The danger of neck compression without restriction of the arterial flow remains unresolved in forensic medicine. There is an ongoing debate concerning life endangerment due to the cardioinhibitory reflex. The aim of this study was to determine what forensic medical experts believe and how they deal with this reflex. An anonymous electronic questionnaire was sent to 1429 forensic medical experts all over the world. We asked them about their opinion on the cardioinhibitory reflex, its role in causing death, and what their diagnostic criteria were. A total of 182 questionnaires were returned. The experts who answered were from 32 different countries. Our survey showed that 80.2% of experts believe that the cardioinhibitory reflex can theoretically cause death. In the practical application opinions diverge though. Apparently, the practical application mainly depends on the habit of the individual expert. We observed no consensus on the diagnostic criteria to be used. Given the potentially frequent use of the concept of the cardioinhibitory reflex in forensic practice and its judicial impact it would be important to reach a consensus.
Investigations into deaths in custody are still very incomplete and insufficiently independent in many countries. This chapter identifies the key elements that should form the basis of all investigations following a death in custody. It also indicates basic evidence-taking acts that can and should be immediately undertaken by any other less-qualified independent investigator if the required competencies mentioned earlier are not completely met. All cases of death under custody should be submitted to autopsy, in order to determine the cause of death. A very thorough autopsy procedure is crucial for shedding light on controversial deaths such as those occurring in custody. It is recommended that all central detention authorities draw up policies and procedures to be followed in the event of any death in custody. The postmortem examination of a body goes from an external examination of the body to a full forensic autopsy completed with ancillary analyses.
In the present study, the effects of amphetamine-class drugs were examined in cases reported to the Victorian coroner from 2001 to 2005 to determine if death can occur from the use of amphetamine-class drugs alone. A total of 169 cases were reviewed where a forensic autopsy detected amphetamine(s) in the blood. Pathology, toxicology, and police reports were analyzed in all cases to ascertain the involvement of amphetamine-class drugs in these deaths. In Victoria, methamphetamine (MA) is the principal abused amphetamine-class followed by methylenedioxymethamphetamine (MDMA). There were six cases in which a cerebral hemorrhage caused death and three cases in which serotonin syndrome was established as being caused by the interaction of MDMA and moclobemide. There were 19 cases in which long-term use of amphetamines was associated with heart disease. There were three cases where amphetamine-class drugs alone were regarded as the cause of death, of which two cases exhibited high levels of MDMA and lesser amounts of MA and/or amphetamine. There were no cases in which significant natural disease was absent and death was regarded as caused by the use of MA. There was no correlation between blood concentration of drug and outcome.
Objective: To evaluate the relative importance of increased lactate production as opposed to decreased utilization in hyperlactatemic patients, as well as their relation to glucose metabolism. Design: Prospective observational study. Setting: Surgical intensive care unit of a university hospital. Patients: Seven patients with severe sepsis or septic shock, seven patients with cardiogenic shock, and seven healthy volunteers. Interventions: 13C-labeled sodium lactate was infused at 10 μmol/kg/min and then at 20 μmol/kg/min over 120 mins each. 2H-labeled glucose was infused throughout. Measurements and Main Results: Baseline arterial lactate was higher in septic (3.2 ± 2.6) and cardiogenic shock patients (2.8 ± 0.4) than in healthy volunteers (0.9 ± 0.20 mmol/L, p < .05). Lactate clearance, computed using pharmacokinetic calculations, was similar in septic, cardiogenic shock, and controls, respectively: 10.8 ± 5.4, 9.6 ± 2.1, and 12.0 ± 2.6 mL/kg/min. Endogenous lactate production was determined as the initial lactate concentration multiplied by lactate clearance. It was markedly enhanced in the patients (septic 26.2 ± 10.5; cardiogenic shock 26.6 ± 5.1) compared with controls (11.2 ± 2.7 μmol/kg/min, p < .01). 13C-lactate oxidation (septic 54 ± 25; cardiogenic shock 43 ± 16; controls 65 ± 15% of a lactate load of 10 μmol/kg/min) and transformation of 13C-lactate into 13C-glucose were not different (respectively, 15 ± 15, 9 ± 18, and 10 ± 7%). Endogenous glucose production was markedly increased in the patients (septic 14.8 ± 1.8; cardiogenic shock 15.0 ± 1.5) compared with controls (7.2 ± 1.1 μmol/kg/min, p < .01) and was not influenced by lactate infusion. Conclusions: In patients suffering from septic or cardiogenic shock, hyperlactatemia was mainly related to increased production, whereas lactate clearance was similar to healthy subjects. Increased lactate production was concomitant to hyperglycemia and increased glucose turnover, suggesting that the latter substantially influences lactate metabolism during critical illness.
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