Australian tiger and brown snake bites

see also:

• Australian snake bites
• toxinology
• RCH guideline - snake bites and envenomation
• Vic. DOH snakebite Mx tools (2019):
  • https://bettersafercare.vic.gov.au/resources/clinical-guidance/emergency-care/management-of-snake-bite
  • flowchart for ED's
  • a clinical pathway for the management of snake bite envenomation
• MJA 2013: Mx of Australian snakebites
• Australian Venom Research Unit (AVRU): Mx of snake bites
• NSW govt - Mx of snake bites and red back spider bites 2007 (pdf)
• SA govt - Mx of snake bites and red back spider bites 2006

• Australian brown and tiger snakes are elapid snakes and have potentially lethal venom (the highest LD50 in mice in the world along with the Australian taipan), but rarely cause bites unless you accidentally step on one or you try to kill it, and then only a minority will develop features of systemic envenomation.
• many more people die from anaphylaxis from honey bee stings in Australia than from snake bites!
• many more people die from falling trees in Australia than from snake bites!
• ~3000 suspect snakebites occur in Australia each year with 10% requiring antivenom.
• consider all Australian endemic snake bites as potentially venomous
• although brown snakes account for most bites Australia-wide, tiger snakes account for the far majority of endemic snake bites in south eastern Australia (eg. Victoria and Tasmania) which occur outside of reptile parks, zoos and those who keep exotic snakes.
• snakes inside houses
  • these are relatively uncommon in SE Australia (it is said that a third of houses on the Gold Coast in Qld harbour at least one python in their ceiling)
  • all venomous snakes in SE Australia can flatten themselves to squeeze under a door
  • the eastern brown snake accounts for over 90% of human bites indoors and one or two bites each year are from snakes who have sort refuge under bedding
  • most snake bites occur outside around houses as snakes seek rats and mice for food and back yards tend to have lots of options for them to seek shelter
• young brown snakes mainly prey on lizards and thus their venom is mainly neurotoxins
• mature brown snakes prey on small mammals such as rodents and their venom is mainly anticoagulant which immobilises their prey by causing stroke ¹⁾
  • there appear to be a difference in toxins which cause clotting between eastern brown snakes in northern parts of Australia compared with southern parts
  • other snakes in Victoria but which are uncommonly associated with bites include:
    • Red-bellied Black snake - relatively common bites but very low death rate as they appear to envenomate less frequently - use tiger snake anti-venom
    • Copperhead snake - use tiger snake anti-venom
    • Sea snake (3 ampoules Tiger snake antivenom if sea snake antivenom unavailable)
• the treatment for all these snakes is essentially the same apart from use of different anti-venom.
• advice on the management of envenomation is available 24 hours a day from the Australian Venom Research Unit on 03 8344 7753 or through the Victorian Poisons Information Centre - Austin Hospital) ph: 13 11 26 for Victoria, after 2100hrs, phone via Austin switchboard on 94965000

• possible puncture marks at bite site +/- local bruising - but unlike redback spider bites, there is not intense pain at the bite site.
• only 5% to 10% of snakebite patients develop severe envenoming and this is manifest within 12 hours of bite
• possible sudden collapse or near syncope within minutes of bite
• NB. snake handlers in particular, are at risk of hypersensitivity reactions to the venom
• evidence of envenoming exists if neurotoxicity develops or the INR, aPTT or CK level becomes abnormal

• sudden collapse or cardiac arrest
  • mainly occurs with brown snake envenomations, but uncommonly occurs with taipan envenomations
  • can occur within 15 minutes of bite with the bite being largely asymptomatic prior to sudden collapse
• severe venom-induced consumption coagulopathy (VICC):
  • often within minutes, and if collapse and head trauma subsequently occur, there is substantial risk of intracranial haemorrhage and death.
  • the main sign of severe envenomation in the far majority of tiger and brown snake severe envenomations
  • at least partial VICC occurs in 20-30% of victims with envenomation due to tiger or brown snakes, and in 50% of those due to taipan envenomation
  • does not usually occur with sea snakes, death adder or black snakes which include the mulga snake (black snakes cause an anticoagulant type of coagulopathy with raised APPT but only mild if any increase in INR and a normal DDimer)
  • severe VICC is indicated by an international normalised ratio (INR) > 3.0 with either:
    • an undetectable fibrinogen level, or,
    • a raised D-dimer level (at least 10 times the assay cut-off or > 2.5mg/L)
• early neurotoxicity causing cranial nerve palsy (especially ptosis) and bulbar respiratory paralysis
  • late neurotoxicity may occur
  • not a significant feature of brown snake or black snake envenomations but common in death adder and taipan envenomations, and uncommon with tiger snakes
• myotoxicity:
  • a creatine kinase (CK) level > 1000 U/L, with myalgia and/or muscle tenderness.
  • severe myotoxicity and raised WCC is more likely with Black snake group and sea snakes rather than Brown Snakes (Pseudonaja spp)
• thrombotic microangiopathy (TMA):
  • intravascular haemolysis on the blood film
  • raised creatinine level with or without acute renal failure
  • thrombocytopaenia
  • 10% of brown snake envenomations and 5% of tiger and taipan envemomations

• at least three of nausea, vomiting, abdominal pain, diarrhoea, diaphoresis and headache), or,
• mild or partial VICC is indicated by maximal INR < 3.0 and evidence of coagulopathy, or,
• mild neurotoxicity or mild myotoxicity

• 9% died within 3 hours
• 8% died in the 3-6 hours period
• 15% died in the 7-12 hours period
• 26% died in the 13-24 hours period
• 42% died after 24hrs
• ie. 82% did not die until at least 7 hours after being bitten, thus there should be adequate time in most cases to reach medical aid & receive antivenom as “no patient is too ill to receive antivenom, & even those with the most severe paralysis may recover”.
• remember that only 5-10% of bites result in severe envenomation

• early death:
  • eastern brown snake or taipan bites may cause sudden collapse and death in under 30 minutes
  • collapse in coagulopathic state with possible hypertensive crisis causing resultant intracranial haemorrhage
  • anaphylactic reaction
  • multiple bites especially toddlers
• delayed medical care or inadequate first aid:
  • geographical isolation from medical care
  • unrecognised snake bite
  • alcohol intake
• inadequate medical care:
  • victim not observed for an adequate period;
  • antivenom withheld when there is clear evidence of systemic envenomation
  • failure to give the correct antivenom
  • inadequate amount of antivenom given

• do not attempt to catch or kill the snake
• do not wash bite site (as this will decrease ability to detect snake type with VDK)
• do not incise or excise bitten area
• do not apply arterial tourniquet
• minimise lymphatic spread of toxin from the bite site
  • splint affected limb to prevent muscle action - avoid walking or running
  • firm elastic bandage (crepe is less effective) around whole of limb including bite site - commencing over bite site & bandaging upwards
    • this must remain in place until patient is in a resuscitation facility with iv access and either antivenom given, or antivenom at hand if no systemic envenomation evident.
• keep nil oral
• minimise risk of trauma such as head injury while potentially coagulopathic
• transport to medical care ASAP in a safe manner
  • facility must be able to do an INR quickly and have access to antivenom and adequate medical expertise to Mx anaphylaxis

• move patient to a resuscitation room
• ensure first aid principles in place
• iv access (avoid multiple attempts or venepunctures as potential coagulopathy)
• send bloods for FBE, U&E,CK, INR, APTT and d-Dimer (NB. an elevated d-Dimer alone does NOT indicate envenomation)
• cardiac monitor
• commence neuro obs - in particular assess for ptosis (eye lid droop on sustained upward gaze), speech difficulty or breathing difficulty (consider regular PEFR measurements)
• ensure adequate iv hydration, particularly if rhabdomyolysis is evident (markedly raised CK)

• if patient is stable and above has been achieved and initial bloods are normal, then if patient is in a facility where there is antivenom available and medical care to manage potential anaphylaxis, remove pressure immobilisation, observing for evidence of envenomation
• take a swab of the bite site in case venom detection kit analysis is required if evidence of envenomation arises, routine VDK analysis of swab or urine is generally not required if there is no evidence of envenomation, as it is expensive and may give false results
• repeat clotting profile at 1 hour after removal of bandage (and then repeat bloods at 6 and 12 hours post bite)²⁾
• repeat neurologic examinations
• if no evidence of envenomation by 12 hours post-bite, then patient can be discharged home if it is daylight hours
  • if PBI has remained in situ for > 6 hours post-bite then the last bloods needed are 6hrs after removal of PBI
  • more caution is needed with children, and many would observe for 12-24 hours.

• see Mx of Australian snake bites with evidence of envenomation