Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/97278
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Type: Journal article
Title: Death adder envenoming causes neurotoxicity not reversed by antivenom - Australian snakebite project (ASP-16)
Author: Johnston, C.
O'Leary, M.
Brown, S.
Currie, B.
Halkidis, L.
Whitaker, R.
Close, B.
Isbister, G.
Nagree, Y.
Ker, F.
Greene, S.
Taylor, M.
Macrokanis, C.
Wilke, G.
Coulson, A.
Barnes, C.
Bonni, R.
Whitake, R.
Halkidis, L.
Isbiste, G.
et al.
Citation: PLoS Neglected Tropical Diseases, 2012; 6(9):e1841-1-e1841-8
Publisher: PLoS
Issue Date: 2012
ISSN: 1935-2727
1935-2735
Statement of
Responsibility: 
Christopher I. Johnston, Margaret A. O, Leary, Simon G. A. Brown, Bart J. Currie, Lambros Halkidis, Richard Whitaker, Benjamin Close, Geoffrey K. Isbister, for the ASP investigators
Abstract: BACKGROUND: Death 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 FINDINGS: Definite 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/SIGNIFICANCE: Death 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.
Keywords: ASP Investigators; Animals; Humans; Elapidae; Nervous System Diseases; Snake Bites; Snake Venoms; Antivenins; Blood Chemical Analysis; Enzyme-Linked Immunosorbent Assay; Treatment Outcome; Respiration, Artificial; Intubation; Adolescent; Adult; Aged; Middle Aged; Child; Child, Preschool; Australia; Female; Male; Young Adult
Rights: © Johnston et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
RMID: 0030040063
DOI: 10.1371/journal.pntd.0001841
Grant ID: http://purl.org/au-research/grants/nhmrc/490305
http://purl.org/au-research/grants/nhmrc/605817
http://purl.org/au-research/grants/nhmrc/1023265
Appears in Collections:Medicine publications

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