Neuromuscular Paralysis in Snake Envenoming Snake venom induced paralysis becomes life threatening with progressive paralysis of the bulbar and respiratory muscles which requires prompt airway assistance and mechanical ventilation. 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). 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. Although 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. Snakebite is a major public health concern in the tropics. Keywords: snake envenoming, paralysis, antivenom, 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. 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. A number of studies demonstrated the efficacy of antivenom in human envenoming by clearing circulating venom. The majority of studies available had deficiencies including poor case definition, poor study design, small sample size or no objective measures of paralysis. 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 search yielded no randomised placebo-controlled trials of antivenom for neuromuscular dysfunction. ![]() We searched MEDLINE (from 1946) and EMBASE (from 1947) until March 2017 for clinical studies. 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. 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. We reviewed the clinical and experimental evidence-base for the efficacy and effectiveness of antivenom in snakebite neurotoxicity. IsbisterĪntivenom therapy is currently the standard practice for treating neuromuscular dysfunction in snake envenoming. “This is just my hypothesis,” the coroner said.Īntivenom for Neuromuscular Paralysis Resulting From Snake EnvenomingĪnjana Silva, Wayne C. The pathologist hands the investigator a snippet of some articles to read.
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