Page 492 - Clinical Small Animal Internal Medicine

460 Section 5 Critical Care Medicine

mechanisms, including interactions with von Willebrand patients bitten by snakes every year is unknown but it is
VetBooks.ir factor (vWF) receptors and fibrinogen receptors. Platelet estimated to be between 150 000 and 300 000. Animals
that are most at risk are those that live in a rural or semi-
activation occurs through a thrombin‐like effect of pro-
teinases and phospholipase A 2 , among other mediators.
in wilderness areas are also at high risk, especially if
Besides the effect of venom on primary and secondary rural environment although dogs that are taken on walks
hemostasis, proteins in the venom can affect the endothe- allowed off leash. There is a strong seasonal influence on
lium. Metalloproteinases, disintegrins, and C‐type lec- the incidence of snake bites, with the majority of bites
tins degrade the blood vessel extracellular matrix, induce occurring in the spring and summer months.
endothelial cell apoptosis, and inhibit platelet binding The severity of a bite depends on several variables,
through interference with vWF. The net result of this including the time that has elapsed since the snake’s last
combined action is consumption of fibrin and develop- meal (it takes approximately 20 days for pit vipers to
ment of bleeding diathesis that is not generally character- replenish venom stores), the motivation of the snake
ized by thrombosis or intravascular coagulation. (defensive or offensive), and its age. Bites from immature
Neurotoxins contained in snake venom exhibit a snakes in the spring months are often more severe than
predilection for peripheral nervous tissue and relatively bites that occur later in the season since juvenile pit vipers
few are capable of crossing the blood–brain barrier. have not developed the ability to control the amount of
Venoms that exert a primarily neurotoxic effect act as venom that is injected with each strike but rather deliver an
either presynaptic (beta‐neurotoxins) or postsynaptic “all or nothing” bite. Therefore, somewhat counterintui-
(alpha‐neurotoxins) neuromuscular blocking agents; tively, it is arguably better for an animal to be bitten by a
most neurotoxic venoms contain toxins that affect both large adult pit viper than a juvenile. The metabolic demands
the pre‐ and postsynaptic neuron. Presynaptic or beta‐ required to synthesize venom are quite high so adult snakes
neurotoxins have been isolated from members of the will often deliver an initial “dry bite” (a bite containing no
Elapidae and Viperidae (including Crotalidae) families. venom) as an attempt to deter a pet from further harassing
Most of these toxins inhibit neurotransmitter (acetyl- them. Subsequent defensive strikes, however, are often
choline) release although a small number have been very severe as the snake continues to feel threatened and is
identified that actually enhance neurotransmitter committed to finally deterring its assailant.
release. Postsynaptic or alpha‐neurotoxins result in a The most common location of bite wounds is the head
curare‐like syndrome by binding acetylcholine recep- (79%) followed by extremities (16%) while bites to the
tors on the postsynaptic membrane or interfering with torso account for less than 2% of confirmed snake bites.
acetylcholine interaction with its postsynaptic recep- Additionally, single bites are much more common than
tors. The degree of inhibition is related to the number multiple bites, with multiple bites occurring approxi-
of receptors occupied by toxin molecules. Most of these mately 15–30% of the time. The small puncture wounds
toxins bind irreversibly to the acetylcholine (ACh) typical of snake bites are often difficult to locate and can
receptor although treatment with antivenin seems to be easily overlooked, especially if no surrounding local
accelerate toxin–receptor dissociation. tissue reaction is present. Only 20–25% of known rattle-
A unique syndrome resulting in myokymia (sponta- snake bites are actually envenomating.
neous undulating fine contractions of multiple individ- Cats appear to be inherently more resistant to pit viper
ual motor units) has been identified with venom from venom than dogs. However, when cats do present for
timber rattlesnakes (Crotalus horridus). Primarily neu- veterinary care, their clinical condition is generally more
rotoxic snake bites result in much less local tissue inflam- advanced. This may be due to cats’ habit of hiding and
mation and pain than their necrogenic counterparts. avoiding human contact following a snake bite compared
Large necrosing wounds are uncommon in these cases. to dogs who are more likely to seek human interaction.
Cats’ smaller body size and inclination to “toy” with
possible prey may also be contributing factors to explain
Epidemiology these findings.
The species of snake is known in less than 50% of cases
Of the approximately 2300 species of snakes worldwide, although this can often be inferred based on the known
about 420 are venomous. Venomous species can be ranges of different species. Owners should be discour-
found on every continent except Antarctica, with mem- aged from attempting to identify the snake due to the
bers of the Viperidae family found throughout the world. danger that is posed with handling a live or very recently
In North, Central, and South America, the Viperidae dead snake. Envenomating bites can occur from recently
family is represented primarily by the pit vipers dead or decapitated snakes. These agonal bites typically
(Crotalidae) and is responsible for the majority of veteri- inject the entire volume of the venom gland, making
nary envenomations. The true incidence of veterinary them very severe.