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Neuromuscular Effects of Common Krait (Bungarus caeruleus) Envenoming in Sri Lanka
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نویسنده
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silva a. ,maduwage k. ,sedgwick m. ,pilapitiya s. ,weerawansa p. ,dahanayaka n.j. ,buckley n.a. ,johnston c. ,siribaddana s. ,isbister g.k.
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منبع
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plos neglected tropical diseases - 2016 - دوره : 10 - شماره : 2
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چکیده
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Objective: we aimed to investigate neurophysiological and clinical effects of common krait envenoming,including the time course and treatment response. methodology: patients with definite common krait (bungarus caeruleus) bites were recruited from a sri lankan hospital. all patients had serial neurological examinations and stimulated concentric needle single-fibre electromyography (sfemg) of orbicularis oculi in hospital at 6wk and 6–9mth post-bite. principal findings: there were 33 patients enrolled (median age 35y; 24 males). eight did not develop neurotoxicity and had normal sfemg. eight had mild neurotoxicity with ptosis,normal sfemg; six received antivenom and all recovered within 20–32h. seventeen patients developed severe neurotoxicity with rapidly descending paralysis,from ptosis to complete ophthalmoplegia,facial,bulbar and neck weakness. all 17 received indian polyvalent antivenom a median 3.5h post-bite (2.8–7.2h),which cleared unbound venom from blood. despite this,the paralysis worsened requiring intubation and ventilation within 7h post-bite. sfemg showed markedly increased jitter and neuromuscular blocks within 12h. sfemg abnormalities gradually improved over 24h,corresponding with clinical recovery. muscle recovery occurred in ascending order. myotoxicity was not evident,clinically or biochemically,in any of the patients. patients were extubated a median 96h post-bite (54–216h). on discharge,median 8 days (4–12days) post-bite,patients were clinically normal but had mild sfemg abnormalities which persisted at 6wk post-bite. there were no clinical or neurophysiological abnormalities at 6–9mth. conclusions: common krait envenoming causes rapid onset severe neuromuscular paralysis which takes days to recover clinically consistent with sfemg. subclinical neuromuscular dysfunction lasts weeks but was not permanent. antivenom effectively cleared venom but did not prevent worsening or reverse neuromuscular paralysis. © 2016 silva et al.
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آدرس
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monash venom group,department of pharmacology,monash university,clayton,vic,australia,faculty of medicine and allied sciences,rajarata university of sri lanka,saliyapura,sri lanka,south asian clinical toxicology research collaboration,university of peradeniya,peradeniya, Sri Lanka, south asian clinical toxicology research collaboration,university of peradeniya,peradeniya,sri lanka,clinical toxicology research group,university of newcastlensw, Australia, south asian clinical toxicology research collaboration,university of peradeniya,peradeniya, Sri Lanka, faculty of medicine and allied sciences,rajarata university of sri lanka,saliyapura, Sri Lanka, faculty of medicine and allied sciences,rajarata university of sri lanka,saliyapura, Sri Lanka, faculty of medicine and allied sciences,rajarata university of sri lanka,saliyapura, Sri Lanka, south asian clinical toxicology research collaboration,university of peradeniya,peradeniya,sri lanka,clinical pharmacology,university of sydney,sydney, Australia, clinical toxicology research group,university of newcastlensw, Australia, faculty of medicine and allied sciences,rajarata university of sri lanka,saliyapura, Sri Lanka, south asian clinical toxicology research collaboration,university of peradeniya,peradeniya,sri lanka,clinical toxicology research group,university of newcastlensw, Australia
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Authors
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