Dataset Information

Death adder envenoming causes neurotoxicity not reversed by antivenom--Australian Snakebite Project (ASP-16).

ABSTRACT:

Background

Death adders (Acanthophis spp) are found in Australia, Papua New Guinea and parts of eastern Indonesia. This study aimed to investigate the clinical syndrome of death adder envenoming and response to antivenom treatment.

Methodology/principal findings

Definite death adder bites were recruited from the Australian Snakebite Project (ASP) as defined by expert identification or detection of death adder venom in blood. Clinical effects and laboratory results were collected prospectively, including the time course of neurotoxicity and response to treatment. Enzyme immunoassay was used to measure venom concentrations. Twenty nine patients had definite death adder bites; median age 45 yr (5-74 yr); 25 were male. Envenoming occurred in 14 patients. Two further patients had allergic reactions without envenoming, both snake handlers with previous death adder bites. Of 14 envenomed patients, 12 developed neurotoxicity characterised by ptosis (12), diplopia (9), bulbar weakness (7), intercostal muscle weakness (2) and limb weakness (2). Intubation and mechanical ventilation were required for two patients for 17 and 83 hours. The median time to onset of neurotoxicity was 4 hours (0.5-15.5 hr). One patient bitten by a northern death adder developed myotoxicity and one patient only developed systemic symptoms without neurotoxicity. No patient developed venom induced consumption coagulopathy. Antivenom was administered to 13 patients, all receiving one vial initially. The median time for resolution of neurotoxicity post-antivenom was 21 hours (5-168). The median peak venom concentration in 13 envenomed patients with blood samples was 22 ng/mL (4.4-245 ng/mL). In eight patients where post-antivenom bloods were available, no venom was detected after one vial of antivenom.

Conclusions/significance

Death adder envenoming is characterised by neurotoxicity, which is mild in most cases. One vial of death adder antivenom was sufficient to bind all circulating venom. The persistent neurological effects despite antivenom, suggests that neurotoxicity is not reversed by antivenom.

SUBMITTER: Johnston CI

PROVIDER: S-EPMC3459885 | biostudies-literature | 2012

REPOSITORIES: biostudies-literature

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Publications

Death adder envenoming causes neurotoxicity not reversed by antivenom--Australian Snakebite Project (ASP-16).

Johnston Christopher I CI O'Leary Margaret A MA Brown Simon G A SG Currie Bart J BJ Halkidis Lambros L Whitaker Richard R Close Benjamin B Isbister Geoffrey K GK

PLoS neglected tropical diseases 20120927 9

<h4>Background</h4>Death adders (Acanthophis spp) are found in Australia, Papua New Guinea and parts of eastern Indonesia. This study aimed to investigate the clinical syndrome of death adder envenoming and response to antivenom treatment.<h4>Methodology/principal findings</h4>Definite death adder bites were recruited from the Australian Snakebite Project (ASP) as defined by expert identification or detection of death adder venom in blood. Clinical effects and laboratory results were collected p ...[more]

PMID: 23029595

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Project description:BackgroundCurrently, there is inadequate evidence on which to base clinical management of neurotoxic snakebite envenoming, especially in the choice of initial antivenom dosage. This randomised controlled trial compared the effectiveness and safety of high versus low initial antivenom dosage in victims of neurotoxic envenoming.Methodology/ principal findingsThis was a balanced, randomised, double-blind trial that was conducted in three health care centers located in the Terai plains of Nepal. Participants received either low (two vials) or high (10 vials) initial dosage of Indian polyvalent antivenom. The primary composite outcome consisted of death, the need for assisted ventilation and worsening/recurrence of neurotoxicity. Hourly evaluations followed antivenom treatment. Between April 2011 and October 2012, 157 snakebite victims were enrolled, of which 154 were analysed (76 in the low and 78 in the high initial dose group). Sixty-seven (43·5%) participants met the primary outcome definition. The proportions were similar in the low (37 or 48.7%) vs. high (30 or 38.5%) initial dose group (difference = 10·2%, 95%CI [-6·7 to 27·1], p = 0·264). The mean number of vials used was similar between treatment groups. Overall, patients bitten by kraits did worse than those bitten by cobras. The occurrence of treatment-related adverse events did not differ among treatment groups. A total of 19 serious adverse events occurred, including seven attributed to antivenom.ConclusionsThis first robust trial investigating antivenom dosage for neurotoxic snakebite envenoming shows that the antivenom currently used in Nepal performs poorly. Although the high initial dose regimen is not more effective than the low initial dose, it offers the practical advantage of being a single dose, while not incurring higher consumption or enhanced risk of adverse reaction. The development of new and more effective antivenoms that better target the species responsible for bites in the region will help improve future patients' outcomes.Trial registrationThe study was registered on clinicaltrials.gov (NCT01284855) (GJ 5/1).

Project description:BACKGROUND:Snakebite envenoming is a major public health problem throughout the rural tropics. Antivenom is effective in reducing mortality and remains the mainstay of therapy. This study aimed to determine the cost-effectiveness of using effective antivenoms for Snakebite envenoming in Nigeria. METHODOLOGY:Economic analysis was conducted from a public healthcare system perspective. Estimates of model inputs were obtained from the literature. Incremental Cost Effectiveness Ratios (ICERs) were quantified as deaths and Disability-Adjusted-Life-Years (DALY) averted from antivenom therapy. A decision analytic model was developed and analyzed with the following model base-case parameter estimates: type of snakes causing bites, antivenom effectiveness to prevent death, untreated mortality, risk of Early Adverse Reactions (EAR), mortality risk from EAR, mean age at bite and remaining life expectancy, and disability risk (amputation). End-user costs applied included: costs of diagnosing and monitoring envenoming, antivenom drug cost, supportive care, shipping/freezing antivenom, transportation to-and-from hospital and feeding costs while on admission, management of antivenom EAR and free alternative snakebite care for ineffective antivenom. PRINCIPAL FINDINGS:We calculated a cost/death averted of ($2330.16) and cost/DALY averted of $99.61 discounted and $56.88 undiscounted. Varying antivenom effectiveness through the 95% confidence interval from 55% to 86% yield a cost/DALY averted of $137.02 to $86.61 respectively. Similarly, varying the prevalence of envenoming caused by carpet viper from 0% to 96% yield a cost/DALY averted of $254.18 to $78.25 respectively. More effective antivenoms and carpet viper envenoming rather than non-carpet viper envenoming were associated with lower cost/DALY averted. CONCLUSIONS/SIGNIFICANCE:Treatment of snakebite envenoming in Nigeria is cost-effective with a cost/death averted of $2330.16 and cost/DALY averted of $99.61 discounted, lower than the country's gross domestic product per capita of $1555 (2013). Expanding access to effective antivenoms to larger segments of the Nigerian population should be a considered a priority.

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Project description:BackgroundSnakebite envenoming (SBE) is an acute, life-threatening emergency in tropical and subtropical countries. It is an occupational hazard and a major socioeconomic determinant. Limited awareness, superstitions, lack of trained health providers, poor utilization of anti-venom results in high mortality and morbidity. India is the snakebite capital of the world. Yet, information on awareness, knowledge, and perceptions about snakebite is limited. Data on capacity building of health systems and its potential impact is lacking. Recommended by the National Task Force on snakebite research in India, this protocol describes the National Snakebite Project aiming for capacity building of health systems on prevention and management of snakebite envenomation in Maharashtra and Odisha states.MethodsA cross-sectional, multi-centric study will be carried out in Shahapur, Aheri blocks of Maharashtra, and Khordha, Kasipur blocks of Odisha. The study has five phases: Phase I involves the collection of retrospective baseline data of snakebites, facility surveys, and community focus group discussions (FGDs). Phase II involves developing and implementing educational intervention programs for the community. Phase III will assess the knowledge and practices of the healthcare providers on snakebite management followed by their training in Phase IV. Phase V will evaluate the impact of the interventions on the community and healthcare system through FGDs and comparison of prospective and baseline data.DiscussionThe National Snakebite Project will use a multi-sectoral approach to reduce the burden of SBE. It intends to contribute to community empowerment and capacity building of the public healthcare system on the prevention and management of SBE. The results could be useful for upscaling to other Indian states, South Asia and other tropical countries. The findings of the study will provide critical regional inputs for the revision of the National Snakebite Treatment protocol.Trial registrationRegistered under the Clinical Trials Registry India no. CTRI/2021/11/038137.

Dataset Information

Death adder envenoming causes neurotoxicity not reversed by antivenom--Australian Snakebite Project (ASP-16).

Background

Methodology/principal findings

Conclusions/significance

Publications

Death adder envenoming causes neurotoxicity not reversed by antivenom--Australian Snakebite Project (ASP-16).

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