First clinical experiences about the neurotoxic envenomings inflicted by lowland populations of the Balkan adder, Vipera berus bosniensis

Malina, Tamás; Krecsák, László; Jelić, Dušan; Maretić, Tomislav; Tóth, Tamás; Šiško, Marijan; Pandak, Nenad

doi:10.1016/j.neuro.2010.11.007

Cited by 23 publications

(17 citation statements)

References 10 publications

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“…Neuromuscular paralysis is classically a descending paralysis which initially involves the eye-lid muscles, clinically manifesting as bilateral ptosis, usually within a few hours of the bite. This is followed by external ophthalmoplegia and diplopia, facial muscle weakness [4,5,7,17] with slurred speech and difficulty in mouth opening [7,18]. The paralysis then descends to the neck muscles and bulbar muscles.…”

Section: Neuromuscular Paralysis In Snake Envenomingmentioning

confidence: 99%

Antivenom for Neuromuscular Paralysis Resulting From Snake Envenoming

Silva

Hodgson

2017

Toxins

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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.

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Section: Neuromuscular Paralysis In Snake Envenomingmentioning

confidence: 99%

Antivenom for Neuromuscular Paralysis Resulting From Snake Envenoming

Silva

Hodgson

2017

Toxins

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“…Haemoglobin may remain high at first, but anaemia may occur later [2,10,14]. Reports of neurotoxic effects [8,[15][16][17], systemic haemorrhage and coagulopathy at Vbb envenomation are rare [2,11].…”

Section: Introductionmentioning

confidence: 99%

Venomics of Vipera berus berus to explain differences in pathology elicited by Vipera ammodytes ammodytes envenomation: Therapeutic implications

Latinović

Leonardi

Šribar

et al. 2016

Journal of Proteomics

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“…Pero en las 2 ú ltimas dé cadas lo que antes era excepcional se ha convertido en habitual, y las manifestaciones neuroló gicas tras la mordedura de algunas de las especies de víbora á spid (V. aspis aspis, V. aspis zinnikeri) y víbora berus (V. berus bosniensis) han pasado a ser la norma, y desde muchos de los países de nuestro entorno se advierte de la gravedad de estas manifestaciones. Esta neurotoxicidad se achaca a la acció n de una fosfolipasa A 2 (PLA 2 ) [18][19][20][21][22][23][24] . Las diferentes isoenzimas de la PLA 2 pueden provocar hemó lisis, miotoxicidad, neurotoxicidad presiná ptica y postsiná ptica, cardiotoxicidad, edemas y actividad anti o procoagulante.…”

Section: Características Del Venenounclassified

“…En Españ a su uso se inició a principios del añ o 2000, pero ya llevaba tiempo empleá ndose en países de nuestro entorno, habié ndose constatado su seguridad 24,32,40,41 . Se trata de un antiveneno de tercera generació n, es decir, anticuerpos de caballo frente al veneno de varias especies de víboras (V. aspis, V. ammodytes y V. berus), tratados posteriormente con pepsinas para separar el fragmento F(ab) 2 del fragmento FC de los anticuerpos, siendo este ú ltimo el responsable de las reacciones anafilá cticas (tipo I) y por inmunocomplejos (tipo III), y por ello ya no es de esperar que las citadas complicaciones aparezcan 19,28,40,41 .…”

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Novedades en el envenenamiento por mordedura de víbora

Martín

Nogué

2015

Medicina Clínica

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First clinical experiences about the neurotoxic envenomings inflicted by lowland populations of the Balkan adder, Vipera berus bosniensis

Cited by 23 publications

References 10 publications

Antivenom for Neuromuscular Paralysis Resulting From Snake Envenoming

Antivenom for Neuromuscular Paralysis Resulting From Snake Envenoming

Venomics of Vipera berus berus to explain differences in pathology elicited by Vipera ammodytes ammodytes envenomation: Therapeutic implications

Novedades en el envenenamiento por mordedura de víbora

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