Australian Snake Bites

In Australia there are about 3,000 snake bites per year, resulting in about 500 hospital admissions (Weldon, 2017). Many receive antivenom; on average two per yearwill prove fatal. About half the deaths are due to bites from the brown snake; the rest mostly from tiger snake, taipan and death adder. While some deaths occur soon after the bite, it is uncommon to die within four hours of a snake bite.

Deaths from anaphylaxis following bee, hornet, tick or other arthopod bite happen as frequently as deaths from snake bite.

Struan Sutherland's 'Death from snake bite in Australia, 1981-1991' (The Medical Journal of Australia, December 1991, Volume 7, pages 740-46) contains some graphic descriptions of the 18 known fatal snake bites in that ten year period.

In 1906, the untreated death rates were as high as 40% to 50% for death adder and tiger snake bites! Improved supportive treatment and the availability of effective antivenoms has reduced this considerably.


For more information go to the Australian Reptile Park or read this excellent Australian Prescriber Review.

CSL provide a smartphone app for Apple and Android.

Snake Identification

Before the advent of polyvalent antivenoms it was extremely important to positively identify the snake. Although less important now, it remains highly desirable, because snake-specific antivenoms are less hazardous to the patient than polyvalent antivenoms. Snake identification can be very difficult if it was seen fleetingly or in poor light. Scale patterns and colours can be quite unreliable, especially for brown snakes.

Venom identification kits, on the other hand, can often accurately identify the type of snake in 30 minutes, and thus reliably and safely reduce the need for administration of polyvalent antivenom.

If identification is uncertain, ALWAYS treat as if the snake was unidentified.

The Australian Reptile Park are experts in snakes and envenomation. If you have the time to visit them I recommend it highly. Brian Bush has a page for WA snake identification. Detailed information with pictures is also available from - click on snakes and select australia as the country.

See also Tamworth Animal Hospital's Snake Envenomation slide s by Peter Best

Common or Eastern Brown Snake Pseudonaja textilis

brownsnake1brownsnaked1The Brown Snake may be found all over Australia. It has extremely potent venom, and although the quantity of venom injected is usually small, this snake causes more snakebite deaths in Australia than any other. Sudden and relatively early deaths have been recorded. Its venom causes severe coagulation disturbances, neurotoxicity, and occasionally nephrotoxicity (by a direct action of the venom), but not rhabdomyolysis. The Gwardir is also known as the Western Brown snake, and the Dugite is a spotted brown snake found in Western Australia. All need brown snake antivenom. See also Venom Supplies brown snake pages, Emedicine Brown Snake guidelines,, AVRU brown snake info and treatment, Australian Reptile Park, Wikipedia. Some more local pics:

Taipan Oxyuranus scuttelatus

taipantaipandThe taipan may be found mostly along the non-desert areas of north and north-east Australia (from Brisbane to Darwin). It is an aggressive, large, slender snake, and may be coloured any shade of brown but always has a rectangular head (large in proportion to the body) and red eye. Venom output is high and causes neurotoxicity, coagulopathy, and rhabdomyolysis, and the amount retrieved from just one milking from one taipan is enough to kill many million mice. Paralysis is difficult to reverse unless treated early. Untreated, a good bite will almost certainly be fatal. See also Venom Supplies, AVRU taipan info and treatment, Wikipedia.

Another picture:Taipan - Oxyuranus scuttelatus (49K jpeg)

Tiger Snake Notechis scutatus

tigersnaketigersnakedThe tiger snake lives in the temperate southern areas of Australia. The characteristic stripes are not seen all year round, and there is a totally black variant found around the Flinders Ranges area of South Australia. As well as neurotoxicity and coagulopathy, rhabdomyolysis (due to Notexin in the venom) is very likely if treatment is delayed. Untreated mortality is about 45%. See also Venom Supplies tiger snake page, AVRU tiger snake info, and treatment, Aust Reptile Park, Wikipedia.

Some more pictures: Eastern Tiger Snake - Notechis scutatis (32K jpeg), Black Tiger Snake - Notechis ater (40K jpeg)

Death Adder Acanthopis antarcticus

deathadderdeathadderdThe death adder has strongly neurotoxic venom; coagulation defects are usually minor and rhabdomyolysis is almost never seen. The postsynaptic paralysis is easily reversed by antivenom. It has characteristic appearance and may be striped. See also Venom Supplies, AVRU death adder page, and treatment, Aust Reptile Park, Wikipedia.

Another picture :Death Adder - Acanthopis antarcticus (22K jpeg)

Copperhead Austrelaps superbus

copperheadcopperheaddThe copperhead is found in Tasmania, Victoria, and the western plains of NSW. Its venom has neurotoxic, coagulopthic and myotoxic actions, however, despite its large venom output, bites are rarely fatal. Use tiger snake antivenom. See also Venom Supplies copperhead page. AVRU copperhead page, Aust Reptile Park, Wikipedia.

Another picture: Copperhead - Austrelaps superbus (29K jpeg)

Rough Scaled Snake Tropidechis carinatus

roughscaledsnakeroughscaledsnakedThe rough scaled snake is found mostly in northeastern non-arid areas. It may be striped, and hence confused with the tiger snake. It is extremely ill-tempered, and has venom with neurotoxic, coagulopthic and myotoxic actions. See also AVRU rough scaled snake page.

Another pic: Rough Scaled Snake - Tropidechis carinatus (45K jpeg)

King Brown or Mulga snake Pseudechis australis

kingbrownkingbrowndThe king brown (or mulga) snake is found in all arid parts of Australia, and has the greatest venom output, with neurotoxic, coagulopthic and myotoxic actions, but of relatively low toxicity. It has a strongly defined dark crosshatched pattern on its scales, and is more related to the black snakes than the brown. The king brown needs black snake antivenom. See also Venom Supplies.

Another picture: Mulga (King Brown) Snake - Pseudechis Australis (20K jpeg)

Redbellied Black Snake Pseudechis porphyriacus

redbellyblackredbellyblackdThe redbellied black snake is found in all eastern non-arid areas. While the venom has neurotoxic, coagulopthic and myotoxic actions, it is not as potent as most, and no deaths after a redbellied black snake have yet been reported. Black or tiger antivenom may be used. Can 'jump' in the air if disturbed or chased. Another picture from John Loadsman during a bushwalk.

See also Venom Supplies, AVRU black snake page, Aust Reptile Park.

Small Scaled or Fierce Snake Oxyuranus microlepidotus

smallscalesmallscaledThe small scaled snake (sometimes called the inland taipan or fierce snake) has the most potent venom in the world, but is restricted to relatively uninhabited areas of south-western Queensland, so, fortunately, not many people get bitten. Use taipan antivenom. More info: Aust Reptile Park, Wikipedia.

Another picture: Fierce (Small Scaled) Snake - Oxyuranus microlepidus (30K jpeg)


Signs and Symptoms

The bite site is usually painless. It may have classical paired fang marks, but this is not the most common picture. Often there are just a few lacerations or scratches, and sometimes these may be painless or go unnoticed. Bruising, bleeding, and local swelling may be present, but significant local tissue destruction is uncommon in Australia.

Regional lymphadenopathy may be marked, even with non-venomous snake bites, and is not by itself an indication for the administration of antivenom. It may contribute to abdominal pain in children.

The usual sequence of systemic symptom development goes something like this:

  • (<1hr) Headache (an important symptom), irritability, photophobia, nausea, vomiting, diarrhoea, confusion; coagulation abnormalities; occasionally sudden hypotension with loss of consciousness.
  • (1-3 hrs) Cranial nerve paralysis (ptosis, diplopia, dysphagia etc), abdominal pain, haemoglobinuria, hypertension, tachycardia, haemmorrhage.
  • (>3hrs) Limb and respiratory muscle paralysis leading to respiratory failure, peripheral circulatory failure with pallor and cyanosis, myoglobinuria, eventually death.

This sequence of events is highly variable. Brown snake bites, even apparently trivial ones, have been associated with acute deterioration over a five minute period leading to death. This may occur as soon as 30 minutes to an hour after the original bite. Acute, severe cardiac depression may be the mechanism for sudden death.

Paralysis, when it occurs, usually commences with cranial nerves, then skeletal muscle, then the muscles of respiration. In small children or with highly venomous snake bites it may happen much more quickly.

Major bleeding disturbances are, as mentioned before, rare with Australian snakes, although the development of coagulopathies and a DIC-like picture are relatively common. Thromboctopaenia and haemolysis may occur. Watch for haematuria, haemoptysis, haematemesis, low bowel haemmorrhage, menorrhagia or haemoglobinuria, and remember that about 20% of patients who die after snake bite have cerebral haemmorrhages.

Muscle destruction from myolytic toxins is not uncommon and may not be associated with muscle tenderness; it may lead to renal failure and should be specifically looked for, because early treatment with antivenom will reduce its severity.

Snake bite should always be considered in any case of unexpected confusion or loss of consciousness following outdoor activities in snake country. In Australia, snake venoms alone cause coagulopathy, so if present you can rule out other forms of envenomation.

Prognosis depends on the type of snake and the quantity of venom injected. An angry snake and multiple bites is associated with greater venom volumes.

Snake bites and domestic pets

Ian Westbrook describes, in this moving story, how an apparently trivial bite from a tiger snake caused the death of one of his dogs. In contrast, Donna describes her experience with a Death Adder bite.

Murdoch University provided a 'pets in summer - snakebite warning' page with some general information for WA.

First Aid for Snake Bites:

Do NOT wash the area of the bite or try to suck out the venom!

It is extremely important to retain traces of venom for use with venom identification kits.

Do NOT incise or cut the bite, or apply a high torniquet!

Cutting or incising the bite won't help. High torniquets are ineffective and can be fatal if released.

Stop lymphatic spread - bandage firmly, splint and immobilise!

The "pressure-immobilisation" technique is currently recommended by the Australian Resuscitation Council - see their guidelines, the Royal Australasian College of Surgeons and the Australian and New Zealand College of Anaesthetists.

The lymphatic system is responsible for systemic spread of most venoms. This can be reduced by the application of a firm bandage (as firm as you would put on a sprained ankle) over a folded pad placed over the bitten area. While firm, it should not be so tight that it stops blood flow to the limb or to congests the veins. Start bandaging directly over the bitten area, ensuing that the pressure over the bite is firm and even. If you have enough bandage you can extend towards more central parts of the body, to delay spread of any venom that has already started to move centrally. A pressure dressing should be applied even if the bite is on the victims trunk or torso.

Immobility is best attained by application of a splint or sling, using a bandage or whatever to hand to absolutely minimise all limb movement, reassurance and immobilisation (eg, putting the patient on a stretcher). Where possible, bring transportation to the patient (rather then vice versa). Don't allow the victim to walk or move a limb. Walking should be prevented.

The pressure-immobilisation approach is simple, safe and will not cause iatrogenic tissue damage (ie, from incision, injection, freezing or arterial torniquets - all of which are ineffective).

This is an example of a suitable compression bandage.

This poster from is worth keeping.

Bites to the head, neck, and back are a special problem - firm pressure should be applied locally if possible.

Removal of the bandage will be associated with rapid systemic spread. Hence ALWAYS wait until the patient is in a fully-equipped medical treatment area before bandage removal is attempted.

Do NOT cut or excise the area or apply an arterial torniquet! Both these measures are ineffective and may make the situation worse.

Joris Wijnker's Snakebite Productions has more information on envenomation and he can supply a suitable first aid kit and booklet.

Medical Management of Snake Bites

Only 1 in 20 snake bites require active emergency treatment or the administration of antivenom, but every snake bite should be managed as a medical emergency until resolved, even if the patent seems well on presentation. Medical management depends on the degree of systemic envenomation, the effectiveness of first aid bandaging, and the type of venom.

Note that local signs of tissue damage, bruising etc are not common following Australian snake bite.

For phone advice in Australia call the National Poisons Information Centre on 13 11 26.

Also see the ARC guidelines on snake bite, Antivenom Update by Ian Whyte in Australian Prescriber 2012, MJA article by Isbister 2013. emedicine Brown Snake envenomation management 2013, RCH Melbourne Snakebite page, .

Critically ill patients

  • Maintain immobilisation, splint and bandage until the situation is under control!
  • Support airway, breathing and circulation.
  • Intubate and ventilate with 100% Oxygen if airway or respiration fail.
  • Give antivenom immediately (See below for details). Intravenous adrenaline should be given only for lifethreatening hypotension or anaphylaxis - its use has been associated with cerebral haemorrhage.
  • Volume expansion may be necessary.
  • Severe coagulation disturbances, electrolyte abnormalities, and muscle damage leading to acute renal failure are likely.
  • Repeat antivenom as clinically indicated.
  • General management as for less seriously ill patients as well (see below).

Less seriously ill patients - no signs of systemic spread

  • Admit to ICU for non-invasive monitoring, strict bedrest and full head injury observations (wake hourly).
  • Leave bandages in place.
  • Obtain appropriate antivenoms and venom detection kit.
  • Obtain intravenous access.
  • Take blood for group and X-match, coagulation screen (including APTT, fibrinogen levels, CK and tests for DIC), full blood count, electrolytes and calcium, creatinine kinase and arterial blood gases. Perform ECG. Repeat at appropriate intervals.
  • Collect urine for microscopy to detect haematuria and for free protein, haemoglobin and myoglobin measurement. Record urine output. Freeze the first sample for venom detection.
  • Draw up adrenaline, antihistamine, and steroids in case of anaphylaxis to antivenom.
  • When ready, cut a hole over the wound site, inspect and take swabs for use with the venom detection kit.
  • Once the results of the venom detection kit are known, slowly and progressively remove the bandages. Don't rush!

If systemic symptoms ensue:

  • Re-apply bandages and give antivenom as clinically indicated.
  • Ensure the patient is well hydrated (to reduce the risk of acute renal failure due to rhabdomyolysis).
  • Repeat blood tests, ECG, etc at clinically relevant intervals.
  • Correct abnormal coagulation; look out for disseminated intravascular coagulation (heparin probably contra-indicated in DIC from snake bite).
  • Analgesia and sedation - be cautious.
  • Correct hypotension, if present, with volume expansion and vasopressors (exclude occult bleeding).
  • Watch for development of renal failure - monitor urine output and composition.
  • Tetanus prohylaxis is recommended.

Usually, if there are no signs of envenomation four hours after removal of the bandages, and if repeat blood tests taken at that time are normal, then it is probable that significant envenomation has not occurred. If laboratory tests are not available, 12 to 24 hours is a reasonable period of observation.

Recovery is usually complete, though the patient usually develops a sensitivity to equine immunoglobulin.

If the patient develops serum sickness (see below), the severity is reduced by steroid administration (eg. prednisolone 1mg/kg every 8 hours) until resolution occurs. A course of steroids is recommended in all patients who receive polyvalent antivenoms.

Antivenoms and Pre-Treatment

Antivenom should be given to all patients who exhibit signs of systemic spread.

If possible choose the appropriate antivenom. Snake identification is unreliable (unless the person works with snakes or was bitten in a zoo and they know what bit them!). Venom detection kits (instructions) may be helpful; if in doubt use tiger snake antivenom in Tasmania, tiger and brown snake antivenom in Victoria, and polyvalent antivenom in all other states and New Guinea. One ampoule (50ml of 17% protein) should neutralise the average venom yield from milking a snake of that species, and is usually enough for all but the most severe envenomations. Severe bites may require much more and a recent in vitro study (Sprivulis, Jelinek and Marshall. Anaesthesia and Intensive Care 1996; 24: 379-381) suggests that much more is also required to neutralize the procoagulant effects of Brown and Tiger snakes (up to 20 times the recommended dose!). If the situation allows, antivenoms should be given slowly (over half an hour, diluted in an IV fluid). A test dose may be advisable, particularly following prior exposure to equine protein.


Antivenoms are prepared from horse serum. The risk of anaphylaxis is very low (less than 1% even for polyvalent antivenoms), but is increased in people who have had prior exposure to horses, equine tetanus vaccines, and a general allergic history. This increased risk is much more common in people aged 50 years or more. About 4% of all administrations are associated with minor reactions.

Pre-treatment with a non-sedating anti-histamine (ie, promethazine 0.25 mg/kg), subcutaneous adrenaline (0.25mg for adults, 0.01mg/kg for children), and iv steroids (hydrocortisone 2mg/kg) is still recommended, athough severe reactions are rare. In general the risk from the snake toxins is much greater than the risk of administering the antivenom.

Each State in Australia has a specifically formulated polyvalent antivenom to suit local snake species, however it is preferable to use a snake-specific antivenom whenever possible to reduce the chance of reactions. Details of which antivenom to use varies from state to state, and are found with the packs and test kits.

If an antivenom is administered, ALWAYS advise the patient of the possibility of delayed serum sickness (up to 14 days later). This is characterised by fever, rash, generalised lymphadenopathy, aching joints and renal impairment. The likelihood of developing this depends on the volume of antivenom required. It occurs in about 10% of patients who are given polyvalent antivenoms. Treatment with steroids is usually all that is needed.

Supplies of antivenoms may be obtained from Commonwealth Serum Laboratories, Australia. Struan Sutherland has suggested that metropolitan and regional hospitals should keep 4 ampoules of polyvalent antivenom and 4 ampoules for each type of snake that is found in the area. He also suggested that smaller centers should stock enough antivenom, as approprite for the local snake population, to manage one bite, unless the incidence of snakebite is unusually high or low in that area. In southern Victoria a combination of tiger (3000 units) and brown snake (1000 units) antivenoms can be used where the identity of the snake is unknown, and in Tasmania tiger snake antivenom alone (6000 units) is suitable. Shelf life is 3 years when stored in a refrigerator. Antivenoms should not be frozen.

Other pages of interest include my general envenomations page (links to other information sources, antivenoms etc) and my pages on Australian spider and marine envenomation.

This page was written from information provided by Dr. Struan K. Sutherland and from published papers. Inaccuracies and errors may exist and the content may become out of date with time.

Last updated Monday, August 21, 2017
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