Anjana Silva1,2,3, Kalana Maduwage3,4, Michael Sedgwick3, Senaka Pilapitiya2, Prasanna Weerawansa2, Niroshana J Dahanayaka2, Nicholas A Buckley3,5, Sisira Siribaddana2, Geoffrey K Isbister3,4. 1. a Monash Venom Group, Department of Pharmacology , Monash University , Clayton , VIC , Australia ; 2. b Faculty of Medicine and Allied Sciences , Rajarata University of Sri Lanka , Saliyapura , Sri Lanka ; 3. c South Asian Clinical Toxicology Research Collaboration , University of Peradeniya, Peradeniya , Sri Lanka ; 4. d Clinical Toxicology Research Group , University of Newcastle , Callaghan , NSW , Australia ; 5. e Clinical Pharmacology , University of Sydney , Sydney , NSW , Australia.
Abstract
CONTEXT: Russell's viper is more medically important than any other Asian snake, due to number of envenoming's and fatalities. Russell's viper populations in South India and Sri Lanka (Daboia russelii) cause unique neuromuscular paralysis not seen in other Russell's vipers. OBJECTIVE: To investigate the time course and severity of neuromuscular dysfunction in definite Russell's viper bites, including antivenom response. METHODOLOGY: We prospectively enrolled all patients (>16 years) presenting with Russell's viper bites over 14 months. Cases were confirmed by snake identification and/or enzyme immunoassay. All patients had serial neurological examinations and in some, single fibre electromyography (sfEMG) of the orbicularis oculi was performed. RESULTS: 245 definite Russell's viper bite patients (median age: 41 years; 171 males) presented a median 2.5 h (interquartile range: 1.75-4.0 h) post-bite. All but one had local envenoming and 199 (78%) had systemic envenoming: coagulopathy in 166 (68%), neurotoxicity in 130 (53%), and oliguria in 19 (8%). Neurotoxicity was characterised by ptosis (100%), blurred vision (93%), and ophthalmoplegia (90%) with weak extraocular movements, strabismus, and diplopia. Neurotoxicity developed within 8 h post-bite in all patients. No bulbar, respiratory or limb muscle weakness occurred. Neurotoxicity was associated with bites by larger snakes (p < 0.0001) and higher peak serum venom concentrations (p = 0.0025). Antivenom immediately decreased unbound venom in blood. Of 52 patients without neurotoxicity when they received antivenom, 31 developed neurotoxicity. sfEMG in 27 patients with neurotoxicity and 23 without had slightly elevated median jitter on day 1 compared to 29 normal subjects but normalised thereafter. Neurological features resolved in 80% of patients by day 3 with ptosis and weak eye movements resolving last. No clinical or neurophysiological abnormality was detected at 6 weeks or 6 months. CONCLUSION: Sri Lankan Russell's viper envenoming causes mild neuromuscular dysfunction with no long-term effects. Indian polyvalent antivenom effectively binds free venom in blood but does not reverse neurotoxicity.
CONTEXT: Russell's viper is more medically important than any other Asian snake, due to number of envenoming's and fatalities. Russell's viper populations in South India and Sri Lanka (Daboia russelii) cause unique neuromuscular paralysis not seen in other Russell's vipers. OBJECTIVE: To investigate the time course and severity of neuromuscular dysfunction in definite Russell's viper bites, including antivenom response. METHODOLOGY: We prospectively enrolled all patients (>16 years) presenting with Russell's viper bites over 14 months. Cases were confirmed by snake identification and/or enzyme immunoassay. All patients had serial neurological examinations and in some, single fibre electromyography (sfEMG) of the orbicularis oculi was performed. RESULTS: 245 definite Russell's viper bite patients (median age: 41 years; 171 males) presented a median 2.5 h (interquartile range: 1.75-4.0 h) post-bite. All but one had local envenoming and 199 (78%) had systemic envenoming: coagulopathy in 166 (68%), neurotoxicity in 130 (53%), and oliguria in 19 (8%). Neurotoxicity was characterised by ptosis (100%), blurred vision (93%), and ophthalmoplegia (90%) with weak extraocular movements, strabismus, and diplopia. Neurotoxicity developed within 8 h post-bite in all patients. No bulbar, respiratory or limb muscle weakness occurred. Neurotoxicity was associated with bites by larger snakes (p < 0.0001) and higher peak serum venom concentrations (p = 0.0025). Antivenom immediately decreased unbound venom in blood. Of 52 patients without neurotoxicity when they received antivenom, 31 developed neurotoxicity. sfEMG in 27 patients with neurotoxicity and 23 without had slightly elevated median jitter on day 1 compared to 29 normal subjects but normalised thereafter. Neurological features resolved in 80% of patients by day 3 with ptosis and weak eye movements resolving last. No clinical or neurophysiological abnormality was detected at 6 weeks or 6 months. CONCLUSION: Sri Lankan Russell's viper envenoming causes mild neuromuscular dysfunction with no long-term effects. Indian polyvalent antivenom effectively binds free venom in blood but does not reverse neurotoxicity.
Entities:
Keywords:
Antivenom; Daboia russelii; paralysis; single fibre electromyography
Authors: Anjana Silva; Sanjaya Kuruppu; Iekhsan Othman; Robert J A Goode; Wayne C Hodgson; Geoffrey K Isbister Journal: Neurotox Res Date: 2016-07-11 Impact factor: 3.911
Authors: Kalana Maduwage; Anjana Silva; Margaret A O'Leary; Wayne C Hodgson; Geoffrey K Isbister Journal: Sci Rep Date: 2016-05-27 Impact factor: 4.379
Authors: Anjana Silva; Christopher Johnston; Sanjaya Kuruppu; Daniela Kneisz; Kalana Maduwage; Oded Kleifeld; A Ian Smith; Sisira Siribaddana; Nicholas A Buckley; Wayne C Hodgson; Geoffrey K Isbister Journal: PLoS Negl Trop Dis Date: 2016-12-02