Brown snakes of the genus Pseudonaja are the most common cause of snakebite and of death from snakebite in Australia. Medically important species are:
Less commonly involved in human bites but still capable of causing significant envenomation are:
Brown snakes have become well adapted to the urban environment and have been known to bite people inside their houses!
Relative to other snakes Brown snakes have small fangs and the bite is painless or almost painless. Not infrequently the snake bite may not be recognised as such.
Coagulopathy is the hallmark of brown snake envenomation and is characterised by complete consumption of circulating fibrinogen and uncoagulable blood. A simple bed side test is to place a blood sample in a clean glass (not plastic) test tube and leave it undisturbed. A whole blood clotting time of greater than 12 minutes is suggestive of coagulopathy; greater than 20 minutes with no clot formation is highly suggestive. The management of Brown snake envenomation and the titration of antivenom is best undertaken by monitoring coagulation studies including INR, APTT, fibrinogen and D-dimer. Once sufficient antivenom has been given fibrinogen levels will be detectable.
For some Australian snake envenomation it has been suggested that more than one vial of antivenom may be required, particularly with regard to Brown snake envenomation in Western Australia. This is currently an area of ongoing study.
This information should be read in conjunction with the detailed background information on Australian snakebite.
|Antivenom||Brown Snake: starting dose 1 ampoules|
|Bite Site||25% effective bite, minimal local pain|
|Principle venom effect||Predominantly coagulopathy|
Brown snakes have adapted well to human land use and are widely distributed throughout mainland Australia. The eastern brown is found throughout the eastern half of the country while the western brown (gwardar) is found everywhere except the SE corner of the continent. Brown snakes cause the majority of snakebites in Australia. However, because of the small amount of venom available (average only 5 mg) and the small fang size (average length only 2.8 mm), many bites do not result in significant envenomation. On average only 1 in 4 or less brown snakebites is severe enough to require antivenom therapy. Nevertheless, when a significant amount of venom is injected, it can cause major and life threatening envenomation very rapidly. All brown snakebites should be treated as potentially lethal.
The colour of even the common or eastern brown snakes is very variable and misleading for identification purposes. They may be brown, red brown, grey, very dark brown and may be plain in colour, have speckling, stripes or bands, or have a dark or black head.
The venom causes coagulopathy, renal failure and (theoretically) paralysis. In practice, the dominant feature of brown snake envenomation is coagulopathy (defibrination type). Rarely, early collapse is seen due to initial intravascular thrombosis as defibrination occurs. Paralysis is only very rarely seen (presynaptic neurotoxin), usually in bites where there has been a long delay in giving antivenom therapy. Renal failure is a moderately common in brown snake envenomation in adults and is usually an acute tubular necrosis, which may occasionally require a period of haemodialysis. If renal failure is present then the coagulopathy is usually of the true DIC type, with thrombocytopenia.
NOTE: Gives positive result in the brown snake tube of the Venom Detection Kit.
Preferred antivenom is CSL Brown Snake Antivenom.
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Hodgson WC. Pharmacological action of Australian animal venoms. Clin. Exp. Pharmacol. Physiol. 1997;24(1):10-7.
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. pp. 286-342.
White J. Clinical Toxicology of Snakebite in Australia and New Guinea. In: Meier J, White J, editors. Handbook of Clinical Toxicology of Animal Venoms and Poisons. 1st ed. New York: CRC Press; 1995. pp 595-618.