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Venomous Snake Bites

Nathan Peterson, DVM, DACVECC

VCA West Los Angeles Animal Hospital, Los Angeles, CA, USA

Etiology/Pathophysiology rattlesnakes (also vipers) produce primarily paralytic
or neurotoxic venoms.
The degree of pathology related to snakebites is determined by The venom of the North American pit vipers (Crotalidae)
two main factors: the composition of the venom and the is typically classified as necrogenic/hemorrhagic and is
amount of venom injected into the victim. In veterinary capable of causing massive tissue damage and inducing
medicine, there are two families of venomous snakes that life‐threatening inflammation or hemorrhage. The venom
are responsible for the vast majority of envenomations: the is primarily composed of water, with proteins and pep-
Viperidae and Elapidae. In general, vipers are capable of tides making up approximately 10% of the total volume. It
injecting venom through hollow fangs and once they is this portion of the venom that is responsible for most of
(vipers) are mature, they have the ability to control the vol- the direct tissue injury and hemostatic perturbation seen
ume of venom injected with each bite. The Elapidae do not with envenomation. It is also this portion that is responsi-
have such an advanced venom delivery system and rely on ble for inducing endothelial cell damage leading to endothe-
introduction of venom secreted from a venom gland lial dysfunction, cell lysis, and ultimately circulatory
through a wound created by biting. These snakes use their collapse. So far, over 60 purified polypeptides and approx-
teeth and underdeveloped fangs in a chewing motion to imately 50 enzymatic fractions have been identified with
create the wound. Therefore, elapid envenomation usually at least 10 enzymes and 3–12 nonenzymatic proteins and
requires a snake to “adhere” or “chew” on a victim for some peptides present in any individual snake’s venom.
amount of time to allow adequate envenomation and con- Hyaluronidase and collagenase act to break down
sequently, these snakes strike and hold to allow for venom connective tissue, facilitating the spread of venom and
introduction whereas vipers strike and retreat, allowing the beginning the digestive process. Together, these enzymes
venom injected during the bite to immobilize the patient. are capable of causing massive tissue damage and necro-
The composition of snake venom is extremely com- sis and are responsible for many of the outward sings of
plex and it varies between species and within species envenomation. The impact of envenomation on hemo-
based on geographic range. Venom composition also stasis is profound and can be considered in light of the
varies with age of the snake and the time of year. There areas of hemostasis that are affected.
are many potential effects of snake envenomation Venom proteins acting directly on coagulation factors
including flaccid paralysis, systemic myolysis, coagu- include procoagulant proteins such as factor V (FV) acti-
lopathy and hemorrhage, renal damage/failure, cardio- vators, FX activators, prothrombin activators, and
toxicity, and local tissue injury at the bite site. While the thrombin‐like enzymes. Anticoagulant venom factors
traditional view of venomous snakes was that vipers also exist and include FIX/X binding proteins, protein C
caused local and hemorrhagic effects (hemotoxic activators, thrombin inhibitors, and phospholipase A 2 .
venom) and elapids caused systemic and nonhemor- Finally, factors acting on fibrinolysis include fibrinolytic
rhagic effects (neurotoxic venom), the reality is that any enzymes (metalloproteinases and serine proteases) and
species of snake is capable of producing venom that plasminogen activator.
can affect one or more of the body systems. Some Asian Many of the components of snake venom exert an effect
and African cobras (vipers) produce profound tissue on platelet function. The C‐type lectins, disintegrins,
injury while some South and Central American and proteinases inhibit platelets by a variety of

Clinical Small Animal Internal Medicine Volume I, First Edition. Edited by David S. Bruyette.
© 2020 John Wiley & Sons, Inc. Published 2020 by John Wiley & Sons, Inc.
Companion website: www.wiley.com/go/bruyette/clinical