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wikitox:2.3.5.3.2_australian_venomous_snakes

Australian Venomous Snakes

ANIMALS INCLUDED IN THIS CATEGORY

OVERVIEW

Australia has a number of species of venomous snakes. Reports by bystanders or the patient are generally unreliable in identifying specific snakes unless the individual has undertaken professional training in snake identification. The clinical approach to snakebite and envenomation centres around several factors:

  • Professional identification of the snake such that clinical features of envenomation can be anticipated and appropriate antivenom sourced
    • Usually only possible in professional snake handlers who get bitten by their own snakes
  • Geographical knowledge of what venomous snakes have been reported to cause bites within the area
  • The clinical and laboratory features that are seen or subsequently manifest themselves

A considerable number of snakebites do not result in clinical envenoming and local effects are also uncommon in Australian snakes with the exception of some myotoxic snakes such as the Black Snake and Tiger Snake groups. Therefore in practice the clinical approach will mostly involve, observation, serial clinical and laboratory examinations until envenoming can be reliably excluded. This process mandates a time frame of at least 12 hours post bite before an individual can be safely judged to be no longer at risk of severe envenoming.

Patients not uncommonly present to a healthcare facility who “may have been bitten by a snake”. Such cases often involve someone walking through long grass or bushland who feels a sting on a limb. Due to the general lack of significant local envenoming in Australian snakebite, a well looking patient who raises this issue cannot be presumed to not have been bitten by a snake on the basis of looking well with minimal clinical features. In such circumstances, if the clinician cannot plausibly exclude an encounter with a venomous snake then the clinician is subsequently committed to a minimum 12 hour period of clinical and laboratory tests.

In practice snakebites present to healthcare facilities as an undifferentiated entity. Thus the priorities of the clinician are to establish:

  1. If the patient has been envenomed
  2. If envenomed, which antivenom should be administered

The flowchart below outlines a clinical pathway of appropriate serial laboratory testing based on 240 envenomed cases from the Australian Snakebite Project. this pathway can be used to reliably exclude severe envenoming, however any patient developing clinical or laboratory features of envenoming should exit the pathway when this becomes evident and be managed as appropriate for an envenomed case.

Flowchart, November 2010 [101 KB]

There are 5 monovalent antivenoms (AV) and 1 polyvalent AV available for terrestrial snakes in Australia. These are:

  • Brown Snake AV
  • Tiger Snake AV
  • Black Snake AV
  • Taipan AV
  • Death Adder AV
  • Polyvalent AV

Clinicians should approach envenoming cases by using clinical laboratory and other features to narrow down individual cases to an AV related group e.g. Rough-scaled snake envenoming is functionally a tiger snake bite/envenoming from the perspective of AV treatment.

MECHANISM OF TOXIC EFFECTS

All significantly venomous Australian snakes are from the elapid family. Their venom can cause a variable mixture of neuromuscular dysfunction, coagulopathy, rhabdomyolysis and renal dysfunction.

Neuromuscular dysfunction

Paralysis (skeletal and respiratory muscles) is generally due to presynaptic toxicity although some snakes have significant postsynaptic neurotoxins.

Coagulopathy

Some snakes may cause a significant coagulopathy as part of envenomation (e.g. brown snakes, tiger snakes, taipans). This is due to potent procoagulants in the venom, which in vivo cause consumption of fibrinogen and fibrinolysis - the DEFIBRINATION SYNDROME. This may occur rapidly after onset of envenomation, and renders the blood UNCLOTTABLE, sometimes within 30 to 60 minutes of the bite.

Platelets are usually unaffected.

Other snakes have a true anticoagulant effect (black snake family) with similar clinical effects but normal fibrinogen.

Myolysis

Generalised destruction of skeletal muscle with high serum CPK and myoglobinuria.

Renal dysfunction

Primary or secondary (myolysis, coagulopathy) acute renal failure.

KINETICS

Not every snakebite is effective in delivering a toxic amount of venom. Venom movement is normally via the lymphatic system. Systemic absorption is rapid if pressure bandage and immobilisation of both limb and patient is not undertaken within minutes of the bite.

CLINICAL EFFECTS

Australian venomous snakes cause principally systemic rather than local effects.

Neuromuscular effects: ptosis, diplopia, ophthalmoplegia, fixed dilated pupils, muscle weakness and respiratory failure
Coagulopathy: asymptomatic laboratory abnormalities, bleeding from bite wound and/or venepuncture sites, rarely haematemesis and spontaneous haemorrhage
Rhabdomyolysis: pain or weakness on muscle movement, compartment syndrome, red or brown urine (mistaken for haematuria)
Nephrotoxicity: oliguria, anuria

For most Australian venomous snakes, reported bites demonstrate at least part of the extent of clinical effects possible. However, we do not have a good indication of the spectrum of envenomation severity, because cases at the more extreme ends of the spectrum tend to be reported more often. It is therefore useful to document prospectively, as completely as possible, all the clinical features, and their severity, for all bites by Australian venomous snakes. This is facilitated by using a formal case record form or a clinical database.

CLINICAL ASSESSMENT

History

  • Was a snake seen to bite (ask about multiple bites) OR were the circumstances such that a bite might have occurred?
  • How long is it since the alleged bite?
  • In which geographic place did the incident occur (snakes in area)?
  • Description of snake if possible (colour, length).
  • Timing and type of first aid and activity after the bite.
    • This is important as a relatively small delay in establishing effective first aid treatment allows systemic distribution of venom.
    • Thus, a patient who is asymptomatic and has not applied effective first aid has a lower likelihood of developing envenomation than a patient who has immediately applied effective first aid.
  • Type and timing of symptoms - specifically:
    • headache, nausea, vomiting or abdominal pain, blurred or double vision, slurring of speech, muscle weakness, respiratory distress
    • bleeding from the bite site or elsewhere
    • passing dark or red urine
    • local pain or swelling at the bite site, pain in lymph nodes draining the bite area
    • loss of consciousness, convulsions
  • Relevant past history; specifically ask about
    • allergy or past exposure to antivenom, atopic (allergy) history, renal, cardiac, or respiratory disease.

Examination

  • Examine patient on exposed areas for bite marks or scratches.
  • Look for local and regional tender lymphadenopathy.
  • Perform a neurological assessment looking specifically for ptosis or diplopia or other evidence of muscle weakness.
  • Examine muscles for tenderness and swelling.
  • Check for myolysis; dark or red urine indicative of myoglobinuria (positive for “blood” and so may be mistaken for haematuria)

INVESTIGATIONS

Biochemistry

Serum creatinine, creatine phosphokinase (CK)

Haematology

Full blood count (FBC) including platelets

Coagulation studies

Prothrombin time (PT) or international normalised ratio (INR), activated partial thromboplastin time (aPTT), thrombin clotting time (TCT) if available, fibrinogen concentration, and fibrin(ogen) degradation products (XDP or FDP). Repeated tests are generally necessary.

If there is no laboratory on site then do whole blood clotting time (5 to 10 mL venous blood in a glass tube, e.g. test tube, and observe time to clot; normal is less than 10 min, if there is a coagulopathy there will be no clot at 15 min).

SNAKE IDENTIFICATION

Most bystanders and victims are unreliable witnesses. If you don't have the snake you should rely on local epidemiology, pattern of toxicity based on your clinical and laboratory examination in conjunction with careful use of the Venom Detection Kit (VDK).

See snake identification using symptoms and signs.

Venom detection kit

The VDK uses an ELISA to detect nanogram quantities of snake venom, and indicates which type of venom is present, corresponding to one of the five monovalent antivenoms. It does not indicate if envenomation has occurred nor is it an indication for antivenom treatment.

The VDK comes in a kit including three separate test boxes, but only one set of instructions.

The best sample is a swab from the bite site:
1. Moisten the swab stick provided, in the solution in the first bottle
2. Rub the swab firmly over the bite site and adjacent skin
3. Place the end of the swab back in the solution in Solution 1 (first bottle) and twirl around for a few moments to get venom into solution
4. Then use the kit as indicated in the instructions

If the patient has evidence of systemic envenomation and the bite site is not available for testing (i.e. been washed, or is not apparent), then URINE is worth testing for venom. Use urine instead of solution 1.

Blood has proved an unreliable sample for venom testing with the VDK, giving both false positives and false negatives. It is not recommended for use with the VDK (despite what the instructions may say).

A positive result is indicated by a colour change (to blue) in one of the tubes plus the control tube, within 10 minutes in the last stage of the test, so watch all tubes carefully throughout this last 10 minute period. If one tube changes colour, all will do so eventually, but only the first tube to change is relevant.

NOTE: There is often a colour change in the plastic tubing joining each of the glass capillary tubes, such a change is irrelevant and should not be taken as a positive result.

If you get a positive result this indicates:

  • that venom was present on the skin
  • the type of snake involved
  • the appropriate monovalent antivenom to use should this be needed

DETERMINATION OF SEVERITY

Criteria for systemic envenomation

  • any degree of paralysis
  • significant coagulopathy (INR > 2.0)
  • significant myolysis (myoglobinuria, CPK > 5,000 U/L)
  • significant renal impairment (creatinine > normal and rising)
  • period of unconsciousness or fitting
  • general systemic symptoms such as headache, vomiting, abdominal pain, but beware of these in isolation (i.e. anxiety reaction only)

NOTE: positive venom detection from the wound site does not imply systemic envenomation and is not in itself an indication for antivenom.

TREATMENT

A considerable number of snakebites do not result in significant illness, and do not require antivenom, but ALL suspected or confirmed snakebites must be admitted for observation at least overnight (18-24 hours), as some serious effects may be delayed.

Initial: First Aid

  • Immediately apply broad compressive bandage to the bitten limb at same pressure as for a sprain. Extend bandage to cover whole of bitten limb from distal to proximal. Splint limb. Keep patient still.
  • DO NOT give alcohol, food, stimulants, cut the wound, or use a tourniquet.
  • DO NOT WASH OR CLEAN THE WOUND.
  • Maintain airway/breathing if imperilled.

In hospital

  • Establish IV line
  • Cut away bandage over bite site and swab for venom detection (CSL Venom Detection Kit)
  • Take blood for investigations
  • Observe patient at least overnight (18-24 hours)
  • If there is evidence of systemic envenomation consider ANTIVENOM therapy

Supportive

  • Insert an IV line (normal saline, run at maintenance, keep the patient fasted).
  • If profound hypotension, IV normal saline solution. A degree of hypertension may be encountered which usually resolves.
  • Respiratory failure: artificial ventilation; mouth to mouth; bag/mask; bag/endotracheal tube as needed.
  • Circulatory failure: if cardiac arrest, cardiopulmonary resuscitation.
  • Apply pressure bandage/immobilisation first aid if not already present (remove when initial antivenom therapy is completed and the patient is clinically stable)

Continuing care includes

  • high intensity nursing, with specific instructions to look for evidence of developing paralysis (ptosis, diplopia)
  • monitor urine output, and if in doubt catheterise
  • serial tidal volume measurement
  • check and update tetanus immunisation status
  • avoid unnecessary venepuncture

Antivenom

All snake antivenoms available in Australia are refined equine F(ab)2 portions of IgG. Antivenom is the definitive treatment of envenomation, and is potentially life saving but as it is refined horse serum, it is also potentially allergenic and therefore its use is not without risk. Therefore, antivenom should only be used if there is systemic envenomation. Overall, only 1 in 4 or less patients require antivenom therapy.

Administration
Antivenom for snakebite should always be given IV (or via bone needle in children), with all facilities ready to hand to treat anaphylaxis in the rare event that it should occur.

  • Have an IV line set up and running, in children consider a bone needle if no other access available
  • Dilute the antivenom about 1:10 (1:5 or less may be needed if volume is a problem, e.g. polyvalent antivenom, paediatric patient) in IV fluid (normal saline, or Hartman's solution)
  • Start infusion very slowly carefully observing patient for reaction
    • look for rash, hypotension, bronchospasm (in children warning signs also include nasal, palatal, or ocular pruritus), coughing, sneezing, profuse sweating, faecal or urinary urgency or incontinence, abdominal pain, and a “sense of impending doom”
  • increase rate aiming to give whole dose over 15 to 20 minutes

Dose
The minimum dose is one ampoule of the appropriate antivenom.

  • Children require the same dose as adults
  • Multiple bites or severe envenomation mandate higher doses; begin with at least 2 ampoules, and be prepared to give more. Four to 6 ampoules is not unusual in a severe snakebite

If there is a coagulopathy then the dose can be titrated against serial coagulation results (see guidelines on managing coagulopathy).

Premedication prior to antivenom therapy
This is controversial with two major viewpoints in Australia. The authors do not use premedication.

One view recommends the routine use of premedication, especially subcutaneous adrenaline, and an antihistamine, to reduce the chance of anaphylaxis. This is considered particularly useful for country doctors. The antivenom manufacturer (CSL) no longer recommends premedication (nor recommends against it).

The opposing view is that such premedication is potentially hazardous (adrenaline may cause hypertension, dangerous if there is a coagulopathy or cardiovascular disease), may obscure signs of envenomation (drowsiness or irritability due to antihistamines), and may not be effective in practice in preventing anaphylaxis. It may therefore be better to be fully prepared to treat anaphylaxis if it occurs with adrenaline, volume loading with SPPS and such other measures as may be indicated.

Treatment of specific complications

Snakebite coagulopathy

Snakebite coagulopathy can prove complex to manage, and it is preferable to treat the patient in a major hospital, with full coagulation laboratory facilities on site.

Expected results in coagulopathy:

  • Whole blood clotting time grossly prolonged (> 15 min (usually will not clot even after 1 hour), normal = less than 10 min)
  • INR grossly prolonged (> 4 (usually infinity), normal = 1.0)
  • aPTT grossly prolonged (> 150 s, normal = less than 35 s)
  • TCT grossly prolonged (>150 s, normal about 15 s)
    • NOTE: TCT may be the first parameter to show improvement because of antivenom therapy, dropping from >150 s to less than 100 s If this occurs it probably indicates that enough antivenom has been given, despite the lack of improvement in other parameters, and so at this stage stop further antivenom therapy and repeat tests in 1-2 h to confirm trend of improvement.
  • Fibrinogen concentration very low or zero (< 0.1 g/L, normal = 1.5 to 4.0 g/L)
  • Fibrin(ogen) degradation products grossly elevated (XDP > 16, normal < 0.25)
    • NOTE: Degradation products are in themselves anticoagulant, and at such high concentrations may interfere with some clotting tests, giving falsely high estimates of abnormality, particularly INR and aPTT on some automated coagulation machines. This may obscure the first signs of recovery. Make sure your laboratory is aware of this problem

Frequency of tests
If initial studies are normal, repeat studies after 2 to 4 hours, or sooner if the patient appears envenomed.
If there is a significant coagulopathy (unclottable blood, or INR > 4) then this must be treated.
Antivenom is the treatment of choice.

Replacement therapy with clotting factors (e.g. whole blood, fresh frozen plasma (FFP), cryoprecipitate) should be avoided, as it is liable to make the coagulopathy worse if there is still active venom.

Once active venom is all neutralised by antivenom normal homeostasis rapidly (often within 2 hours) rectifies the problem, placing the patient out of danger (i.e. INR < 4), usually without need of any other treatment.

Antivenom therapy
Antivenom therapy can be titrated against the resolution of the coagulopathy.

After the initial dose of antivenom retest clotting studies about 1 to 2 hours later. If still showing a coagulopathy, give more antivenom and repeat tests in 2 hours, continuing this process until there is evidence of resolution, or 6 ampoules of antivenom have been given. If after 6 ampoules of antivenom there is no resolution then expert advice should be sought.

LATE COMPLICATIONS, PROGNOSIS - FOLLOW UP

All patients who receive any antivenom should be warned of the potential development of serum sickness. This is a reaction to foreign protein comprising fever, malaise, skin rash, joint pain, lymphadenopathy and proteinuria which occurs one to three weeks after exposure. Serious reactions may require steroid treatment.

REFERENCES

Fulltext

  1. Yeung JM, Little M, Murray LM, Jelinek GA, Daly FFS. Antivenom dosing in 35 patients with severe brown snake (Pseudonaja) envenoming in Western Australia over 10 years. Med. J. Aust. 2004 Dec 6;181(11-12):703-705.
  2. Isbister GK. Antivenom, anecdotes and evidence. Med. J. Aust. 2004 Dec 6;181(11-12):685-686.
  3. Isbister GK, Brown SG, MacDonald E, White J, Currie BJ. Current use of Australian snake antivenoms and frequency of immediate-type hypersensitivity reactions and anaphylaxis. Med. J. Aust. 2008 Apr 21;188(8):473-476.
  4. Isbister GK, Tankel AS, White J, Little M, Brown SGA, Spain DJ, et al. High rate of immediate systemic hypersensitivity reactions to tiger snake antivenom. Med. J. Aust. 2006 Apr 17;184(8):419-420.
  5. Isbister GK, Duffull SB, Brown SGA. Failure of antivenom to improve recovery in Australian snakebite coagulopathy. QJM. 2009 Aug;102(8):563-568.
  6. Currie BJ. Snakebite in tropical Australia: a prospective study in the “Top End” of the Northern Territory. Med. J. Aust. 2004 Dec 6;181(11-12):693-697.

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wikitox/2.3.5.3.2_australian_venomous_snakes.txt · Last modified: 2018/09/01 09:00 (external edit)