Mx of Australian snake bites with evidence of envenomation

see also:

• first aid and Mx of suspected Australian brown and tiger snake bites
• Australian snake bites
• RCH guideline - snake bites and envenomation in children in Victoria
• 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
• 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
• Western Health: Management of Snake Bite and Snake Antivenom Administration (doc) - WH intranet only

• see Australian tiger and brown snake bites for general Mx and clinical features of envenomation

• move patient to a resuscitation room
• ensure first aid principles in place (ie. pressure immobilisation bandage / splint) until antivenom has been given
• 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)
  • DO NOT use point of care tests for INR or D-Dimer as these may give false negative results with 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)

• do not rely on witness identification of the snake unless it is a snake handler
• the choice of antivenom now is more dependent upon local geographical snake prevalence and upon clinical patterns of envenomation rather than snake identification via VDKs as these can be unreliable.
• utility of the CSL Venom Detection Kit (VDK):
  • DOES NOT indicate or diagnose envenomation!
  • even for envenomed patients, the SVDK has shown high rates of inaccuracy
    • 25% false negative rate in envenomed patients
    • 10% of tiger snake bites mis-identified as brown snake
  • VDK probably not required unless clinical envenomation has occurred and type of snake is unclear from based on region in Australia and clinical features, in these instances, consider swabbing site but not running VDK unless envenomation develops
  • whilst leaving immobilisation bandage in place, gain access to the bite site and using the CSL Venom Detection Kit (VDK) swab (perhaps moistened with solution from the sample bottle), swab the site and place swab in the bottle and consider the need to process the swab using the VDK if evidence of envenomation (this takes at least 20 minutes, but most cases in Victoria probably do not need use of VDK).
  • if the bite site has been thoroughly cleaned, consider using urine sample instead.

• general consensus for most brown or tiger snake bites is to:
  • give 1 vial of specific CSL antivenom in 500ml 0.9% saline over 30-60min
  • if snake not identified by VDK and antivenom indicated:
    • in Tasmania give 2 vials of tiger snake antivenom¹⁾
    • in Victoria, give 1 vial of brown snake antivenom and 1 vial tiger snake antivenom
    • in other states, give 1 vial polyvalent antivenom.
  • be ready to temporarily cease administration of antivenom if evidence of anaphylaxis occurs (rare) and in which case give slow iv adrenaline or perhaps s/c adrenaline but avoid im adrenaline as the coagulopathy will result in substantial haematoma.
  • no need for premed with steroids unless past history of sensitivity to horse sera or giving polyvalent antivenom

• reported sudden collapse, seizure or cardiac arrest
• abnormal INR
• any evidence of paralysis, with ptosis and/or ophthalmoplegia being the earliest signs

• systemic symptoms (vomiting, headache, abdominal pain, diarrhoea)
• leukocytosis
• abnormal APTT
• creatine kinase level > 1000U/L

1. stop antivenom infusion
   • many reactions will resolve with this step, and the infusion can then be restarted at a slower rate.
2. lie patient flat, commence high-flow oxygen, support airway and ventilation if required.
3. for hypotension, give rapid infusion of 1 L normal saline (20mL/kg in children).
   • severe antivenom reactions with hypotension will have reduced venous return;
   • supine posture and fluid resuscitation are essential.
4. for hypotension, hypoxaemia, wheeze or upper airway obstruction, give intramuscular adrenaline (0.01mg/kg to a maximum of 0.5mg).
   • alternatively, those experienced with intravenous infusions of adrenaline may go straight to next step
5. consider a cautious intravenous infusion of adrenaline / epinephrine — avoid blood pressure surges.
   • patients with envenoming may be severely coagulopathic, and high blood pressure may cause or worsen intracerebral haemorrhage. Some patients can have exaggerated, hypertensive responses to intramuscular bolus adrenaline, especially to second doses.
   • if there is no response to Steps 1–4, consider starting a cautious and closely monitored intravenous infusion of adrenaline, which can be reduced as soon as blood pressure starts to recover, preventing blood pressure surges.
   • use 1mg in 100mL by infusion pump: start at 0.5mL/kg/h and titrate according to response; monitor blood pressure every 3–5min (using the arm opposite to the infusion). Be aware that as the reaction resolves, adrenaline requirements will fall, the blood pressure will rise and the infusion rate will need to be rapidly reduced.
6. for persistent hypotension, repeat normal saline bolus.
7. for bronchospasm, consider nebulised salbutamol.
8. for upper airway obstruction, consider nebulised adrenaline.
9. seek further advice from a National Poisons Information Centre consultant.

• remove the pressure immobilisation bandage once antivenom has been given and patient is stable
• take bloods after removal of bandage for FBE, U&E, LFTs, INR, APPT, D-Dimer, CK
• indications for admission to an intensive care unit
  • only necessary for patients with major complications, including:
    • neurotoxic paralysis
      • severe neuromuscular paralysis may require intubation and mechanical ventilation for days or weeks.
    • thrombotic microangiopathy (TMA)
    • severe myotoxicity requiring mechanical ventilation
• if no indications for ICU admission, monitoring in an ED observation unit may be appropriate
• Mx of coagulopathy:
  • consensus appears to be that coagulopathy should NOT be corrected by FFP unless there is active uncontrolled bleeding and antivenom has already been given, otherwise there is risk of further DIC and microemboli.
  • the median time to recovery to an INR < 2.0 in VICC is ~15 hours, and the INR will normalise 24–36 hours after the bite, after which most patients can be discharged.
  • appropriate investigation for occult bleeding, such as a cerebral computed tomography scan, should be undertaken if clinically indicated.
  • thrombotic microangiopathy (TMA) should be excluded in all patients with VICC by observing no change in creatinine level and platelet count over the first 24 hours.
    • thrombotic microangiopathy may require haemodialysis.
• Mx of raised CK:
  • significant rhabdomyolysis with acute kidney injury (AKI) / acute renal failure (ARF) is rare but should be treated with generous fluid therapy and close monitoring for electrolyte imbalances (eg, hyperkalaemia).
• once coagulopathy has resolved, consider tetanus prophylaxis
• repeat blood tests at 6hr, 12hr, and 24hr post-removal of bandage
• any patient who has received antivenom should receive advice at the time of discharge about the possibility of symptoms of serum sickness occurring 4 to 14 days later.