the timing of the traumatic event in traumatic brain injury.