The concern of a terrorist attack using cyanide, as well as the gradual awareness of cyanide poisoning in fire victims, has resulted in a renewed interest in the diagnosis and treatment of cyanide poisoning. The formerly academic presentation of cyanide poisoning must be replaced by more useful knowledge, which will allow emergency physicians and rescue workers to strongly suspect cyanide poisoning at the scene. Human cyanide poisonings may result from exposure to cyanide, its salts, or cyanogenic compounds, while residential fires are the most common condition of exposure. In fire victims, recognition of the cyanide toxidrome has been hampered by the short half-life in blood and poor stability of cyanide. In contrast, carboxyhemoglobin, as a marker of carbon monoxide poisoning, is easily measured and long-lasting. No evidence supports the assumption of the arbitrary fixed lethal thresholds of 50% for carboxyhemoglobin, and 3 mg/L for cyanide, in fire victims. Preliminary data, drawn when comparing pure carbon monoxide and pure cyanide poisonings, suggest that a cyanide toxidrome can be defined considering signs and symptoms induced by cyanide and carbon monoxide, respectively. Prospective studies in fire victims may provide value in clarifying signs and symptoms related to both toxicants. Cyanide can induce a lifethreatening poisoning from which a full recovery is possible. A number of experimentally efficient antidotes to cyanide exist, whose clinical use has been hampered due to serious side effects. The availability of potentially safer antidotes unveils the possibility of their value as first-line treatment, even in a complex clinical situation, where diagnosis is rapid and presumptive.

Introduction: Prognostic factors in intentional insulin self-poisoning and the significance of plasma insulin levels are unclear. We therefore conducted this study to investigate prognostic factors in insulin poisoning, in relation to the value of plasma insulin concentration. Methods: We conducted a prospective study, and used logistic regression to explore prognostic factors and modelling to investigate toxicokinetic/toxicodynamic relationships. Results: Twenty-five patients (14 female and 11 male; median [25th to 75th percentiles] age 46 [36 to 58] years) were included. On presentation, the Glasgow Coma Scale score was 9 (4 to 14) and the capillary glucose concentration was 1.4 (1.1 to 2.3) mmol/l. The plasma insulin concentration was 197 (161 to 1,566) mIU/l and the cumulative amount of glucose infused was 301 (184 to 1,056) g. Four patients developed sequelae resulting in two deaths. Delay to therapy in excess of 6 hours (odds ratio 60.0, 95% confidence interval 2.9 to 1,236.7) and ventilation for longer than 48 hours (odds ratio 28.5, 95% confidence interval 1.9 to 420.6) were identified as independent prognostic factors. Toxicokinetic/toxicodynamic relationships between glucose infusion rates and insulin concentrations fit the maximum measured glucose infusion rate (E_max) model (E_max 29.5 [17.5 to 41.1] g/hour, concentration associated with the half-maximum glucose infusion rate [EC₅₀] 46 [35 to 161] mIU/l, and R² range 0.70 to 0.98; n = 6). Conclusion: Intentional insulin overdose is rare. Assessment of prognosis relies on clinical findings. The observed plasma insulin EC₅₀ is 46 mIU/l.