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Antivenom for Neuromuscular Paralysis Resulting From Snake Envenoming.
Toxins (Basel) 2017; 9(4)T

Abstract

Antivenom therapy is currently the standard practice for treating neuromuscular dysfunction in snake envenoming. We reviewed the clinical and experimental evidence-base for the efficacy and effectiveness of antivenom in snakebite neurotoxicity. The main site of snake neurotoxins is the neuromuscular junction, and the majority are either: (1) pre-synaptic neurotoxins irreversibly damaging the presynaptic terminal; or (2) post-synaptic neurotoxins that bind to the nicotinic acetylcholine receptor. Pre-clinical tests of antivenom efficacy for neurotoxicity include rodent lethality tests, which are problematic, and in vitro pharmacological tests such as nerve-muscle preparation studies, that appear to provide more clinically meaningful information. We searched MEDLINE (from 1946) and EMBASE (from 1947) until March 2017 for clinical studies. The search yielded no randomised placebo-controlled trials of antivenom for neuromuscular dysfunction. There were several randomised and non-randomised comparative trials that compared two or more doses of the same or different antivenom, and numerous cohort studies and case reports. The majority of studies available had deficiencies including poor case definition, poor study design, small sample size or no objective measures of paralysis. A number of studies demonstrated the efficacy of antivenom in human envenoming by clearing circulating venom. Studies of snakes with primarily pre-synaptic neurotoxins, such as kraits (Bungarus spp.) and taipans (Oxyuranus spp.) suggest that antivenom does not reverse established neurotoxicity, but early administration may be associated with decreased severity or prevent neurotoxicity. Small studies of snakes with mainly post-synaptic neurotoxins, including some cobra species (Naja spp.), provide preliminary evidence that neurotoxicity may be reversed with antivenom, but placebo controlled studies with objective outcome measures are required to confirm this.

Authors+Show Affiliations

Monash Venom Group, Department of Pharmacology, Biomedicine Discovery Institute, Monash University, Clayton, VIC 3800, Australia. anjana.silva@monash.edu. Faculty of Medicine and Allied Sciences, Rajarata University of Sri Lanka, Saliyapura 50008, Sri Lanka. anjana.silva@monash.edu.Monash Venom Group, Department of Pharmacology, Biomedicine Discovery Institute, Monash University, Clayton, VIC 3800, Australia. wayne.hodgson@monash.edu.Monash Venom Group, Department of Pharmacology, Biomedicine Discovery Institute, Monash University, Clayton, VIC 3800, Australia. geoff.isbister@gmail.com. Clinical Toxicology Research Group, University of Newcastle, Callaghan, NSW 2308, Australia. geoff.isbister@gmail.com.

Pub Type(s)

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

Language

eng

PubMed ID

28422078

Citation

Silva, Anjana, et al. "Antivenom for Neuromuscular Paralysis Resulting From Snake Envenoming." Toxins, vol. 9, no. 4, 2017.
Silva A, Hodgson WC, Isbister GK. Antivenom for Neuromuscular Paralysis Resulting From Snake Envenoming. Toxins (Basel). 2017;9(4).
Silva, A., Hodgson, W. C., & Isbister, G. K. (2017). Antivenom for Neuromuscular Paralysis Resulting From Snake Envenoming. Toxins, 9(4), doi:10.3390/toxins9040143.
Silva A, Hodgson WC, Isbister GK. Antivenom for Neuromuscular Paralysis Resulting From Snake Envenoming. Toxins (Basel). 2017 04 19;9(4) PubMed PMID: 28422078.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Antivenom for Neuromuscular Paralysis Resulting From Snake Envenoming. AU - Silva,Anjana, AU - Hodgson,Wayne C, AU - Isbister,Geoffrey K, Y1 - 2017/04/19/ PY - 2017/03/22/received PY - 2017/04/11/revised PY - 2017/04/13/accepted PY - 2017/4/20/entrez PY - 2017/4/20/pubmed PY - 2017/8/5/medline KW - antivenom KW - neurotoxicity KW - paralysis KW - snake envenoming JF - Toxins JO - Toxins (Basel) VL - 9 IS - 4 N2 - Antivenom therapy is currently the standard practice for treating neuromuscular dysfunction in snake envenoming. We reviewed the clinical and experimental evidence-base for the efficacy and effectiveness of antivenom in snakebite neurotoxicity. The main site of snake neurotoxins is the neuromuscular junction, and the majority are either: (1) pre-synaptic neurotoxins irreversibly damaging the presynaptic terminal; or (2) post-synaptic neurotoxins that bind to the nicotinic acetylcholine receptor. Pre-clinical tests of antivenom efficacy for neurotoxicity include rodent lethality tests, which are problematic, and in vitro pharmacological tests such as nerve-muscle preparation studies, that appear to provide more clinically meaningful information. We searched MEDLINE (from 1946) and EMBASE (from 1947) until March 2017 for clinical studies. The search yielded no randomised placebo-controlled trials of antivenom for neuromuscular dysfunction. There were several randomised and non-randomised comparative trials that compared two or more doses of the same or different antivenom, and numerous cohort studies and case reports. The majority of studies available had deficiencies including poor case definition, poor study design, small sample size or no objective measures of paralysis. A number of studies demonstrated the efficacy of antivenom in human envenoming by clearing circulating venom. Studies of snakes with primarily pre-synaptic neurotoxins, such as kraits (Bungarus spp.) and taipans (Oxyuranus spp.) suggest that antivenom does not reverse established neurotoxicity, but early administration may be associated with decreased severity or prevent neurotoxicity. Small studies of snakes with mainly post-synaptic neurotoxins, including some cobra species (Naja spp.), provide preliminary evidence that neurotoxicity may be reversed with antivenom, but placebo controlled studies with objective outcome measures are required to confirm this. SN - 2072-6651 UR - https://www.unboundmedicine.com/medline/citation/28422078/Antivenom_for_Neuromuscular_Paralysis_Resulting_From_Snake_Envenoming L2 - http://www.mdpi.com/resolver?pii=toxins9040143 DB - PRIME DP - Unbound Medicine ER -