The exact mechanisms of action of AC are not well defined, but the compound has been shown to have both a dose-dependent depressant and stimulant effect on the central nervous system (CNS) in various animal species and in humans (1). Intoxication may lead to sudden onset of lethargy, ataxia, hypersensitivity, muscle tremors, seizures and comatose state. Increased drooling, and symptoms of cranial nerve disorders such as contracted or dilated pupils is frequently described in reports on intoxication in humans and other animal species. In individuals where lethargy is present or consciousness is lost, bradycardia, hypotension, bradypnea and hypothermia may be present, and if not treated or reversed in time hypothermia could contribute to a lethal outcome (6, 1). As there is no antidote or specific treatment for AC intoxication, treatment is supportive and symptomatic, including maintaining a normal body temperature, minimising external stimuli and, when indicated, anticonvulsants (2).
The toxicity of AC, including lethal dose (LD50), is reported to vary between different species (table 1). The therapeutic index in cats has never been fully determined, although reports on use of AC as a feline anaesthetic are available. For example, Kullman et al. used continuous intravenous infusion of AC at a dose of 5mg/kg/h after an initial bolus of 65–75mg/kg as anaesthesia in cats used for experimental research not related to AC toxicosis (7).