Summary For more than 50 years, ketamine has proven to be a safe anesthetic drug with potent analgesic properties. The active enantiomer is S(+)‐ketamine. Ketamine is mostly metabolized in norketamine, an active metabolite. During “dissociative anesthesia”, sensory inputs may reach cortical receiving areas, but fail to be perceived in some association areas. Ketamine also enhances the descending inhibiting serotoninergic pathway and exerts antidepressive effects. Analgesic effects persist for plasma concentrations ten times lower than hypnotic concentrations. Activation of the (N‐Methyl‐D‐Aspartate [NMDA]) receptor plays a fundamental role in long‐term potentiation but also in hyperalgesia and opioid‐induced hyperalgesia. The antagonism of NMDA receptor is responsible for ketamine's more specific properties. Ketamine decreases the “wind up” phenomenon, and the antagonism is more important if the NMDA channel has been previously opened by the glutamate binding (“use dependence”). Experimentally, ketamine may promote neuronal apoptotic lesions but, in usual clinical practice, it does not induce neurotoxicity. The consequences of high doses, repeatedly administered, are not known. Cognitive disturbances are frequent in chronic users of ketamine, as well as frontal white matter abnormalities. Animal studies suggest that neurodegeneration is a potential long‐term risk of anesthetics in neonatal and young pediatric patients.

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: Hemostasis disorders are one of the major clinical conditions of snakebites and are because of mechanisms which may disrupt vessels, platelets, clotting factors and fibrinolysis. Thromboelastography (TEG) could help to understand these effects in the clinical practice. A retrospective study reports a series of patients presenting a snakebite-related coagulopathy, treated with antivenom and monitored with conventional tests and TEG in a French military treatment facility (Republic of Djibouti, East Africa) between August 2011 and September 2013. Conventional coagulation assays (platelets, prothrombin time, activated partial thromboplastin time, fibrinogen) and TEG measurements were taken on arrival and at various times during the first 72 h of hospitalization, at the discretion of the physician. The study included 14 patients (median age 28 years). Bleedings were present in five patients. All patients received antivenom. A coagulopathy was present in all patients and was detected by both conventional assays and TEG. None exhibited thrombocytopenia. Prothrombin time and fibrinogen remained abnormal for most of patients during the first 72 h. The TEG profiles of 11 patients (79%) showed incoagulability at admission (R-time > 60 min). TEG distinguished 10 patients with a generalized clotting factor deficiency and 4 patients with an isolated fibrinogen deficiency after an initial profile of incoagulability. Hyperfibrinolysis was evident for 12 patients (86%) after Hour 6. Snake envenomations in Djibouti involve a consumption coagulopathy in conjunction with delayed hyperfibrinolysis. TEG could improve medical management of the condition and assessment of additional therapeutics associated with the antivenom.

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Hypertonic saline improves organ perfusion and animal survival during hemorrhagic shock because it expands plasma volume and increases tissue oxygenation. Because both decreased and increased myocardial performance have been reported with hypertonic saline, the effects of hyperosmolarity and the mechanism accounting for it were investigated in isolated blood-perfused rabbit hearts. Coronary blood flow (CBF), myocardial contractility, relaxation, and oxygen consumption were measured during administration of blood perfusates containing 140-180 mmol sodium concentrations ([Na+]). In two other series of experiments, the role of Na(+)-Ca2+ exchange in the inotropic effect of hyperosmolarity (160 mmol sodium concentration) and hypertonicity (sucrose) were also investigated. Hypertonic [Na+] induced a significant increase in contractility and relaxation, combined with a coronary vasodilation. Myocardial oxygen consumption (MVO2) increased at all hypertonic [Na+] without significant change in coronary venous oxygen tension (PVO2) and content (CVO2). Amiloride (0.3 mmol) inhibited the improved contractility observed with 160 mmol sodium. Similar Na(+)-Ca2+ exchanger blockade did not inhibit the inotropic effect of sucrose. These results confirm the positive inotropic effect of hypertonic [Na+]. The inhibition of this improvement by amiloride suggests that calcium influx through the sarcolemna could be the major mechanism of this effect.

Pain was reduced or abolished in two-thirds of patients under ketamine therapy; ketamine was effective for patients taking opioids and resulted in few adverse effects.