Dr Nick Erskine
Emergency Registrar
Peer review / Editor: Dr Hector Thomson | Dr David McCreary
I grew up in New Zealand and therefore snakebites were never something that particularly crossed my mind. I was far more afraid of falling into quicksand or tripping a yellow barrel of radioactive green sludge than I was of creepy crawlies.
However, since migrating across the ditch, my need to fear and understand venom-induced consumptive coagulopathies has grown. In fact, diving into toxinology study may have well driven me back to the safety of New Zealand if not for the discovery of a cannibalistic New Zealand sea-slug that’s riddled with tetrodotoxin.
Let’s talk about Snakes, baby
Despite Australia’s reputation for being fraught with deadly animals, snake bites are a relatively rare event here. Exact estimates vary, but the incidence is in the ballpark of 3 envenomations per 100,000 people per year.[1, 2]
Importantly, most snakebites in Australia do not result in envenomation [3]. This may either be from a non-venomous snakebite, or from a “dry bite” by a venomous snake where insufficient venom is injected to cause envenomation in a person.
Whilst there are dozens (and dozens and dozens!) of different snakes in Australia the big ones we are concerned about when it comes to envenomation are
Black Snake Group (Pseudochis)
Brown Snake (Pseudonaja)
Death Adder (Acanthophis)
Sea Snake (Hydrophiliadae)
Taipan Snake (Oxyuranus)
Tiger Snake Group (Notechis)
It is rare that someone can reliably tell you which snake bit them (snake handlers undergoing workplace accidents excepted). We all know of cases where malicious sticks on the ground have stabbed someone in the ankle whilst an innocent snake happened to be nearby.
Rather than relying on the patient’s blurred description of colours and patterns, take guidance from the environment around you and the toxidrome before you.
Wherefore art my snake?
Every state has different endemic snake populations, and you’ll likely be able to tell which snakes are around by which types of snake antivenom you keep in stock in your ED.
In broad strokes for those planning an interstate vacation
Black Snake Group – Most of Australia except Tasmania and the South Coast
Brown Snake Group – Most of Australia except Tasmania
Death Adder – Most of Australia except Tasmania, Victoria, and the southern parts of Western Australia
Sea Snake – In the sea (again, excepting some of Tasmania and a good chunk of the South Coast)
Taipan – Northern and Central Australia
Tiger – Southern Australia and Tasmania
However, with the exception of the Bass Strait, borders are largely just guidelines for snakes so it’s not impossible to find snakes outside their home turfs.
Additionally, snake wranglers and handlers can bring different species all over Australia so it’s worth understanding the toxidromes you may come across irrespective of which AFL team you support.
What to expect when you’re expecting (an envenomated patient)
After the initial snakebite, the patient may notice localised symptoms at the bite site (E.g. pain, muscle tenderness).
As the venom spreads through the lymphatic system people may develop non-specific systemic features (E.g. nausea, vomiting, abdominal pain, diarrhoea, diaphoresis, headache) before proceeding to specific systemic envenomation.
To mitigate the spread of venom through the lymphatics (and therefore reduce the risk of systemic envenomation) a pressure bandage immobiliser (PBI) should be placed within the first four hours of the bite. This should not be removed until certain criteria are met (stay tuned for that later in the post)
Despite the early application of a PIB, people can still progress to specific snake envenomation syndromes. The features of which can be grouped into
1) Cardiovascular Collapse
- Syncope (often within one hour of the bite)
- Hypotension (that may spontaneously resolve before medical contact)
- Rarely (<5%) cardiac arrest
2) Coagulopathy
Venom Induced Consumptive Coagulopathic (VICC)
Prothrombin activator toxins cause widespread activation of the clotting cascade and a consumptive coagulopathy
Extremely high (or unrecordable) INR
Extremely low (or unrecordable) fibrinogen
Extremely high D-Dimer (usually >100x normal)
Associated with Microcytic Microangiopathy – a haemolytic anaemia, thrombocytopenia, and acute kidney injury
Partial VICC
Anticoagulant Coagulopathy
3) Myotoxicity
- Localised or systemic myalgias or muscle tenderness
- Biochemical evidence of Rhabdomyolysis (rising CK) can lag by up to 24 hours
- Hyperkalaemia and renal impairment in severe cases
4) Neurotoxicity
- Descending flaccid paralysis
- Eyes (Ophthalmoplegia, ptosis) -> Bulbar Palsy -> Respiratory -> Limb paralysis
But which envenomation goes with which snake?
This is one of those situations where ultimately you just have to rote learn some patterns. Perhaps one day there’ll be a SnakeGPT app that uses AI to determine things for you, but in the meantime, we rely on that gigantic medical brain you’ve spent years developing.
The most important trio of snakes to learn about are the ones that cause VICC, as they’re responsible for nearly 90% of our need for antivenom across Australian EDs.[3]
The Brown, Tiger, and Taipan snakes are the three groups that cause VICC. I listed them non-alphabetically to save the best for last. The Taipan snake not only causes VICC but also causes neurotoxicity. A two-for-one deal for our colleagues in Northern and Central Australia.
Continuing with the Neurotoxicity theme is the Death Adder. Death Adders don’t cause any form of coagulopathy but (alongside the Taipan) will cause a neurotoxic descending paralysis.
Jumping over to the Myotoxicity category you’ll find the Sea Snakes and the Black Snake Groups. Sea Snakes are probably the one time where a patient’s description of the snake does help determine which one bit them (“It was in the ocean, doc”). Helpfully, the black snake group are the only Australian snakes to commonly give you the heparin-like “Anticoagulant Coagulopathy”. So, if it comes from the sea or prolongs your APTT, think myotoxicity.
And finally, the snake that makes you collapse – the brown snake. We touched on this cheeky fella in the VICC category already. I flag it separately within Cardiovascular because it can be the early clue that a brown snake has been involved. Nearly a third of Brown Snake envenomed patients have a syncope early in the envenomation process, significantly higher than any of the other ones on the list.
(Adapted from Ibister GK, Brown SGA, Page CB et al Snakebite in Australia: a practical approach to diagnosis and treatment Med J Aust 2013; 199 (11): 763-768)
Envenomation kits – or how to occupy a distracting Intern’s time
“Ah, but what about our department’s Snake Venom Detection Kit?” I hear you ask. “Wouldn’t that tell me which snake was carrying the smoking gun?”
The cynic in me would say that getting someone to use one of those kits is just a good way to get noisy and chaotic person out of a noisy and chaotic resuscitation. Perhaps the more diplomatic way to say that is to say that its clinical use is limited and the reliance on an SVDK can distract from resuscitation efforts.
First and most importantly, the kits do not tell you if a patient is envenomated. That is not their role, and they cannot and must not be used at such.
They can be used as a guide to which monovalent antivenom to use for an envenomated patient, however, there are a number of caveats to their use.
For starters, they have a lot of false positives and false negatives. And I mean a lot.
One Australian Snakebite Project (ASP) study showed an incorrectly identified positive result in nearly 15% of cases[4], with another ASP study reporting up to 25% of envenomated patients showed no venom detected.[5] This inaccuracy is not helped by the relative inexperience of clinicians or laboratory staff using them (when’s the last time you picked one up and read the instructions?)
Additionally – the geographic distribution of snakes and clinical envenomation syndromes means identification of the snake group is usually possible without using a detection kit. Especially in the more snakeless areas such as Tasmania, Victoria, and the Southern Coast.
Even when exact identification is not clinically possible, it is often safer or more practical to administer two vials of different monovalent antivenoms based on the species endemic to an area (E.g. a vial of Tiger and Brown snake antivenom for a patient with VICC in Victoria), than it is to rely on an SVDK.
And finally, there’s always Polyvalent antivenom
Polyvalent Antivenom
So, if we have an antivenom for all of the snakes, why don’t we just use that?
The primary reason being a significantly greater risk of anaphylaxis when the polyvalent is used.[6] Up to 1% of patients getting a Monovalent Antivenom may experience anaphylactic symptoms, which climbs to 5% of those getting Polyvalent.
Most often this reaction will resolve with just stopping the antivenom infusion, and usually it can be restarted at a lower rate without incident.
If the anaphylactic reaction is non-responsive to this simple measure, then proceed along standard anaphylaxis pathways – lie the patient down, apply 15L/min O2 via Hudson Mask or Non-Rebreather, bolus crystalloid for hypotension, and give IM Adrenaline 0.5mg as required.
Caution should be taken if commencing IV Adrenaline – as most patients receiving antivenom will be profoundly coagulopathic (~90% of patients getting antivenom have VICC) so a sudden surge in blood pressure may precipitate intracranial haemorrhage.
Note: the risk: benefit and cost:benefit ratios to stocking certain monovalent antivenoms changes with different locations and different snake populations. It would be impractical to carry multiple monovalent antivenoms for snakes that are rarely seen or treated, so sometimes polyvalent antivenom is a necessary evil.
Woah woah woah, you’ve jumped ahead there Nick. Why am I giving antivenom?
A fine question my hypothetical friend.
Absolute indications
Immediate life threat: Cardiac arrest
Imminent life threat: Descending paralysis, or seizure
Expected life threat: VICC
Relative indications:
Rhabdomyolysis
Coagulopathic states other than VICC
Protracted, treatment-resistant systemic symptoms (GI etc)
A single vial of antivenom is sufficient, and no pre-medication is required.
Remember to warn any patient that receives any form of snake antivenom that one-third of people may get serum sickness (fevers, myalgias, rash) 5-14 days after administration and if that occurs they should seek immediate medical attention and steroid prescription.
Let's be fair, my patient was "bitten" by a stick. When can I take off their pressure bandage and let them go home?
Ah yes, the far less exciting but far more common scenario. The patient without evidence of systemic envenomation and without the need for antivenom heroics.
The overarching time-based rules to remember are
1) At least 12 hours of observation
2) Never at night
It is worth telling this to your patient upfront. The moment the word “snake” left their lips, they were committed to the long haul in ED.
First, the pressure bandage immobilisation
It should only be taken off if:
There are no clinical or laboratory signs of envenomation (cardiovascular collapse, coagulopathy, myotoxicity, neurotoxicity)
There are appropriate staff to manage envenomation if it occurs (emergency/critical care staff, laboratory staff)
There is immediate access to antivenom should envenomation occur
OR
Antivenom has been administered (because you don't want to keep the venom and antivenom separated now, do you?)
This means if you’re working somewhere without the required clinical and laboratory staff, the PBI stays on until they’ve been transferred somewhere else.
Next, the observation period
Irrespective of how well the patient is and how not-snakey the wound appears, all patients with a potential snakebite need a clinical and laboratory assessment for envenomation at:
Time of arrival
1-hour post PBI removal
6 hours post-bite
12 hours after bite
Neurotoxicity can be subtle and clinician accuracy dips overnight, so being confident that there are no toxinological findings is significantly harder after hours.
Additionally, community response teams (E.g. ambulance) availability overnight are lower should the patient deteriorate after discharge – so snakebite discharges should only ever occur when they’re safe and well-lit.
From Toxicology and Wilderness Expert Group. Summary management of snake bite (Figure 17.3) [revised 2012 June]. In: eTG complete [internet]. Melbourne: Therapeutic Guidelines Limited, Jul 2013.
If your patient is bored during their observation period, they can always watch Snakes on a Plane...13 times.
References & Resources
[1] Australian Institute of Health and Welfare Injury in Australia: Contact with living things Report July 2023 https://www.aihw.gov.au/reports/injury/contact-with-living-things
[2] Kasturiratne A, Wickremasinghe AR, de Silva N, et al. The global burden of snakebite: a literature analysis and modelling based on regional estimates of envenoming and deaths. PLoS Med. 2008;5(11):e218.
[3] Ibister GK, Brown SG, Page CB et al Snakebite in Australia: a practical approach to diagnosis and treatment Med J Aust 2013; 199 (11): 763-768
[4] Isbister GK, Brown SG. Bites in Australian snake handlers — Australian snakebite project (ASP-15). QJM 2012; 105: 1089-1095.
[5] 12. Isbister GK, O’Leary MA, Elliott M, Brown SG. Tiger snake (Notechis spp) envenoming: Australian Snakebite Project (ASP-13). Med J Aust 2012; 197: 173-177.
[6] Isbister GK. Antivenom efficacy or effectiveness: the Australian experience. Toxicology. 2010;268(3):148-154. doi:10.1016/j.tox.2009.09.013
[7] General thanks to LITFL (https://litfl.com/approach-to-snakebite/, https://litfl.com/snakebite/, https://litfl.com/snakebite-envenoming-challenge/)
DR NICK ERSKINE
Emergency Registrar
Nick is an Advanced Trainee working at Alfred Hospital. At work, he is moderately obsessed with point-of-care ultrasound and can usually be seen skulking the halls of the department with a Sonosite. Outside of work he lives in fear of needing a FAST himself after coming off his mountain bike on a downhill course too advanced for him. So far he’s always made it to post-ride beers with all his limbs and solid viscera intact, although will never live down the AC joint disruption he sustained when attempting to show off to the Orthopod he was riding with.
