WikiTox

Animals Included in this Category

Overview

Australia has a number of species of venomous snakes. However the incidence of snakebite and envenoming is low in comparison to many low-middle income countries. This is due to in part to the relatively low population density overall.

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 envenoming centres around several factors :

The clinical and laboratory features that are seen or subsequently manifest themselves
Geographical knowledge of what venomous snakes have been reported to cause bites within the area
Professional identification of the snake (in practice this is often only possible in professional snake handlers who get bitten by their own snakes)

Classification

Snakes can be classified by genera and species however such a classification is impractical for clinicians. It is therefore better to think of snakebite encounters as envenomed or non-envenomed.

Envenomed cases are then most practically thought of in terms of which monovalent antivenom(s) should be administered. There are 5 monovalent anti venom (AV) preparations and 1 polyvalent AV available for terrestrial snakes in Australia.

These are:

Brown Snake AV
Tiger Snake AV
Black Snake AV
Taipan AV
Death Adder AV
Polyvalent AV

Mechanism of Toxic Effects

All significantly venomous Australian snakes are from the elapid family. Their venom can cause a variable mixture of neuromuscular dysfunction, heamatological toxicity and myotoxicity.

Neuromuscular toxicity

Paralysis (skeletal and respiratory muscles) is generally due to presynaptic toxicity although some snakes have significant postsynaptic neurotoxins.

Haematological toxicity

Some snakes may cause a significant coagulopathy as part of envenomation. This is due to potent procoagulants in the venom, which in vivo cause consumption of fibrinogen and fibrinolysis and is referred to as Venom Induced Consumption Coagulopathy (VICC).

Some snake species have a true anticoagulant effect with similar clinical effects but normal fibrinogen. This is thought likely due to inhibition rather than consumption of coagulation factors however the exact mechanism remains unconfirmed.

Myotoxicity

Destruction of skeletal muscle which is postulated to be due to phospholipase A2 (PLA2) toxins in venom.

Kinectics

Snake venom is delivered percutaneously and absorbed via lymphatics. Once it enters the vascular compartment it can then distribute to other parts of the body such as the CNS and skeletal muscle bed causing systemic toxicity.

The absorption/distribution phases can be potentially influenced by use of pressure immobilisation bandaging (PIB) and splinting of an affected limb. Antivenom does not reverse the effects of venom but can prevent further damage by binding it to facilitate elimination. Hence the administration of AV before systemic dissemination is a key goal of management.

Clinical Effects

Australian venomous snakes cause principally systemic rather than local effects.

Non-specific systemic effects

Collapse/syncope can occur early in the course of envenomation and can be difficult to distinguish from other causes. Less commonly it is associated with severe cardiovascular collapse and cardiac arrest. In such circumstances a fatal outcome is common. Most of these events occur pre hospital.

Less severe effects include nausea, vomiting, and headache.

Neuromuscular effects

Neurological effects begin with ocular/cephalic toxicity such as ptosis, diplopia, and ophthalmoplegia. Toxicity can progress in a caudal direction ultimately leading to muscle weakness and respiratory failure.

Haematological effects

VICC is an often-asymptomatic laboratory abnormality which can lead to bleeding from bite wound and/or venepuncture sites and rarely haematemesis and intracranial haemorrhage.

Associated laboratory abnormalities are:

Raised, often unrecordable, INR
Low, often undetectable, fibrinogen
Raised d-dimer reflecting excessive fibrinogen degradation products.

A raised d- dimer is often the first abnormality detected and the presence of a fivefold or more rise within 2 hours of a snakebite is highly suggestive of an evolving VICC pattern.

VICC is described as ‘compete’ (INR >3, undetectable fibrinogen) or ‘partial’ (INR abdnormal but <3, low but detectable fibrinogen)

Anticoagulant coagulopathy: Laboratory abnormalities include a raised APTT and sometimes a very modestly raised INR. This abnormality is sometimes absent despite envenoming occurring depending on the particular laboratory assay being used.

TMA: Characterised by thrombocytopaenia, intravascular haemolysis and a rising serum creatinine, this effect occurs later in the clinical picture.

Myotoxic effects

Rhabdomyolysis: pain or weakness on muscle movement, compartment syndrome, red or brown urine (mistaken for haematuria). The main laboratory effect is a raised Creatinine Kinase (CK) which tends to occur at the 6 to 8 hours point post bite, after the haematological effects.

An early CK rise (< 1000 iu/L) is not uncommonly seen due to activities associated with snake encounters such as bushwalking, and is not a marker of envenoming.

Renal Dysfunction

Primary acute kidney injury (AKI) is uncommon in snakebite. However AKI may occur either secondary to rhabdomyolysis or as part of the TMA picture.

Clinical Assessment

History

Was the encounter a witnessed snakebite? OR were there circumstances such that a bite might have occurred ? (The relative lack of local signs and pain secondary to elapid bites mean that a ‘scratch’ occurring on a limb in long grass could potentially be a snakebite, sometimes referred to as a ‘stick bite’.)
When did the bite occur ?
What venomous snake groups are found locally and thus what clinical effects should we potentially anticipate ?
Has PIB been applied and has the patient been immobile since the encounter ?.
- headache, nausea, vomiting or abdominal pain
- blurred/double vision, slurring of speech, muscle weakness, respiratory distress
- bleeding from the bite site or elsewhere
Relevant past history; specifically ask about
- allergy or past exposure to antivenom - snake AV is made from horse serum so specifically ask about horse allergy
- Is the patient a snake handler ? This increases the likelihood of anaphylaxis to the snake venom !!

Examination

Examine bite site if exposed but leave if covered by PIB.
Perform a brief, focused, neurological assessment looking specifically for ptosis, diplopia or other evidence of muscle weakness.
Monitor vital signs regularly

Investigations

Laboratory Tests

These should be done as per the snakebite pathway and should include :

Full blood count
Coagulation profile including fibrinogen and d-dimer
Urea, electrolytes, Creatinine
Creatinine kinase

The above tests need to be undertaken by a laboratory with appropriate capability. Point of care testing e.g. for INR is unreliable due to both false positive and false negative results. It therefore should not be undertaken.

Whole blood clotting times are no longer recommended for the assessment of coagulopathy in snakebite in Australian practice.

Venom detection kits (VDK) are likewise no longer recommended in assessment of snakebite cases.

Determining Envenoming Status

General systemic symptoms such as headache, vomiting and abdominal pain, have become increasingly recognised as early potential predictors of envenoming.
Demonstrable ocular or cephalic neurological signs or any degree of paralysis
A d-dimer raised greater than five times the upper reference range occurring within 2 hours of bite is indicative of an emerging VICC state.
A raised INR > 1.2, though often unrecordable, associated with low/undetectable fibrinogen levels.
A raised APTT suggesting an anticoagulant coagulopathy.
Raised CK, although this is rarely the first sign of envenoming due to occurring relatively late in the clinical picture.

Treatment and Disposition

First Aid

This is usually performed in the community or by attending ambulance service personnel. Ideally snakebite victims should remain immobile from the time of bite onwards. This may be challenging in practice if the patient is alone in a remote place with limited cellphone reception and thus has to leave the scene to access assistance.

An elasticated bandage is applied to the bitten limb firmly and tightly.
The bandage is extended to cover whole of bitten limb from distal to proximal.
The limb is splinted and the patient kept still.

In hospital

Snakebite victims should be transferred to the closest facility that can administer AV if there are clinical grounds for AV administration (see Treatment section). This requires the receiving facility:

To have appropriate AV available
To be able to treat anaphylaxis if it occurs

If there is no requirement for AV administration on clinical grounds then the patient will require to be transferred to a facility with 24/7 laboratory testing capability. This will enable all suspected or confirmed snakebites to be managed with the use of the snakebite pathway. This pathway commences at the time of bite and involves clinical observation and serial laboratory testing until 12 hours post bite. Thus in practice a patient cannot be declared to be unenvenomed until 13 to 14 hours post bite. (The latter one or two hours due to the time taken for 12 hours post lab test results to be available).

Envenomed patients may require AV but this depends on the picture of envenoming and several other factors. A clinical toxicologist should always be contacted for expert input in this context.

Premedication is not advised routinely when administering AV within Australia. However adrenaline should always be available as there is a risk of anaphylaxis occurring.

Blood products, such as FFP, have been shown to be effective at reducing the INR in VICC cases if administered within 4 hours on AV. In practice this is only performed in scenarios where bleeding complications have occurred. Advice from a clinical toxicologist should be sought.

All envenomed patients require a minimum 24-hour admission. Depending on the envenoming syndrome occurring this may be to the Emergency department short stay unit, inpatient ward or a high dependency type environment.

Antivenom

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.

Administration
Antivenom for snakebite should always be given IV , with all facilities ready to hand to treat anaphylaxis in the event that it should occur.

Dilute the antivenom about 1:10 (1:5 or less may be needed if volume is a problem, e.g. polyvalent antivenom, paediatric patient) in IV fluid (normal saline, or Hartman's solution)
Start infusion slowly, observing patient for reaction
- look for rash, hypotension, bronchospasm, coughing, sneezing, profuse sweating, faecal or urinary urgency or incontinence, abdominal pain, and a “sense of impending doom”
increase rate aiming to give whole dose over 15 to 20 minutes
If a pressure immobilisation bandage is in situ, take it off halfway through the infusion

Dose
The dose is one ampoule of the appropriate antivenom (or one of each appropraite AV e.g. 1 vial of brown and 1 vial of tiger AV are often given when a patient had VICC in an area where Taipans are not found). The dose is the same for children and adults.

Specific Complications of envenoming

Anaphylaxis to venom is a well-documented risk in snake handlers. Anaphylaxis to AV can also occur in any patient and varies depending on the type(s) AV administered.

Serum sickness can occur within 5 to 10 days of AV administration and is a less severe form of allergic reaction. Nonetheless, all patients receiving AV should be counselled in regard to this potential scenario prior to discharge.

Thrombotic microangiopathy can occur and is usually managed by observation. Plasmapheresis is not recommended. Dialysis is occasionally required for renal impairment.

Intracranial haemorrhage is relatively rare but documented to occur with haemorrhagic envenomation syndromes. These tend to occur around 12 hours or more following a snake bite.

Australian Venomous Snakes

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