Snake bite

First Aid on scene

  • BLS
  • Pressure immobilisation bandage (PIB)
    • For technique to be effective, must employ both pressured bandage and immobilisation of the bitten limb
    • Do not wash wound
    • Swab bite site and put in fridge if no signs of envenoming
    • Broad elasticized pressure bandage (if available) below bite site upwards along bitten limb
    • Leave tips of digits uncovered to test circulation
    • Do not remove pants or trousers, bandage over them
    • Mark location of bite
    • Bind a splint  to the limb after this and keep patient as still as possible

On arrival

  • ABCDE
  • IVC and bloods
    • Initial bloods: FBC and film, Coags (APTT, PT, Fibrinogen, D-dimer), CK, U&E, LDH, LFT
    • Serial bloods: INR, APTT, Fibrinogen, CK, FBC, U&E
  • Bite swab (to keep in fridge)
  • Monitoring
  • Ensure adequate urine output
    • 1-2mL/kg/hr if myoglobinuria evident
  • Assess (see below)

Resuscitation

  • Cardiac arrest
    • Paediatric ALS + Polyvalent AV if snakebite thought to be cause
    • If resuscitation successful, return to usual snakebite + post-arrest management
  • Always consider anaphylaxis to venom
    • Antivenom may be a useful adjunct in management of this as well as usual adrenaline protocol
    • If treated successfully, return to usual snakebite + post-anaphylaxis management
  • Severe respiratory distress may be impending compromised airway, respiratory paralysis or severe bronchospasm from anaphylaxis

Assessment

  • Circumstances
    • Witnessed bite or possible bite
    • Multiple bites?
    • Where/when/how
    • First aid
    • Past history
    • Medications esp. anticoagulants
    • Allergies
    • Past exposure to antivenom or snakebite

Assessment

  • Symptoms
    • Headache
    • Nausea/vomiting
    • Abdominal pain
    • Blurred vision
    • Slurred speech
    • Muscle weakness
    • Respiratory distress
    • Bleeding from bite site, gums or elsewhere
    • Passing dark or red urine
    • Local pain or swelling at site
    • Pain in draining lymph nodes
    • Loss of consciousness and/or convulsions

Problem presentations

  • Unexplained collapse
  • Convulsion
  • Progressive unwellness
    • Lethargic, vomiting, mild fever, abdominal pain, haematuria (= myoglobinuria), progressive paralysis and ptosis
  • Renal failure without clear cause

Assessment

  • Examination
    • Evidence of bite/scratch. May be multiple. Take swab.
    • Bruising around bite site (typical of Tiger snake)
    • Evidence of venom movement e.g. swollen or tender nodes
    • Neurotoxic
      • Ptosis, ophthalmoplegia, diplopia, dysarthria, limb weakness, respiratory distress
    • Myotoxic
      • Muscle tenderness, pain with movement, dark or red urine
    • Coagulopathy
      • Bleeding gums, prolonged bleeding from venepuncture site or wounds or bite site

Role of VDK

  • Takes 20-30 minutes
  • In inexperiened hands (most of us), have significant rates of misidentification, false positives and false negatives
  • Results should never override clinical or geographic data
  • Discuss use and results with clinical toxicologists
  • Can use bite site swab or urine (only if sample provided after symptoms/signs of envenomation arose) for test

When can PIB be removed?

  • Patient must be stable with no clinical or lab signs of envenoming
  • Can then remove in resuscitation area
  • Antivenom should be ready for delivery with adrenaline and resuscitation equipment at hand
  • Re-apply PBI if envenoming arises after removal and deliver antivenom

Major venomous snakes

Major venoms

  • Brown snake – VICC +- MAHA + Sudden collapse + presynaptic neuro (mild)
  • Black snake – Rhabdo + anticoagulants
  • Taipan/Tiger – Rhabdo + Neuro + VICC
  • Black- and blue-bellied black snakes rarely cause systemic envenoming

Definitions

  • VICC
    • Venom-induced consumptive coagulopathy
    • Fibrinogen reduced, D-dimer elevated
    • Raised INR
  • Anticoagulant coagulopathy
    • APTT 1.5-2.5x normal +- minor INR elevation
    • D-dimer and fibrinogen usually normal
  • MAHA
    • Microangiopathic haemolytic anaemia
    • Fragmented red cells on film, thrombocytopaenia and rising creatinine

Black snakes

  • Mulga snake, Collett’s snake, Butler’s snake, Papuan black snake
    • Large painful bite with extensive local tissue swelling and local lymphadenitis
    • Systemic features rapidly, generalized myalgia and muscle weakness within 6 hours
    • Myotoxicity is frequent
    • Anticoagulant coagulopathy is frequent but bleeding is rare
    • Acute haemolysis may occur
  • Red-bellied and blue-bellied black snake
    • Local pain and systemic features
    • Myotoxicity is rare
    • Anticoagulant coagulopathy may occur but is usually mild
    • Long-term anosmia, paraethesia and pain at bite site can occur

Black snakes

  • Antivenom within 3 hours prevents myotoxicity
  • 1 ampoule of black snake antivenom if:
    • CK >1000
    • Systemic features
    • Anticoagulant coagulopathy
  • Can use black snake or tiger antivenom for blue-bellied and red-bellied black snake (tiger cheaper, more widely available and smaller volume)
  • Mulga snake is referred to as a King Brown, however, it is NOT a brown snake

Brown snake

  • Most common cause of severe envenoming and death from snakebite in Australia
  • Presyncope or sudden collapse is typical
  • VICC is common
  • MAHA in 10%
  • Myotoxicity does NOT occur
  • Neurotoxicity is rare and mild

Brown snake

  • Complete VICC vs. partial VICC
    • Complete = INR >3, undetectable fibrinogen, D-dimer >100x normal
    • Incomplete = INR <3, low but detectable fibrinogen
  • Recovery from VICC takes around 20 hours
  • Monitor for MAHA with LDH and free Hb/fragmented red cells
  • If received antivenom, can discharge after 24 hours if INR <2, no MAHA and clinically well
  • Clotting factors increase rate of recovery from VICC but not duration of hospitalization
  • Antivenom may not hasten recovery from VICC

Brown snake vs. Tiger snake

  • May be clinically indistinguishable initially as both can cause collapse and VICC
  • Tiger have more significant neurotoxicity and myotoxicity over ensuing hours

Death adder

  • Bites and envenoming are uncommon
  • Not in Victoria or Tasmania
  • Progressive symmetrical descending flaccid paralysis within 6 hours
  • Non-specific systemic symptoms are common
  • Myotoxicity is uncommon and mild
  • Antivenom – 1 vial for objective paralysis
  • No VICC, anticoagulant coagulopathy or MAHA
  • Typically bitten at night walking barefeet. May not even notice bite
  • Can be complicated by cellulitis at bite site

Tiger snake

  • Mostly southern Australia (vs. taipan in northern Australia)
  • The only venomous snakes in Tasmania
  • Classically VICC, myotoxicity, delayed neurotoxicity (in 30%)
  • MAHA can occur but is less common than with brown snakes
  • Rough scaled snake is very similar
  • Tiger vs. Taipan
    • Taipan has more rapid onset of neuro and myotoxicity
    • Both have VICC
    • Taipan Northern and Tiger southern Australia

Taipan snake

  • Rare but frequently lethal
  • Mostly northern Australia
  • Often no specific history of bite
  • Collapse then paralysis within 1-2 hours + VICC + myotoxicity
  • MAHA occurs
  • Differentiated from Brown snake by more severe neuro and myotoxicity

Sea snake

  • Neurotox and myotoxicity
  • No VICC/anticoagulant coagulopathy
  • Unclear if tiger snake antivenom (3:1 sea snake) is still effective as previously described

When to give antivenom?

  • Absolute indications
    • Any evidence of neurotoxic envenomation
      • Ptosis, ophthalmoplegia, limb weakness, respiratory distress
    • Significant coagulopathy
      • Unclottable blood, INR >1.3 or prolonged bleeding clinically
    • History of unconsciousness, collapse, convulsions or cardiac arrest
    • Evidence of acute renal damage
  • Relative (discuss with clinical toxicologist before)
    • Significant systemic symptoms e.g. headache, abdo pain, vomiting
    • Abnormal INR, APTT, fibrinogen, D-dimer, FBC (leukocytosis or evidence of MAHA) or CK >1000

Timing of antivenom therapy

  • It is never too late to deliver antivenom in the presence of severe envenomation
  • Less effective the longer the delay
  • Seek expert advice if >24 hours after the bite as benefits may be outweighed by risks

Choice of antivenom

  • Always preferable to use monovalent antivenom as uses less volume and has less adverse effects (serum sickness specifically)
  • If impractical to consider type (i.e. cardiac arrest), can give polyvalent, which covers 5 snake venom immunotypes predominating in land snakes in Australia and PNG
  • In some regions, using two monovalent types based on geographic range is practical (seek expert advice)
    • In Tasmania and Kangaroo Island, only need Tiger snake antivenom

Monovalent antivenoms

  • Brown
  • Black
  • Taipan
  • Tiger
  • Death adder
  • Sea snake (not included in polyvalent)

Polyvalent antivenom

  • Covers all land-based snakes in Australia 
  • Product information states to use 1 vial but that more may be required depending on clinical effect
  • Expert consensus states that dosing should be as per number recommended for corresponding monovalent i.e. if known brown snake but only have polyvalent, give 2 vials of polyvalent as per brown snake guidelines

Preparation for antivenom delivery

  • 2x IV access
  • 20mL/kg IV N/saline ready for pressure bolus if required
  • IM adrenaline 0.01mg/kg of 1:1000 in case of anaphylaxis
  • Dilute antivenom up to 1 in 10 normal saline (not to exceed 10mL/kg in small children)
  • Start slowly and then increase rate gradually to deliver over 30 minutes

Observations during antivenom delivery

  • Must remain in critical care area
  • Warning signs of anaphylaxis in children
    • Rash, hypotension, bronchospasm
    • Nasal, palatal or ocular pruritis
    • Coughing
    • Sneezing
    • Profuse sweating
    • Faecal or urinary incontinence
    • Abdominal pain
    • Impending sense of doom

What if there is an adverse reaction?

  • May be related to rate of infusion
  • May respond to temporarily stopping, waiting to ensure it settles and then re-starting at a slower rate
  • If sudden fall in BP or bronchospasm:
    • Stop infusion
    • Lie supine
    • 100% O2
    • Rapid fluid bolus 20mL/kg IV N/saline
    • Adrenailne 0.01mg/kg 1:1000 IM
    • If remains hypotensive – repeat fluid bolus and commence IV adrenaline infusion
  • In most cases cautious re-introduction of antivenom is possible and necessary

Adverse reaction risk factors

  • Atopic family history
  • Previous exposure to equine protein
  • Delayed reactions more likely with multiple doses
  • Polyvalent antivenom
  • Repeat doses
  • IV use without dilution

Adverse reactions to antivenom

  • Serious adverse reactions seen in 1% of patients
  • Rash: May be mild or herald more severe reaction
  • Pyrexia
  • Anaphylaxis/anaphylactoid reaction
  • Serum sickness
    • Up to 30% of patients
    • Flu-like syndrome with fever, myalgia, arthalgia and rash developing 4-14 days post-antivenom
    • Management
      • Oral corticosteroid short course
      • Consult with clinical immunologist

What happens after antivenom delivery?

  • PIB can be removed
  • Admit for observation and ongoing treatment
    • Strict fluid balance chart looking for declining urine output
    • Usually repeat blood tests at 6, 12 and 24 hours post-antivenom followed by daily testing until all within normal limits (some caveats as per discharge criteria)

Repeated antivenom dosing

  • Venom-induced consumptive coagulopathy can take up to 6 hours to start improving after antivenom delivery and repeated dosing of antivenom does not provide additional benefit
    • Takes this long for depleted coagulation factors to start being replenished
    • If active bleeding (incl. ICH), need to consider repeat antivenom dosing in conjunction with FFP (>1 hour and <4 hours post-antivenom delivery) with expert advice
  • Anticoagulant coagulopathy rarely requires repeated antivenom dosing

Repeated antivenom dosing

  • Myolysis
    • CK level usually peaks at 24 hours then returns to baseline over several days
    • If second peak or continued rapid rise after antivenom therapy, consider repeat dose
  • Neurotoxicity
    • All Australian snakes that cause paralysis, produce venoms containing both pre- and post-synaptic neurotoxins. Pre-synaptic neurotoxins are not reversible and therefore it is crucial to deliver antivenom as early as possible once neurotoxicity is recognised
    • No benefit in repeated doses of antivenom 

Is there a role for FFP/cryoprecipitate?

  • Very limited
  • If bleeding due to coagulopathy and antivenom already delivered in adequate dose, then there may be a place for blood constituents but need to discuss with clinical toxicologist

Discharge criteria if no antivenom

  • Patient can be discharged (in daylight hours) if all results within normal limits (Initial, 1-hour post-PIB removal, 6 and 12 hours post-bite) and no signs of neurotoxicity
  • Education re: serum sickness

Discharge criteria after antivenom

  • As per Victoria ED management flow chart
    • Uncomplicated myotoxicity and mild neurotoxicity
      • Once clinical features resolving and blood tests normalising at least 12 hours post-antivenom
    • Venom-induced consumptive coagulopathy
      • INR, aPTT, creatinine and platelet count normalising
    • Always in daylight hours

Last Updated on October 28, 2020 by Andrew Crofton