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.
Highlights
Snakebite is a major public health concern in the tropics
This is well supported by clinical observations that neurotoxic snake envenoming almost exclusively results in flaccid paralysis [4,5,6,7,8,9,10,11,12] which is due to the blockade of neurotransmission at the neuromuscular junction by venom neurotoxins [13,14,15,16]
The efficacy of antivenom against a particular venom is due to the ability of antivenom molecules to bind with toxins in the venom [61]. i.e., with respect to neurotoxicity, this is the ability of the antivenom molecules to bind with the neurotoxins in the venom
Summary
Snakebite is a major public health concern in the tropics. An accurate figure of the burden of global snakebite is unavailable, an estimate of 5.5 million annual snakebites across the globe is considered realistic [1,2]. South and Southeast Asia, sub-Saharan Africa and Latin America are the most affected regions, with more than two-thirds of the global snakebite burden reported to arise from Asia [1]. Neuromuscular paralysis due to snake envenoming is common, including envenoming by elapid snakes such as kraits (genus: Bungarus), cobras (genus: Naja and Ophiophagus), coral snakes (genus: Calliophis and Micrurus), taipans (genus: Oxyuranus), tiger snakes (genus: Notechis) and death adders (genus: Acanthophis). Snake venom induced paralysis becomes life threatening with progressive paralysis of the bulbar and respiratory muscles which requires prompt airway assistance and mechanical ventilation [3]
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