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Death adder envenoming causes neurotoxicity not reversed by antivenom--Australian Snakebite Project (ASP-16).
PLoS Negl Trop Dis 2012; 6(9):e1841PN

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.

Authors+Show Affiliations

School of Medicine Sydney, University of Notre Dame Australia, Darlinghurst, New South Wales, Australia.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

23029595

Citation

Johnston, Christopher I., et al. "Death Adder Envenoming Causes Neurotoxicity Not Reversed By antivenom--Australian Snakebite Project (ASP-16)." PLoS Neglected Tropical Diseases, vol. 6, no. 9, 2012, pp. e1841.
Johnston CI, O'Leary MA, Brown SG, et al. Death adder envenoming causes neurotoxicity not reversed by antivenom--Australian Snakebite Project (ASP-16). PLoS Negl Trop Dis. 2012;6(9):e1841.
Johnston, C. I., O'Leary, M. A., Brown, S. G., Currie, B. J., Halkidis, L., Whitaker, R., ... Isbister, G. K. (2012). Death adder envenoming causes neurotoxicity not reversed by antivenom--Australian Snakebite Project (ASP-16). PLoS Neglected Tropical Diseases, 6(9), pp. e1841. doi:10.1371/journal.pntd.0001841.
Johnston CI, et al. Death Adder Envenoming Causes Neurotoxicity Not Reversed By antivenom--Australian Snakebite Project (ASP-16). PLoS Negl Trop Dis. 2012;6(9):e1841. PubMed PMID: 23029595.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Death adder envenoming causes neurotoxicity not reversed by antivenom--Australian Snakebite Project (ASP-16). AU - Johnston,Christopher I, AU - O'Leary,Margaret A, AU - Brown,Simon G A, AU - Currie,Bart J, AU - Halkidis,Lambros, AU - Whitaker,Richard, AU - Close,Benjamin, AU - Isbister,Geoffrey K, AU - ,, Y1 - 2012/09/27/ PY - 2012/06/25/received PY - 2012/08/16/accepted PY - 2012/10/3/entrez PY - 2012/10/3/pubmed PY - 2013/1/29/medline SP - e1841 EP - e1841 JF - PLoS neglected tropical diseases JO - PLoS Negl Trop Dis VL - 6 IS - 9 N2 - 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. SN - 1935-2735 UR - https://www.unboundmedicine.com/medline/citation/23029595/Death_adder_envenoming_causes_neurotoxicity_not_reversed_by_antivenom__Australian_Snakebite_Project__ASP_16__ L2 - http://dx.plos.org/10.1371/journal.pntd.0001841 DB - PRIME DP - Unbound Medicine ER -