Venomous snakes of North America are members of 2 families: 1) the Elapidae or coral snakes (Micrurus spp); and 2) the Crotalidae, or pit vipers (rattlesnakes [Crotalus spp], cottonmouth moccasin [Agkistrodon piscivorus], and copperhead [A cortortrix]). Elapids are generally restricted to southern edges of the USA, while crotalids are widely dispersed across the continent. Because of their wider distribution and less secluded natures, bites by crotalids are much more common than elapid bites. Rattlesnakes account for the majority of snakebite-related deaths in humans and domestic animals in the USA.
Elapids have short fangs and tend to hang on and “chew” venom into their victims. Their venom is neurotoxic and paralyzes the respiratory center. Animals that survive these bites seldom have any sequelae. Crotalids have long, hinged, hollow fangs with which they strike, inject venom (a voluntary action), and withdraw. Many bites by vipers reportedly do not result in injection of substantial quantities of venom and are therefore termed “dry bites.” Crotalid venom is typically hemotoxic, necrotizing, and anticoagulant, although a neurotoxic component is present in the venom of some species, eg, the Mojave rattlesnake (C scutulatus scutulatus).
Fatal snakebites are more common in dogs than in other domestic animals. Due to the relatively small size of some dogs in proportion to the amount of venom injected, the bite of even a small snake may be fatal. In dogs and cats, mortality is generally higher in bites to the thorax or abdomen than bites to the head or extremities. Because of their larger sizes, horses and cattle seldom die as a direct result of snakebite, but deaths may follow bites on the muzzle, head, or neck when dyspnea results from excessive swelling. Serious secondary damage sometimes occurs; livestock bitten near the coronary band may slough a hoof.
Snakebite with envenomation is a true emergency. Rapid examination and appropriate treatment are paramount. Owners should not spend time on first aid other than to keep the animal quiet and limit its activity. The following commonly touted measures have been shown to be ineffective and can be potentially harmful: use of ice, cold packs, or sprays; incision and suction; tourniquets; electric shock; hot packs; and delay in presentation for medical treatment (waiting until problems develop).
In many instances, the bite has been witnessed, and diagnosis is not a problem. However, fractures, abscesses, spider envenomations, or allergic reactions to insect bites or stings could all potentially be confused with a snakebite by the inexperienced eye. When possible, the dead snake should be brought along with the bitten animal; mutilation of the snake's head should be avoided as this may hinder proper identification. Some bites do not result in envenomation or have been made by nonvenomous snakes.
Typical crotalid bites are characterized by severe local tissue damage that spreads from the bite site. The tissue becomes markedly discolored within a few minutes, and dark, bloody fluid may ooze from the fang wounds if not prevented by swelling. The epidermis may slough when the overlying hair is clipped or parted. Hair may hide the typical fang marks. Sometimes, only one fang mark or multiple punctures are present. In elapid snakebites, pain and swelling are minimal, and systemic neurologic signs predominate.
Intensive therapy should be instituted as soon as possible because irreversible effects of venom begin immediately after envenomation. The bite site(s) should be shaved and the wounds cleansed thoroughly with germicidal soap. For animals bitten by crotalids, the leading edge of tissue swelling should be marked on the skin with a magic marker at frequent intervals to monitor the spread of tissue injury. All snakebite victims should be monitored closely for a minimum of 24 (crotalid) to 48 (elapid) hr for the development of clinical signs.
Treatment for crotalid envenomation should be directed toward preventing or controlling shock, neutralizing venom, preventing or controlling coagulopathy, minimizing necrosis, and preventing secondary infection. Any dog or cat presented within 24 hr of a snakebite showing signs of crotalid envenomation requires intensive treatment, starting with IV crystalloids to combat hypotension. Rapid-acting corticosteroids may be of benefit in the first 24 hr to help control shock, protect against tissue damage, and minimize the likelihood of allergic reactions to antivenin. Monitoring for the development of echinocytes or coagulopathy is recommended, as these are often early signs of severe envenomation.
Antivenin is it the only direct and specific means of neutralizing snake venom. The polyvalent antivenin (horse-serum origin) against North American pit vipers that was once readily available for use with crotalid bites is no longer being manufactured. The currently available crotalid antivenin is a sheep-derived product that neutralizes the action of venom from North American crotalids. This antivenin utilizes the Fab components of the immunoglobulin molecule, resulting in an antivenin that has lower risk of allergic reaction, faster reconstitution, and has efficacy against crotalid venom equal to that of the horse-derived product. Antivenin is most effective if administered in the first 6 hr after the bite, although improvement in clinical condition may be seen following antivenin administration at ≥24 hr after the bite. In the unlikely event of an anaphylactic reaction to the antivenin, 0.5–1 mL of 1:1,000 epinephrine should be administered SC.
Antivenin generally helps significantly in managing the pain of a crotalid bite, but opioid analgesics may be used as needed for residual pain. If coagulopathy (thrombocytopenia, DIC, etc) occurs, appropriate treatment, including blood replacement products and heparin sodium (in mini dose at 5–10 U/kg/hr or low dose at 50–100 U/kg, SC, tid), should be administered. Hemoglobin glutamer-200 (bovine) or hetastarch may be helpful in managing hypovolemia; however, colloids should be used with caution due to their potential to leak out of damaged vessels and pull fluids into tissue beds.
Broad-spectrum antibiotics should be given to prevent wound infection and other secondary infections. Several potential pathogens, including Pseudomonas aeruginosa, Clostridium spp, Corynebacterium spp, and staphylococci have been isolated from the mouth of rattlesnakes. Antibiotics should be continued until all superficial lesions have healed.
Tetanus antitoxin also should be considered, especially in horses, and other supportive treatment should be administered as needed (eg, blood or plasma transfusions in the case of hemolytic or anticoagulant venoms). In most cases, surgical excision of tissue is impractical or unwarranted. Antihistamines have been reported to be contraindicated, but diphenhydramine hydrochloride (10–50 mg, SC or IV) has been shown to be helpful in managing fractious patients and may possibly assist in minimizing risk of allergic reactions to antivenin.
Animals bitten by coral snakes may be treated with supportive care as needed (IV fluids, ventilatory support, anticonvulsants, etc) and antivenin, if available (the producer of North American coral snake antivenin has discontinued manufacture as of 2009). As with crotalid bites, broad-spectrum antibiotics are indicated to reduce the risk of infection of the bite wound.
The prognosis of snakebite depends on the type and species of snake, location of the bite, size of the victim, degree of envenomation, and the time interval between the bite and institution of treatment. Animals surviving elapid bites generally have full recoveries, but crotalid bites can result in longterm sequelae due to tissue necrosis (amputation, loss of function, etc), depending on the severity of the bite and the promptness and aggressiveness of treatment instituted.
Last full review/revision March 2012 by Sharon M. Gwaltney-Brant, DVM, PhD, DABVT, DABT