Used for neutralising systemic envenoming by members of the Australian black snake group. It is made from horse IgG. Each ampoule contains 18000 units of neutralising capacity against the target venoms. Average volume per ampoule is 30-50mL. The immunising venom is mulga snake venom.
The main species for which this antivenom is used are the mulga snake (=king
brown), Butler's mulga snake, Collett's snake and the Papuan black snake. It
is also effective for bites by other members of this genus, namely the red bellied
black snake and the blue bellied black snake (=spotted black snake). However,
CSL Tiger Snake Antivenom is usually used in preference for treating bites by
these latter three species. For this reason, details about these snakes is given
in the section on CSL Tiger Snake Antivenom.
The mulga snake or king brown is a large land snake which may exceed 2.5m in length. It has moderately large fangs and produces more venom than any other Australian snake. It is fortunate that this venom is less toxic than some of the other species. It is brown to red brown in body colour, with cream coloured belly scales. The body scales have distinctive colouration, being paler brown or cream on the inner aspect, darkening towards the margin of each scale. This gives the snake a subtle reticulated appearance, but is easily mistaken for a uniform brown colour. The head is large and triangular in shape, compared to the true brown snake.
Butler's mulga snake is similar except it has more distinct yellow or cream markings on the body, producing a speckled pattern in some specimens.The appearance of the other species is listed in the section on CSL Tiger Snake Antivenom.
Collett's snake may exceed 2.5m in length. It is brown with pinkish specs on the body which is almost banded in some specimens.
|Mulga or king brown snake Pseudechis australis|
|(no photo)||Butler's mulga snake Pseudechis butleri|
|Collett's snake Pseudechis colletii|
The mulga snake is common in arid and semi arid areas through to tropical areas in northern Australia. It is found in some urban areas in central and northern Australia. Butler's mulga snake is restricted to inland areas of thesouthern half of WA. Collett's snake is found in a restricted area of central Queensland.
Mulga snake venom contains several potent phospholipase toxins that are either myotoxins or neurotoxins. There is also an anticoagulant toxin, but no procoagulant is present. Butler's mulga snake is presumed to have a similar venom. Collett's snake has venom similar to the mulga snake.
It is not known what proportion of mulga snake bites would be lethal if no treatment were given, though a figure of 30% has been estimated. Because of the size of these snakes and the large amount of venom available, it may be expected that most cases will be envenomed. Locally, bites cause pain and extensive swelling, which may involve much of the bitten limb, however tissue damage is rare and the swelling usually subsides over 2-4 days. The principal clinical problem with mulga snake bites is myolysis, which may be severe, with potential for secondary kidney failure and hyperkalaemia. The usual clinical features of myolysis may be expected, including myoglobinuria (red to brown urine testing positive for blood), skeletal muscle weakness and pain on movement.
Defibrination coagulopathy is not seen, but there may be slight elevation of clotting times due to anticoagulants in the venom. Because there are neurotoxins in the venom, paralysis might be predicted theoretically, but in clinical practice, neuromuscular paralysis of clinical significance is rarely seen (except for ptosis), though there may be detectable muscle weakness secondary to muscle damage. Occasionally there may be an anticoagulant coagulopathy, with prolonged prothrombin time and aPTT, but normal fibrinogen and no fibrin(ogen) degradation products. Collett's snake and probably Butler's mulga snake cause similar clinical effects.
As with most antivenoms, CSL Black Snake Antivenom should only be given if there is clear evidence of envenoming. See potential complications. It should be given intravenously, through a drip set. If possible, dilute antivenom up to 1 in 10, with an isotonic crystaloid solution (eg saline, Hartmans or dextrose). In general, each ampoule/dose should be run over 15-30 minutes.Prior to commencing antivenom therapy, make sure everything is ready to treat anaphylaxis, should this occur. Specifically, have adrenaline ready to give. If there is an infusion pump available, have this set up to run through a side arm of the drip set, with a solution of dilute adrenaline (eg 6mg adrenaline in 100mL of saline or 5% dextrose, or equivalent dilution). Clearly mark this pump, so that it is not accidentally started.
The use of adrenaline as pre-treatment when using antivenoms is still being debated. The risk of anaphylaxis varies from antivenom to antivenom. People who have had previous exposure to equine derived products may be at greater risk. It is recommended that the Product Information be read before use and if necessary, contact be made with a specialist in the field.
The antivenom of choice for envenoming by mulga snakes is CSL Black Snake Antivenom. It should be used in every case where there is evidence of systemic envenoming. Because whole blood clotting time is unlikely to be prolonged greatly in mulga snake bites, it is not a useful measure of systemic envenoming in these cases. Therefore, in any case of mulga snake bite, Collett's snake bite or Butler's mulga snake bite, if there are general symptoms of envenoming present, such as persistent headache with nausea/vomiting or abdominal pain, it is generally advisable to give 1 vial of antivenom. If there is already severe myolysis established at the time of presentation, it may be necessary to give a second vial of antivenom.
For bites by the red bellied black snake and the blue bellied black snake (=spotted black snake), see the section on CSL Tiger Snake Antivenom. Should this antivenom be unavailable, then the initial dose of CSL Black Snake Antivenom for bites by these species requiring antivenom therapy (many bites don't need antivenom), is often listed as 1/3 to 1/2 a vial. Except in smaller children, where volume is an issue, in practice it is probably best to give a full vial. This ensures a very adequate dose is given and avoids wastage of antivenom. It may increase the risk of serum sickness, but this is a lesser consideration.
Any patient who has received antivenom may develop serum sickness, from 4 to 14 days later. Before leaving hospital, they should be advised of the symptoms of serum sickness, such as rash, fever, joint aches and pains, malaise, and told to return immediately for review and probable commencement of oral steroid therapy. If there was major envenoming, organise follow up. This is usually not necessary for minor envenoming. It may be useful to give a 5 day course of oral steroids as prophylaxis for serum sickness (eg 30-50mg daily of prednisolone, for adults).