snake bites

...now browsing by tag

 
 

Possible new directions in Australian toxinology

Friday, June 26th, 2009

There were a couple of very interesting presentations at the ACEM Winter Symposium in Darwin this week relating to Australian toxinology by A/Prof Geoff Isbister and Dr Bart Currie, and in particular, discussions surrounding antivenom usage.

Box jelly antivenom, whilst binding the venom in vitro, is NOT likely to be of benefit in actual poisonings as mortality cases usually occur within 20 minutes and for the antivenom to be effective in vivo, it would seem that it needs to be given BEFORE the envenomation.

Red back spider (Latrodectus sp) bites are well recognised for causing local severe pain (which appears to be neuropathic type pain and not well controlled by conventional analgesics), localised sweating, and systemic features, has been traditionally been managed in the ED with im red back antivenom, although recent studies have suggested that 2 vials iv is more likely to give demonstrable circulating antivenom, although similar response to pain (~60%) and reduction in systemic features.

Given the absence of detectable circulating redback antivenom when given im, and the similar response rates to iv doses, one hypothesis may be that the responses may be primarily placebo effect and this will need further studies to verify. Of course, anecdotally, there does usually seem to be a response and so if this is a placebo effect, then its a pretty good one!

Now for the Australian snake bite conundrum.

Bites from the Australian Brown Snakes are well recognised for causing:

  • a possible initial hypotensive collapse and possible sudden death – often associated with intracranial haemorrhage which may have resulted from fall to ground, and head strike in an anticoagulated state due to the intravascular coagulation from the bite.
  • profound coagulopathy due to the procoagulant in the venom causing a consumptive coagulapathy which once it has occurred, in particular, depletes factor V, factor VIII, and fibrinogen levels until the liver can restore these level some 8-14 hours later.
  • a late onset neuropathy due to neurotoxins although there appears to be some controversy regarding this

A/Prof Geoff Isbister has shown that you ONLY NEED 1-2 vials of CSL antivenom to neutralise the venom from brown snake bites and 1 vial to neutralise venom from tiger snake bites, and furthermore, that there is NO POINT giving more antivenom to try to reverse the coagulopathy – this may need early FFP to achieve this although studies will need to be done to confirm this hypothesis. The main benefit of giving the antivenom appears to be in reducing the late neurotoxic effects – NOT the coagulopathy although having been given the antivenom, it lasts in the body a couple of weels or so, and may prevent a coagulapathy in a subsequent snake bite during this time period although this is speculative!

Furthermore, it has been shown that CSL tiger snake and brown snake antivenoms are actually polyvalent, and thus there is a push to have CSL just market them as a single brown snake/tiger snake antivenom, but this would need re-submission for marketing approval.

The possible conseqence of this, could be that in areas of Australia where the snake bites are almost entirely either brown snake or tiger snake such as in south-eastern Australia, the snake bite venom detection kits may become redundant!

An interesting question then arises in my mind:

Currently the practice with asymptomatic Australian Elapid snake bites managed with early pressure immobilisation is that once iv access and resuscitation equipment and antivenom is available, that the pressure immobilisation be removed in the ED under close observation, and if signs of envenomation occur such as coagulopathy or neurotoxicity (test by looking for ptosis on prolonged upward gaze of 30sec), then the pressure immobilisation is temporarily re-applied whilst antivenom is given.

The potential problem with this approach is that once you have allowed the coagulopathy to occur – assuming early pressure immobilisation prevents this – it is now too late to stop it using antivenom.

Thus, if you really believe the patient has been bitten by a brown snake, and likely to have been envenomated, and the risks of coagulopathy outweigh the risks of 1 vial of antivenom administration, then perhaps we should give that vial of antivenom BEFORE removing the pressure immobilisation – this of course may mean many more would get a vial of antivenom even though they may not be envenomated but it seems to me something to consider. Now, I am NOT a toxinology expert but it does seem to me the logical course to take.

Well it is all fascinating stuff – and maybe in the end, we can save the hospitals considerable amounts of money in VDK’s and antivenom, while the patients will hopefully have lower doses of antivenom and less serum sickness as a result – seems like a win-win situation to me – except there does not seems to be much incentive for CSL to play ball and help us achieve this.

Post script:
A paper published in the Emergency Medicine Australasia (EMA) this month (2009 21, 184-190) by Canale, Isbister and Currie suggests that pressure immobilisation bandaging (PIB) for snakebite may not be adequate when crepe bandages are used, and only adequate some 50% of the time when elasticized bandages are used. The recommendation is that people should be made aware of the relative inadequacy of crepe when compared to elasticized bandages, and that perhaps more important is the need for immobilisation.