The Tiger Snakes are the only venomous snake in Tasmania and coexist with brown snakes in Australia with similar clinical features in early envenomation. Also behind the brown snake they can also cause death. The Tiger Snake has a number flavours including: Pygmy copperhead, common copperhead, pale-headed snake, broad-headed snake, Stephen’s banded snake, western or black tiger snake, common or eastern tiger snake and the rough-scaled snake.
The classic presentation of envenoming will be a patient with a venom induced consumptive coagulopathy and a symmetrical descending paralysis +/- collapse pre-hospital.
- Potential to be immediately life threatening, the patient should initially be managed in an area capable of resuscitation.
- Early threats to life include hypotension, uncontrolled haemorrhage and descending flaccid paralysis.
- If respiratory failure occurs regardless of whether antivenom has been given, provisions should be made to secure the airway and to ventilate the patient.
- In cardiac arrest, 1 ampoule of tiger snake antivenom should be administered as an IV push and resuscitation continued under standard protocols.
Typical symptoms include:
- Pain at the bite site – puncture wounds may not be apparent
- Local swelling and bruising – sometimes the wounds can develop cellulitis
- Non-specific symptoms including nausea, vomiting, headache and abdominal pain.
- Rarely collapse and cardiac arrest.
- Venom induced consumptive coagulopathy (VICC) both complete and partial occur early on in envenomation. Clinically there will be bleeding at IV sites, gums but rarely intracranial. VICC resolves within 10-20 hours spontaneously.
- Neurotoxicity occurs in 30% of envenomings, it is slow in onset (usually within 2 hours) and progresses over time. The early features include ptosis, blurred vision, diplopia and difficulty swallowing. Rarely cases progress to respiratory failure requiring intubation and ventilation.
- Myotoxicity occurs in 20% of envenomed patients manifested by myalgia, myoglobinuria and rarely renal failure.
- As with all snakes that can produce VICC, thrombotic microangiopathy is a possible complication. Characterised by thrombocytopenia, microangiopathic haemolytic anaemia (MAHA) and acute renal failure.
- Symptomatic relief – IV fluids (if hypotensive / raised CK), antiemetics, analgesia.
- Intubation and Ventilation if respiratory failure is present.
- Pressure bandage with Immobilisation (PBI) – Should have been applied pre-hospital, if not apply while awaiting initial investigations.
1. Laboratory Tests (At presentation, 1 hour post PBI removal, 6 and 12 hours following the bite): FBC, EUC, CK, INR, APTT, Fibrinogen, D-dimer. Never use point of care testing for D-dimer or INR. If there is no evidence of envenoming at 12 hours after the bite (including 6 hours post PBI removal), the patient is fit for discharge (although not during the night as subtle neurotoxicity maybe missed).
2. Tiger snake envenoming is characterised by a VICC or a Partial VICC:
- Elevated INR (>3 or laboratory max or unrecordable)
- Undetectable fibrinogen
- Elevated D-dimer (>100 x normal)
- Partial VICC:
- INR abnormal but <3
- Low but detectable fibrinogen
- Recovery from VICC or partial VICC (INR <2) takes on average 15 hours.
3. Monitor renal function and if VICC has occurred there is a risk of thrombotic microangiopathy indicated by a rise in LDH, deteriorating renal function and platelets with fragmented red blood cells.
4. Clinical exam for descending paralysis and spirometry can be a good measure of pending respiratory decline alerting you to the potential for intubation and ventilation. Check these every time you do bloods as a minimum.
5. The CK maybe elevated and urine should be check for myoglobinuria
Laboratory Results seen in the Australian Snake Envenomations
4. The Snake Venom Detection Kit (SVDK): This is not used to diagnose envenoming but can be used to determine which monovalent antivenom to use if more than one snake could be responsible for the observed clinical features. This kit does produce false positives and false negatives, caution needs to be used and contacting a clinical toxicologist is highly recommended if your patient is envenomed.
- Tiger and brown snake envenomations are very similar early on (both cause VICC), the main difference is between the two is significant paralysis or myotoxicity rarely occurs with the brown snake.
- Taipans are also similar to the tiger snake but cause rapid onset paralysis and myotoxicity. They are like the tiger snake but on steroids!!
- Black snakes can cause myotoxicity but have an anticoagulant coagulopathy not VICC.
- Death adders can cause paralysis but have no clotting disorders.
- 1 amp CSL monovalent Tiger Snake Antivenom: Used in the treatment of envenomation by the tiger snake.
- It will not reverse paralysis but dose halt further progression.
- See Tiger Snake Antivenom for dosing, administration and complication details
- All patients must be observed in a hospital capable of managing a potential snake bite envenomation, this involves adequate laboratory cover and the ability to administer antivenom and manage potential anaphylaxis.
- Patients with no clinical evidence of paralysis or coagulopathy at 12 hours post bite are not envenomed and maybe discharged in daylight hours.
- Envenomed patients can be discharged following antivenom, improving coagulation studies with an INR <2, no evidence of thrombotic microangiopathy and no evidence of significant renal failure. If paralysis has occurred the resulting disability will determine if discharge is feasible.
- Administration of antivenom does not appear to hasten the recovery from VICC, but it may reverse or prevent other manifestations of envenoming.
- Plasmapheresis has been used to treat thrombotic microangiopathy but its utility is still undefined.
- Administration of Fresh Frozen plasma or cryoprecipitate after antivenom administration is associated with earlier recovery from VICC but it does not effect time to discharge and the exact utility to this approach has not be well defined in clinical practice.
References and Additional Resources:
- Tiger Snake Antivenom
- Approach to the Snakebite Patient
- Tox Conundrum 005 – Snakebite vs Stickbite
- Tox Conundrum 026 – Snakebite Envenoming Challenge
Zeff – James Hayes Fellowship teaching Snakebite
- Brown SG, Caruso N, Borland M et al. Clotting factor replacement and recovery from snake venom-induced consumptive coagulopathy. Intensive Care Medicine 2009; 35(9): 1532-538
- Gan M, O’Leary MA, Brown SG et al. Envenoming by the rough-scaled snake (Tropidectis carinatus): a series of confirmed cases. Medical Journal of Australia 2009; 191(3):183-186
- Isbister GK, Buckley NA, Page CB et al. A randomised controlled trial of fresh frozen plasma for treating venom-induced consumption coagulopathy in case of Australian snakebite (ASP-18). Journal of Trombosis and Haemostats 2013; 11:1310-1318
- Isbister GK, Duffel SB, Brown SGA. Failure of antivenom to improve recovery in Australian snakebite coagulopathy. Quarterly Journal of Medicine 2009; 102(8):563-568
- Isbister GK, O’leary MA, Elliott M, Brown SGA. Tiger snake (Notechis spp) envenoming: Australian Snakebite project (ASP-13). Medical Journal of Australia 2012; 197(3):173-177
- Isbister GK, White J, Currie BJ et al. Clinical effects and treatment of envenoming by Hoplocephalus app. snakes in Australia: Australian Snakebite Project (ASP-12). Toxicant 2011; 58:634-640
- Scop J, Little M, Jelinek GA et al. 16 years of severe tiger snake (Notechis) envenoming in Perth, Western Australia. Anaesthesia and Intensive Care 2009; 37:613-618
Dr Neil Long BMBS FACEM FRCEM FRCPC. Emergency Physician at Burnaby Hospital in Vancouver Emergency. Loves the misery of alpine climbing and working in austere environments. Supporter of FOAMed, toxicology, tropical medicine, sim and ultrasound
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