Abstract
BackgroundDeath adders (Acanthophis spp) are found in Australia, Papua New Guinea and parts of eastern Indonesia. This study aimed to investigate the clinical syndrome of death adder envenoming and response to antivenom treatment.Methodology/Principal FindingsDefinite death adder bites were recruited from the Australian Snakebite Project (ASP) as defined by expert identification or detection of death adder venom in blood. Clinical effects and laboratory results were collected prospectively, including the time course of neurotoxicity and response to treatment. Enzyme immunoassay was used to measure venom concentrations. Twenty nine patients had definite death adder bites; median age 45 yr (5–74 yr); 25 were male. Envenoming occurred in 14 patients. Two further patients had allergic reactions without envenoming, both snake handlers with previous death adder bites. Of 14 envenomed patients, 12 developed neurotoxicity characterised by ptosis (12), diplopia (9), bulbar weakness (7), intercostal muscle weakness (2) and limb weakness (2). Intubation and mechanical ventilation were required for two patients for 17 and 83 hours. The median time to onset of neurotoxicity was 4 hours (0.5–15.5 hr). One patient bitten by a northern death adder developed myotoxicity and one patient only developed systemic symptoms without neurotoxicity. No patient developed venom induced consumption coagulopathy. Antivenom was administered to 13 patients, all receiving one vial initially. The median time for resolution of neurotoxicity post-antivenom was 21 hours (5–168). The median peak venom concentration in 13 envenomed patients with blood samples was 22 ng/mL (4.4–245 ng/mL). In eight patients where post-antivenom bloods were available, no venom was detected after one vial of antivenom.Conclusions/SignificanceDeath adder envenoming is characterised by neurotoxicity, which is mild in most cases. One vial of death adder antivenom was sufficient to bind all circulating venom. The persistent neurological effects despite antivenom, suggests that neurotoxicity is not reversed by antivenom.
Highlights
Death adders are a member of the snake family Elapidae
The study is a prospective cohort study of definite death adder (Acanthophis spp) bites recruited to the Australian Snakebite Project (ASP)
Of the 14 death adder bites that occurred in the wild, nine of them occurred in the evening/night between 6pm and 6am
Summary
Death adders (genus Acanthophis) are a member of the snake family Elapidae. They inhabit most of Australia (excluding Victoria and Tasmania), Papua New Guinea, Irian Jaya and the Indonesian islands of Seram, Halmahera, Obi and Tanimbar. Death adders are readily distinguishable from other Australian snakes by their ‘‘viperlike’’ appearance. They differ to other Australian elapids because they are ambush predators, being primarily active at night. Death adder venom has been the subject of considerable in vitro investigation and several venom components have been isolated and identified. This study aimed to investigate the clinical syndrome of death adder envenoming and response to antivenom treatment
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