Snakebite envenomation
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Snakebite is an uncommon presentation to Australian emergency departments. Most snakebites do not result in serious envenomation and don’t require anti-venom. True envenomation is rare. However, snakebite can be a potentially life-threatening emergency, even in patients who initially appear well. First aid can be life-saving. Venom travels via lymph – and first aid measures are design to reduce the flow of lymph – you should immobilise the limb, and also try to keep the patient completely immobile – remembering that lymph only flows passively via compression from moving muscles.  This reduces the chance of the venom ending up in the general circulation.

Bites tend to occur in warmer months of the year, and are more common in regional and rural areas.

The major life-threatening complication of venomous snakebite is venom-induced consumption coagulopathy – VICC. Snake bites can also cause myotoxicity (muscle necrosis), neurotoxicity and renal failure. Different snake venoms tend to cause different patterns of these toxicities and can help identify the snake.

All patients with suspected snakebite should be monitored in hospital (e.g. in an emergency short stay unit) for at lest 12 hours, and receive serial blood tests for creatine kinase, activated partial thromboplastin time and INR.

Anti-venom is the mainstay of envenomation treatment. There are effective anti-venoms against all major Australian groups of snakes. Use anti-venom as soon as there is evidence of envenomation. Identification of the snake, by appearance (only by a snake expert!), geographical location and toxic syndrome induced in the patient is possible, but less important with the advent of polyvalent anti-venom. However, monovalent anti-venom is less hazardous to the patient and should be used if the snake can be positively identified. Venom detection kits can help to confirm. Don’t delay anti-venom whilst using a venom detection kit – consider giving polyvalent anti-venoms or multiple monovalent anti-venoms if necessary when there is uncertainty.

Due to the widespread public awareness about the dangers of snakebites, there are also a large number of false alarms (e.g. walkers or gardeners who “felt something” on their leg – but never saw it) – often affectionately known as “stick bites”.

If in doubt or need of assistance at any point – call the National Poisons Information Centre (in Australia) on 13 11 26


  • 3,000 snake bites per year in Australia, resulting in about 500 hospital admissions
  • On average, snake bite causes 2 deaths in Australia each year
  • About 50% of deaths are due to brown snake bites. The other 50% are caused by taipan, black snake, tiger snake and death adder combined
  • Death rarely occurs in under 4 hours
  • Anaphylaxis from insect bite or sting causes more deaths than snake bite


Most snakebites don’t result in envenomation – either because the bite is “dry”, or because the snake is non-venomous. The most common cause of VICC is a brown snake bite.

  • Typically, brown snake bites don’t cause local effects, but some patients may have some localised pain and swelling
  • The textbook two fang marks are often not present. There may be some simple scratches or lacerations, but often no wound site is visible at all

Tiger snake and black snake bites typically cause severe localised pain and swelling – and may lead to myotoxicity (muscle necrosis).

Consider snake bike in any case of unexpected confusion, syncope or collapse which occurs outdoors in Australia.

Clinical Features

  • Collapse / syncope
    • Often sudden and usually the result of hypotension
    • Most patients will regain consciousness shortly afterwards
    • around 5% of patients may have cardiac arrest or seizure
  • VICC – venom induced consumption coagulopathy
    • The result of activation of the clotting pathway by the venom
    • Causes “consumption” of clotting factors (fibrinogen, factor V and factor VIII)
    • INR raised (may be unrecordable)
    • Prolong aPTT
    • D-Dimer markedly elevated (up to 1,000x upper limit of normal)
    • Fibrinogen may be low or undetectable
    • Usually VICC symptoms are present by the time of arrival in the emergency department (85% of cases) but can take up to 6 hours to occur
    • Usually VICC is “complete” or “Severe” but in some cases a milder form may occur
  • Neurotoxicity
    • Usually a descending flaccid paralysis
    • Eye muscles involved first, followed by bulbar palsy, respiratory muscle paralysis and limb paralysis
    • Evolves over a period of hours. May not be present when patient presents
  • Myotoxicity
    • Local and generalised myalgia
    • CK initially normal and rises within 24-48 hours – anywhere between 1,000 and 100,000 U/L
    • Hyperkalaemia
    • Also evolves over a period of hours and may not be present when patient presents
  • Systemic features
    • Nausea
    • Vomiting
    • Abdominal pain
    • Diarrhoea
    • Headache
    • Diaphoresis (sweating)
    • Tender nodes draining from bite site
  • Thrombotic microangiopathy
    • Small fragmented RBCs on blood film
    • Can lead to acute renal failure – and may require dialysis
  • Anticoagulant coagulopathy
    • Occurs in black snake bites
    • Causes mildly elevated aPTT and D-dimer
    • Not clinically significant, but can help in identifying the snake
    • Snake venoms tend to cause either VICC or anticoagulant coagulopathy

Snakes and the features of their envenomation

  • Brown snake
    • Vast majority of cases of envenomation
    • Frequently causes collapse
    • VICC
    • Rarely, a mild neurotoxicity
    • No Myotoxicity
    • Systemic symptoms occur in <50% of patients
    • Thrombotic microangiopathy in about 10%
    • Found throughout Australia except TAS
  • Tiger Snake
    • VICC
    • Neurotoxicity and myotoxicity are rare
    • Systemic symptoms are common
    • Thrombotic microangiopathy in about 5%
    • Found in costal areas in southern QLD, NSW, VIC, SA, TAS and WA
  • Black snake
    • Anticoagulatn coaguloapthy
    • No VICC
    • No neurotoxicity
    • Commonly causes myotoxicity
    • Systemic symptoms common
    • Found all along the east coast
  • Death adder
    • No VICC or anticoagulant coagulopathy
    • Commonly causes neurotoxicity
    • No Myotoxicity
    • Found throughout Australia except southern VIC and TAS
  • Taipan
    • Very deadly – but thankfully bites are rare
    • VICC
      • Partial VICC in up to 50% of cases
    • Neurotoxicity common
    • Myotoxicity rare
    • Systemic symptoms common
    • Thrombotic microangiopathy in about 5%
    • Found in costal areas in QLD and the NT


  • Coagulation studies
    • INR
    • aPTT
    • Fibrinogen
    • D-Dimer
    • Point-of-care testing devices can give false negatives and should be avoided
  • FBC
    • Red cell fragmentation on film – diagnostic for thrombotic microangiopathy
    • Platelets often low at 24 hours after bite
  • CK
    • Indicates muscle damage but results lag behind clinical features by up to 24 hours
  • Snake venom detection kit (SVDK)
    • Can be used to assist identifying the type of snake, and thus the type of anti-venom
    • May be inaccurate and should not be relied upon to confirm diagnosis of envenomation
    • Often, geographical knowledge, along with the clinical syndrome is enough to diagnose the type of snake bite and thus the anti-venom to administer
    • In particular:
      • False negative results in 25% of envenomation patients
      • Wrong about 15% of the time when expert snake identification was available
      • It reports brown snake envenomation in up to 10% of tiger snake bites
    • Bite site swab is the most accurate
    • Urine testing is also possible – but NOT on first pass urine since envenomation – as this contains urine produced before envenomation and thus may report false negative

First Aid

  • Do NOT wash the wound site (this can prevent the use of SVDK later-on)
  • Apply pressure bandage and immobilise the limb and the entire patient. This is sometimes called Pressure bandage with immobilisation (PBI). 
    • Venom travels via lymph and not via the blood. Immobilisation greatly reduces flow of lymph
    • Bandage the bite site
    • Pressure similar to that of a sprained ankle bandage. You should not be able to get a finger easily between the bandage and skin
    • Then, bandage the rest of the limb, starting at the fingers or toes and moving upwards
    • Elasticised bandage is most appropriate, 15cm broad bandage is best
    • Immobilise the limb – sling for an arm, or a splint for the leg
    • Do not move the patient. Transport should come to the patient
    • Bandage can be removed when either:
      • Envenomation has been confirmed and anti-venom has been given
      • Clinical and laboratory data suggest no envenomation has occurred AND the patient is in a hospital with anti-venom and can be closely monitored
      • There are cases of apparently well patients with no symptoms who subsequently develop envenomation after removal of the pressure bandage and mobilisation. 
  • Common misconceptions
    • Do NOT wash the wound or try to “suck out” the venom
    • Do NOT apply a high tourniquet. They are ineffective and can be fatal when removed
    • Do NOT cut or incise the bite mark


No evidence of envenomation

  • Patients with snake bite but no evidence of envenomation either clinically or on laboratory tests should have their pressure bandage removed whilst in a hospital with resuscitation and anti-venom facilities
  • Closely monitor in the first 1-2 hours
    • Particularly for ptosis – the first sign of neurotoxicity – as neurotoxicity has the most delayed onset of the clinical syndromes
    • Repeat bloods (FBC, INR, aPTT, CK) at 1 hour after removal of the bandage, and 6 and 12 hours after the snake bite. 
  • If they remain well, envenomation is highly unlikely
  • They should be monitored for at least another 12 hours (for death adder bites (usually in the NT) some centres recommend longer than this. If the 12 hours expires in the middle of the night, the patient should be kept overnight and discharged in the morning
  • Usually this in the short stay unit of an appropriate emergency department
  • Wound infection is rare and there is no recommendation for antibiotics unless there is obvious evidence of infection
  • All patients should receive tetanus vaccination

Evidence of envenomation

  • Anti-venom is the mainstay of treatment
    • It is thought to be very effective in preventing toxic syndromes, but to have little effect once the syndromes have developed – but evidence for its effects is lacking
    • Absolute Indications
      • Collapse, secure or cardiac arrest
      • Raised INR
      • Any evidence of paralysis (ptosis and ophthalmoplegia are earliest signs)
    • Relative indications
      • Systemic symptoms
      • Elevated aPTT
      • CK >1,000 U/L
    • Choosing anti-venom
      • Can be based on geographical location and clinical syndrome
      • Can be based on results of SVDK
      • If in doubt, administer multivalent anti-venom or multiple single-talent anti-venoms
        • Usually brown snake and tiger snake antivenom as this will cover most snake bites for south Australian and central Eastern Australia. The total volume of this is only around 5-10mls, compared to 40-50mls for the polyvalent antivenoms. Larger volume is associated with increased risk of allergy and anaphylaxis.
      • Polyvalent antivenoms are often variable in their constituents by geographical location based on the snakes in the area
      • Seek expert advice
  • in coagulopathy disorders, it takes several hours for clinical signs and symptoms to improve, even after all the venom has been neutralised
  • In rhabdomyolysis – the process can be prevented but not reversed
  • The effect against neurotoxicity is variable
  • The reversibility of the generalised systemic symptoms is often rapid
  • Anaphylaxis to anti-venom occurs in about 5% of patients, and generalised allergy in up to 20% of patients. Previous exposure to antivenom is not thought to be an important risk factor
  • Should be given in 1:10 dilution with normal saline via IV push
  • Multiple doses are not recommended
  • Serum sickness is a delayed reaction to anti-venom, causing a flu-like illness – fevers, myalgia, rash and arthralgia. It is treated with 7 days of corticosteroids (usually 25mg daily of prednisolone). Patients who received >25mls of anti-venom should be given a prophylactic course of steroids

Supportive Management

Manage the sick, envenomated patient like any other acutely unwell patient

  • ABC – Airway, breathing and circulation assessment in a resuscitation area
    • Intubate and ventilate if airway or breathing fail
    • Give antivenom immediately in this scenario
    • Give fluid resuscitation as required – consider blood replacement if obvious signs of bleeding
  • Most patients are well, and the life threatening complications are rare
  • Intensive care is only rarely required and tends to be in late presentations
    • As a result, most patients do not require tertiary centre care, and can be treated in any hospital with resuscitation facilities, laboratory facilities (available 24 hours) and supplies of antivenom
  • Use of fresh frozen plasma (FFP) is recommended for patients with active bleeding and an immediate threat to life, but evidence is not great. It reduces the time to normalisation of clotting factors, but does not improve time to discharge. Early use of FFP is less effective as the factors are consumed as part of the process of VICC
  • Death from snakebite is usually due to complications from bleeding caused by VICC. Watch for:
    • Haematuria
    • Haematemesis
    • Melaena
    • Menorrhagia
    • Intracranial haemorrhage (consider CT brain in any patient with severe VICC)
  • Be aware of severe myalgia as a sign of rhabdomyolysis – early antivenom use can prevent this, and its associated renal failure (Which may require dialysis)
  • After administration of antivenom, mean time to resolution of VICC is 15 hours
  • Most patients can be discharged at about 24-36 hours


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Dr Tom Leach

Dr Tom Leach MBChB DCH EMCert(ACEM) FRACGP currently works as a GP and an Emergency Department CMO in Australia. He is also a Clinical Associate Lecturer at the Australian National University, and is studying for a Masters of Sports Medicine at the University of Queensland. After graduating from his medical degree at the University of Manchester in 2011, Tom completed his Foundation Training at Bolton Royal Hospital, before moving to Australia in 2013. He started almostadoctor whilst a third year medical student in 2009. Read full bio

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