Background: The influence of the early COVID-19 pandemic on non-COVID-19 emergencies is uncertain. We conducted a systematic review and a meta-analysis to evaluate the impact of the first months of the COVID-19 pandemic on the presentation, management, and prognosis of patients presenting with ST-segment elevation myocardial infarction (STEMI). Methods: We searched the PubMed, Scopus, and Embase databases from January to August 2020. A meta-analysis of studies comparing the profile, STEMI severity at presentation, reperfusion delay, and in-hospital mortality for patients presenting before and during the early COVID-19 pandemic was conducted. Fifteen cross-sectional observational studies including 20,528 STEMI patients from the pre-COVID period and 2190 patients diagnosed and treated during the first months of the COVID-19 pandemic met the inclusion criteria. Results: Patients presenting with STEMI during the pandemic were younger and had a higher comorbidity burden. The time interval between symptoms and first medical contact increased from 93.22 ± 137.37 min to 142 ± 281.60 min (p < 0.001). Door-to-balloon time did not differ significantly between the two periods (p = 0.293). The pooled odds ratio (OR) for low left ventricular ejection fraction at presentation during the pandemic was 2.24 (95% confidence interval (CI) 1.54–3.26) and for a presentation delay >24 h was 2.9 (95% CI 1.54–5.45) relative to before the pandemic. In-hospital mortality did not increase significantly during the outbreak (p = 0.97). Conclusion: During the first months of the COVID-19 pandemic, patients presenting with STEMI were addressed later in the course of the disease with more severe left ventricular impairment. In-hospital emergency circuits and care functioned properly with no increase in door-to-balloon time and early mortality.

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.

Carbon monoxide (CO) and hydrogen cyanide (HCN) are two common toxic products of combustion. HCN concentrations of fire victims are not routinely determined in most legal medicine services in Romania. We present the case of a room fire victim in which we evaluated the concentrations of HCN and carboxyhemoglobin (COHb), their contribution to the mechanism of death, and the possibility that HCN concentration can be interpreted as vital sign. COHb was determined by spectrophotometry. HCN was spectrophotometrically determined with ninhydrin in postmortem blood samples after its removal with 20% phosphoric acid and uptake into a solution of potassium carbonate. The presence of ethyl alcohol was determined by gas chromatography. The COHb concentration was 6.15%, while the blood HCN concentration was 1.043 µg × mL−1 and the total HCN was 1.904 µg × ml−1. A blood alcohol content of 4.36 g‰ and a urine alcohol content of 5.88 g‰ were also found. Although the fire produced a considerable amount of soot, and there were signs of inhalation of soot particles, the COHb level cannot be interpreted as a vital sign. Toxic concentrations of HCN and total HCN can be interpreted as a vital sign and indicates a contributive effect of HCN in the mechanism of death.

Craniocerebral 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.

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