Snake envenomation is a toxicity that requires immediate action in any veterinary practice, regardless of whether a snake has been identified or not. In Queensland alone, there are approximately 120 known species of snakes, of which 65% are venomous (80). And if you’re practicing in the warmer parts of Australia, there’s a fair chance you’ve encountered a snake bite case in your clinic! That’s why we’ve put together a series of articles all about snake envenomation in dogs and cats to guide you through your next case.
But snake detection can be difficult and owner recognition is reported as being poor, making each presenting patient a challenge whether they’re happily walking or being carried moribund through the door. Given the major neurological consequences and coagulopathies that can arise, detecting and appropriately treating a patient with a suspected snake bite can prove challenging for even the most experienced veterinary professional.
In our first article, we’ll provide you with the various pathophysiology behind snake envenomation in dogs and cats and the mechanisms triggered by envenomation. In order to understand this, it’s vital to first understand the main categories of snakes, particularly those that are capable of causing life-threatening illness. Snakes can be divided into two broad categories: the front-fanged snakes (Elapids) and the rear-fanged snakes (Colubrids).
An Example of Some Venomous Elapids:
Elapids contain some of the most venomous snakes in the world and include species like the Eastern Brown, Tiger Snake, Taipan, and Death Adder (to name just a few). A list of common Elapids is located in the images above to allow direct identification when required. In comparison, some Colubrids produce weak venom and as their fangs are located at the back of their mouth, they are also considered poor envenomators and non-life threatening (e.g., Whip snakes). Boids and Pythons are also commonly seen, which are considered non-venomous.
An Example of Some Non-Venomous Species:
Regardless of whether a venomous or non-venomous snake is suspected, all owners should be advised to have their pet assessed, and a snake detection test performed on the patient where applicable. For the safety of the owner, they should NOT be advised to capture the snake, though if it has been obviously killed in the process (ie: in more than one piece), then identification of the snake can be made in house (ie: counting scales – ventral, dorsal mid-body, anal division or single, and subcaudal tail division, single or both). Your official state government website can also be highly useful in aiding with snake identification.
The Mechanisms of Snake Envenomation in Dogs and Cats
Although snake venom varies significantly between species, the majority of the toxic enzymes in venomous snakes are phospholipases, more specifically a phospholipase A2. As a result they act on cell membranes, leading to neurotoxic, myotoxic, haemotoxic, cardiotoxic and nephrotoxic effects. Coagulopathies are also present due to either activation of the common coagulation pathway (pro-coagulant) or from anti-coagulant effects, or a combination of both.
Pre-paralytic signs have been shown to be a result of acute prothrombin activation and obstruction to the outflow of the right ventricle, leading to cor pulmonale, impedance of left ventricular filling and sudden acute hypotension. It is now also suspected to be related to an acute hypersensitivity response and release of vasoactive substances causing an acute hypotensive response.
What Does Snake Envenomation in Dogs and Cats Cause?
There are several distinct mechanisms by which snake envenomation in dogs and cats can lead to acute and fatal life-threatening illness. This includes:
Neurotoxicity
The severity of neurological impairment depends on whether the particular toxin attaches to the pre-synaptic terminal or post-synaptic terminal at the neuromuscular junction (NMJ). Neurotoxins attached to the pre-synaptic terminal tend to have a greater affinity for their receptors, are less responsive to antivenene administration, and cause more severe neurological disease.
Coagulopathy
There are varying degrees of coagulopathies amongst snake species, and their severity depends on whether they are caused pro-coagulant or anti-coagulant toxins. The most severe coagulopathies are caused by pro-thrombotic toxins and mimic factor-Xa, combining with endogenous factor Va to cleave prothrombin into thrombin and proceed into Venom Induced
Consumptive Coagulopathy (VICC)
This mechanism leads to increased fibrin degradation products (FDP), and prolonged PT, APTT and ACT. Copperhead snakes are the only snake that show anti-PLT activity, so most snakes will have a normal PLT number initially, though can be reduced in time due to blood loss.
Nephrotoxicity
Although this is not well understood, nephrotoxicity from snake envenomation is thought to arise from indirect actions of tubular damage associated with myoglobinuria and bilirubinuria, hypovolaemia, procoagulation and hypoxaemia-ischemia injury at the glomerulus.
Myotoxicity
Rhabdomyolysis from a myotoxin is common and can lead to elevated creatine kinase and subsequent renal tubular damage if not treated. Other intra-cellular components will also lead to hyperphosphatemia, hyperkalemia, hypermagnesemia and a metabolic acidosis.
Haemotoxicity
Haemolysis is also variable amongst snake venom, however, their potency tends to be more exaggerated in species seen in the eastern states of Australia and can require blood transfusions if global hypoxia is evident (ie: elevated lactate, low ScvO2, low base excess, tachycardia). Disruption to the cell membrane by phospholipase causes water to enter the cell, allowing it to swell and causing cell destruction.
Cardiac Toxicity
This is typically specific for Taicotoxin from the Taipan, and it has been shown to inhibit calcium channels in the myocardium, leading to prolonged repolarisation and arrhythmias. Caution is used in relation to possible fluid overload due to its effects as a negative inotrope and chronotrope, and positive lusitrope. Other cardiac toxins have not been ruled out from other elapids, though are weak in nature if present.
Now that we have an understanding of the mechanisms behind snake envenomation in dogs and cats, our next article on snake envenomation will guide you through one of the most important and challenging steps in the suspected snake bite patient: diagnosis of snake envenomation. For more on snake envenomation, but sure to access the full Snake Envenomation Protocol at VetAPedia.
