Snakebite in Australia: Moving from anecdotes to prospective studies

Currie, Bart J.

doi:10.1046/j.1442-2026.2003.00492.x

Cited by 9 publications

(13 citation statements)

References 5 publications

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“…The cut‐off values used to define abnormal results were: INR > 1.2, aPTT outside the reference range (depending on the individual laboratory), CK > 250 U/L, and WCC > 11.0 × 10 9 /L. Based on previous concerns about cases of isolated neurotoxicity occurring in death adder envenoming, 9 we included a neurological exam‐ination in cases of neurotoxicity as part of the analysis.…”

Section: Methodsmentioning

confidence: 99%

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Changes in serial laboratory test results in snakebite patients: when can we safely exclude envenoming?

Ireland

Brown

Buckley

et al. 2010

Medical Journal of Australia

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Objectives: To determine which laboratory tests are first associated with severe envenoming after a snakebite, when (ie, how long after the bite) the test results become abnormal, and whether this can determine a safe observation period after suspected snakebite. Design, patients and setting: Prospective cohort study of 478 patients with suspected or confirmed snakebite recruited to the Australian Snakebite Project from January 2002 to April 2009, who had at least three sets of laboratory test results and at least 12 hours of observation in hospital after the bite. Severe envenoming was defined as venom‐induced consumption coagulopathy (VICC), myotoxicity, neurotoxicity or thrombotic microangiopathy. Main outcome measures: International normalised ratio (INR), activated partial thromboplastin time (aPTT), creatine kinase (CK) level, and neurological examination. Results: There were 240 patients with severe envenoming, 75 with minor envenoming and 163 non‐envenomed patients. Of 206 patients with VICC, 178 had an INR > 1.2 (abnormal) on admission, and the remaining 28 had an INR > 1.2 within 12 hours of the bite. Of 33 patients with myotoxicity, a combination of CK > 250 U/L and an abnormal aPTT identified all but two cases by 12 hours; one of these two was identified within 12 hours by leukocytosis. Nine cases of isolated neurotoxicity had a median time of onset after the bite of 4 hours (range, 35 min – 12 h). The combination of serial INR, aPTT and CK tests and repeated neurological examination identified 213 of 222 severe envenoming cases (96%) by 6 hours and 238 of 240 (99%) by 12 hours. Conclusion: Laboratory parameters (INR, aPTT and CK) and neurological reassessments identified nearly all severe envenoming cases within 12 hours of the bite, even in this conservative analysis that assumed normal test results if the test was not done.

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Section: Methodsmentioning

confidence: 99%

“…‐ 8 According to one study from southern Queensland, some hospitals discharge asymptomatic patients with normal blood test results 4 to 6 hours after the bite. However, the study included only 34 envenomed patients, and there are concerns about its applicability to other geographical regions 9 …”

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confidence: 99%

Changes in serial laboratory test results in snakebite patients: when can we safely exclude envenoming?

Ireland

Brown

Buckley

et al. 2010

Medical Journal of Australia

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“…Its combination with the previous mechanical approach (PIB and LCPI) might additionally delay the venom movement in the body fluids. To evaluate the efficacy of these first aid measures, prospective, comparative, randomized, and controlled clinical studies (Currie, 2003;Currie et al, 2008) should be carried out that involve identified bites by several species of venomous snake. Such studies could resolve questions of efficacy, application difficulties, and possibilities of improvements in existing first aid techniques, to make them effective and affordable.…”

Section: Discussionmentioning

confidence: 99%

Inclusion of incorrect information on snakebite first aid in school and university teaching materials in Nepal

P¹

2013

J. Toxicol. Environ. Health Sci.

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In previous studies in Nepal, snakebite victims were found to either not have Pressure Immobilization Bandaging (PIB) or Local Compression Pad Immobilization (LCPI) performed for first aid, or had it performed incorrectly. The goal of this study was to evaluate training texts regarding first aid measures for snakebite and the rates of performance of both methods currently recommended, as well as ineffective or harmful practices. The study was conducted from September, 2009 to November, 2010. It evaluated the venomous snakebite first aid measures recommended in the 31 most recently published and commonly used Nepalese reference works and textbooks aimed at paramedical personnel, primary health care workers, medical undergraduates, and students of class five to bachelor´s degree. It compared the suggestions of these with those of published guidelines for the management of snakebite envenomation. Up to 100% of first aid measures advocated in these materials differed significantly from published guidelines. This included the omission of appropriate activities, misstatements and prescription of inappropriate treatments. Among appropriate recommendations that were missing was the advice to apply PIB or LCPI, and the suggestion to go to a snakebite treatment center. Fifty-five percent of the references did recommend emergency transport. Inclusion of accurate evidence-based information regarding first aid measures for venomous snakebite in commonly used texts could help to reduce the application of ineffective or harmful pre-hospital practices, their associated morbidity and mortality, and increase the use of appropriate methods.

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“…More recent studies have found myotoxicity present in the directly-stimulated chick biventer cervicis nerve-muscle (CBCNM) preparation after incubation with some species of death adder, however A. antarcticus whole venom was devoid of myotoxic activity [8]. Significantly, delayed-onset neurotoxicity is a problem in death adder envenomations, occasionally with late presentation of neurotoxicity as the first feature of envenoming [2,9,10]. This has resulted in a recommended hospital admission period of 24 hours for patients in Papua New Guinea and both central and northern Australia, and for children in any region [11].…”

Section: Introductionmentioning

confidence: 99%

Characterisation of the heterotrimeric presynaptic phospholipase A2 neurotoxin complex from the venom of the common death adder (Acanthophis antarcticus)

Blacklow

Escoubas

Nicholson

2010

Biochemical Pharmacology

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While Australo-Papuan death adder neurotoxicity is generally considered to be due to the actions of reversible competitive postsynaptic alpha-neurotoxins, the neurotoxic effects are often poorly reversed by antivenom or anticholinesterases. This suggests that the venom may contain a snake presynaptic phospholipase A(2) (PLA(2)) neurotoxin (SPAN) that binds irreversibly to motor nerve terminals to inhibit neurotransmitter release. Using size-exclusion liquid chromatography under non-reducing conditions, we report the isolation and characterisation of a high molecular mass SPAN complex, P-elapitoxin-Aa1a (P-EPTX-Aa1a), from the venom of the common death adder Acanthophis antarcticus. Using the chick biventer-cervicis nerve-muscle preparation, P-EPTX-Aa1a (44,698Da) caused inhibition of nerve-evoked twitch contractions while responses to cholinergic agonists and KCl remained unaffected. P-EPTX-Aa1a also produced significant fade in tetanic contractions and a triphasic timecourse of neuromuscular blockade. These actions are consistent with other SPANs that inhibit acetylcholine release. P-EPTX-Aa1a was found to be a heterotrimeric complex composed of alpha, beta and gamma-subunits in a 1:1:1 stoichiometry with each subunit showing significant N-terminal sequence homology to the subunits of taipoxin, a SPAN from Oxyuranus s. scutellatus. Like taipoxin, only the alpha-chain produced any signs of neurotoxicity or displayed significant PLA(2) enzymatic activity. Preincubation with monovalent death adder antivenom or suramin, or inhibition of PLA(2) activity by incubation with 4-bromophenacyl bromide, either prevented or significantly delayed the onset of toxicity by P-EPTX-Aa1a. However, antivenom failed to reverse neurotoxicity. Early intervention with antivenom may therefore be important in severe cases of envenomation by A. antarcticus, given the presence of potent irreversible presynaptic neurotoxins.

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Snakebite in Australia: Moving from anecdotes to prospective studies

Cited by 9 publications

References 5 publications

Changes in serial laboratory test results in snakebite patients: when can we safely exclude envenoming?

Changes in serial laboratory test results in snakebite patients: when can we safely exclude envenoming?

Inclusion of incorrect information on snakebite first aid in school and university teaching materials in Nepal

Characterisation of the heterotrimeric presynaptic phospholipase A2 neurotoxin complex from the venom of the common death adder (Acanthophis antarcticus)

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