Design, setting and participants: We conducted a prospective cohort study within the Australian Snakebite Project, reviewing all definite tiger snake envenoming cases between October 2004 and June 2011. Definite cases were identified by venom-specific enzyme immunoassay or expert snake identification.
Results: Fifty-six definite tiger snake envenomings were identified. Clinical effects included venom-induced consumption coagulopathy (VICC) (n = 53), systemic symptoms (n = 45), myotoxicity (n = 11) and neurotoxicity (n = 17). Thrombotic microangiopathy occurred in three patients, all of whom developed acute renal failure. There were no deaths. A bite-site snake venom detection kit test was done in 44 patients, but was positive for tiger snake in only 33 cases. Fifty-three patients received TSAV and eight of these patients had immediate hypersensitivity reactions, severe enough in one case to satisfy diagnostic criteria for severe anaphylaxis. The median peak venom concentration in 50 patients with pretreatment blood samples available was 3.2 ng/mL (interquartile range [IQR], 1–12 ng/mL; range 0.17–152 ng/mL). In 49 patients with post-treatment blood samples available, no venom was detected in serum after the first antivenom dose. Ten patients were given 1 vial of TSAV; the median dose was 2 vials (range, 1–4 vials). Pretreatment serum venom concentrations did not vary significantly between patients given 1 vial of TSAV and those given 2 or more vials.
Conclusion: Tiger snake envenoming causes VICC, systemic symptoms, neurotoxicity and myotoxicity. One vial of TSAV, the dose originally recommended when the antivenom was first made available, appears to be sufficient to bind all circulating venom.
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