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 :
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:
All significantly venomous Australian snakes are from the elapid family. Their venom can cause a variable mixture of neuromuscular dysfunction, heamatological toxicity and myotoxicity.
Paralysis (skeletal and respiratory muscles) is generally due to presynaptic toxicity although some snakes have significant postsynaptic neurotoxins.
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.
Destruction of skeletal muscle which is postulated to be due to phospholipase A2 (PLA2) toxins in venom.
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.
Australian venomous snakes cause principally systemic rather than local 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.
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.
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:
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.
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.
Primary acute kidney injury (AKI) is uncommon in snakebite. However AKI may occur either secondary to rhabdomyolysis or as part of the TMA picture.
These should be done as per the snakebite pathway and should include :
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.
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.
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:
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.
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.
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.
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.
Video: Does post-synaptic neurotoxicity occur in snakebite - Dr Anjana Silva - TAPNA ASM 2019
Video: D-dimer in snakebite - Dr Geoff Isbister - TAPNA ASM 2020
Video: The golden hours for snake antivenom - Prof Geoff Isbister - TAPNA ASM 2021
Video: Thrombotic microangiopathy in snakebite: What’s new - Dr Tina Noutsos - TAPNA ASM 2021
Video: Snakebite Quiz - Prof Geoff Isbister - TAPNA ASM 2022
Video: Snake Venom Proteomics - Dr Theo Tasoulis - TAPNA ASM 2022