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:
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:
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:
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.
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.
Paralysis (skeletal and respiratory muscles) is generally due to presynaptic toxicity although some snakes have significant postsynaptic neurotoxins.
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.
Generalised destruction of skeletal muscle with high serum CPK and myoglobinuria.
Primary or secondary (myolysis, coagulopathy) acute renal failure.
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.
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.
Serum creatinine, creatine phosphokinase (CK)
Full blood count (FBC) including platelets
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).
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).
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:
NOTE: positive venom detection from the wound site does not imply systemic envenomation and is not in itself an indication for antivenom.
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.
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.
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.
The minimum dose is one ampoule of the appropriate antivenom.
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.
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:
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 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.
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.
ADVICE on Australian venomous snakebite is available from the Poisons Information Service, telephone 131126 in Australia.
Broad AJ, Sutherland SK, Coulter AR. The lethality in mice of dangerous Australian and other snake venom. Toxicon 1979;17(6):661-4. 3.
Buckley N, Dawson AH. Unusual results of brown snake envenomation. Med.J.Aust. 1993;158(12):866, 868.
Currie BJ. Clinical toxicology: A tropical Australian perspective. Ther.Drug Monit. 2000;22(1):73-8.
Currie BJ. Snakebite in tropical Australia, Papua New Guinea and Irian Jaya. Emerg.Med. 2000;12:285-94.
Hodgson WC. Pharmacological action of Australian animal venoms. Clin.Exp.Pharmacol.Physiol. 1997;24(1):10-7.
Howarth DM, Southee AE, Whyte IM. Lymphatic flow rates and first-aid in simulated peripheral snake or spider envenomation. Med.J.Aust. 1994;161(11-12):695-700.
Isbister GK, Dawson AH, Whyte IM. Two cases of bites by the black-bellied swamp snake (Hemiaspis signata). Toxicon 2002;40(3):317-9.
Jelinek GA, Breheny FX. Ten years of snake bites at Fremantle Hospital. Med.J.Aust. 1990;153(11-12):658-61.
Mead HJ, Jelinek GA. Suspected snakebite in children: a study of 156 patients over 10 years. Med.J.Aust. 1996;164(8):467-70.
Mirtschin PJ, Crowe GR, Thomas MW. Envenomation by the inland taipan, Oxyuranus microlepidotus. Med.J.Aust. 1984;141(12-13):850-1.
Morrison JJ, Tesseraux I, Pearn JH, Harris J, Masci PP. Venom of the Australian rough-scaled snake, Tropidechis carinatus: lethal potency and electrophysiological actions. Toxicon 1984;22(5):759-65.
Pearn J, McGuire B, McGuire L, Richardson P. The envenomation syndrome caused by the Australian red-bellied Black Snake Pseudechis porphyriacus. Toxicon 2000;38:1715-29.
Shea GM. The distribution and identification of dangerously venomous Australian terrestrial snakes. Aust.Vet.J. 1999;77(12):791-8.
Sutherland SK, Tibballs J. Treatment of snake bite in Australia. In: Sutherland SK, Tibballs J, editors. Australian Animal Toxins. 2nd ed. Melbourne: Oxford University Press; 2001. p. 286-342.
Sutherland SK, Leonard RL. Snakebite deaths in Australia 1992-1994 and a management update. Med.J.Aust. 1995;163(11-12):616-8.
White J. Envenoming and antivenom use in Australia. Toxicon 1998;36(11):1483-92.