Snake Bite
Written 3rd August 2020 - Last Update 23rd July 2026
Snake Bite
Rewritten (2026-07-23) against the current NSW Health Snake and Spider Bites Clinical Management guideline (GL2024_007, June 2024, 4th edition) — its major change from the 3rd edition (2013) is that snake venom detection kits (VDKs) are no longer recommended, reversing this note’s prior advice. Aligned with the current Australian Therapeutic Guidelines approach.
Epidemiology
Up to ~3000 snake bites occur in Australia each year; envenomation is rare (only a few hundred confirmed cases/year) and antivenom is required 100–200 times per year. 1–4 deaths annually, usually from brown snakes. Most bites occur in warmer months, in regional/rural areas, during activities like bushwalking and gardening. ~10% of bites occur in snake handlers — relevant when choosing antivenom, since the snake involved may not match those normally found in the region.
Clinical effects
In most bites, insufficient venom is injected to cause clinical effects (a “dry bite”). Local effects are not a major feature of Australian snake bites and don’t indicate severity — brown snake bites are often minimal locally despite being the most frequently lethal, whereas black and tiger snake bites more often cause local pain/swelling/bruising.
Systemic envenomation is indicated by:
- Non-specific symptoms — nausea, vomiting, headache, abdominal pain, diarrhoea, diaphoresis
- Sudden collapse — usually within an hour of the bite, often before hospital presentation; the leading cause of fatal envenomation
- Venom-induced consumption coagulopathy (VICC) — the most common severe complication, causing ~75% of antivenom administrations. A subset develop thrombotic microangiopathy (thrombocytopenia, haemolytic anaemia with schistocytes >1.0% on film, AKI) — most common with brown snakes
- Anticoagulant coagulopathy (ACC) — seen with black snake envenomation; no increased bleeding risk (unlike VICC)
- Neurotoxicity — descending flaccid paralysis, ptosis is the earliest sign
- Myotoxicity — regional myalgia/swelling, elevated CK, rarely rhabdomyolysis-related AKI
Snake type and typical picture
| Snake type | Major effect | Other effects | Geography |
|---|---|---|---|
| Brown snake | VICC | Often asymptomatic locally; thrombocytopenia | Mainland Australia |
| Tiger snake group* | VICC | Systemic symptoms, myotoxicity, neurotoxicity | South-eastern Australia |
| Hoplocephalus spp. (broad-headed, pale-headed, Stephen’s banded) | VICC | Often asymptomatic | South-eastern Australia |
| Red-bellied black snake | Systemic symptoms | ACC, myotoxicity | Eastern Australia |
| Death adder | Neurotoxicity | Systemic symptoms | Mainland Australia |
| Taipan | VICC, neurotoxicity | Systemic symptoms | Northern Australia |
| Mulga snake† | Myotoxicity, ACC | Systemic symptoms | Not eastern seaboard |
* Includes Notechis spp. and the rough-scaled/Clarence River tiger snake (Tropidechis carinatus). † Collett’s snake causes similar effects, almost exclusively in snake handlers.
First aid: pressure bandage with immobilisation (PBI)
Apply a broad (10–15 cm) elasticised bandage (preferred over crepe) directly over the bite site (do not remove clothing), then wrap distally then proximally to cover the whole limb — firm and tight, similar to a sprained ankle bandage (you shouldn’t be able to easily slide a finger underneath). Splint the limb and keep the patient still; monitor distal circulation.
- If an inadequate PBI is already in place, apply a new one over the top — do not remove it.
- PBI must stay on until the patient reaches a facility with antivenom, critical care/HDU and 24-hour pathology, and is only removed after antivenom is given, or clinical assessment plus formal laboratory (not point-of-care) results show no envenomation.
- Check/give a tetanus booster if the wound is tetanus-prone.
Assessment and diagnosis
The priority is determining whether envenomation has occurred — any sign requires antivenom. Early collapse strongly suggests severe brown-snake envenomation. Snake colour alone doesn’t reliably identify species.
Examine for: bite-site findings (if no PBI in place) and painful draining lymph nodes; bleeding from the bite/cannula/occult sites (GI, urinary, intracranial); neurotoxicity (ptosis, ophthalmoplegia, bulbar weakness, dysphagia, limb/respiratory weakness); non-specific systemic signs.
Investigations
Baseline bloods for all suspected bites: FBC + blood film, coagulation studies (INR, aPTT, fibrinogen, D-dimer), EUC, LFT, CK, LDH. Snake venom detection kits are no longer recommended (high false-positive rate, mostly operator error), and point-of-care (bedside) INR/D-dimer testing must not be used — both give false negatives in severe VICC; only formal laboratory testing is reliable. Antivenom choice is based on clinical effects and geography, not a VDK result.
Timing of serial bloods:
| Patient | Timing |
|---|---|
| Non-envenomed (normal baseline, asymptomatic) | 1 hour post-PBI-removal, then 6 hours, then 12 hours post-bite |
| Envenomed | 6, 12, 24, and (if needed) 36–48 hours post-bite; blood film + LDH at 6 or 12 hours if VICC present |
Non-envenomed disposition: observe for 12 hours from the time of the bite. If labs at 6 and 12 hours are normal and the patient feels well, discharge without follow-up is appropriate.
Antivenom timing
| Time since bite | Action |
|---|---|
| Within 6 hours | Antivenom recommended if signs of envenomation |
| 6–12 hours | Decision made in consultation with a clinical toxicologist |
| After 12 hours | Antivenom not generally recommended |
Early administration (ideally within 2 hours) is most effective at preventing/ limiting neurotoxicity, myotoxicity and AKI. Give antivenom to an obviously envenomed patient even at a smaller hospital (if anaphylaxis can be managed) without waiting for laboratory results or retrieval — consult a clinical toxicologist or the NSW/Australian Poisons Information Centre (13 11 26) before administering, to guide monovalent vs polyvalent antivenom choice by geography and clinical picture.
- Antivenom binds and neutralises venom but does not reverse already established effects — recovery depends on the body’s own repair (e.g. synthesising new clotting factors); giving more antivenom doesn’t speed this up and adds risk.
- Major bleeding with VICC is managed as any severe coagulopathy (FFP, surgical intervention); pre-emptive clotting factor replacement is not indicated.
- Uncomplicated VICC (INR <2) typically resolves in 24–48 hours; AKI from thrombotic microangiopathy can take weeks and may leave residual impairment.
Antivenom adverse effects
- Allergy/anaphylaxis — up to 25% have an allergic/anaphylactoid reaction; ~5% have a severe reaction with hypotension. Highest risk is in the first hour post-administration.
- Serum sickness — develops 4–14 days later: fever, rash, arthralgia, myalgia. For moderate–severe cases, prednisolone 25–50 mg daily for up to 7 days. Warn every antivenom recipient about this at discharge.
From eTG (Toxicology and Wilderness guideline) and NSW Health GL2024_007.