Venomous snakes of North America are members of either of two families: 1) the Elapidae or coral snakes (Micrurus spp); or 2) the Crotalidae, or pit vipers (rattlesnakes [Crotalus spp], cottonmouth moccasin [Agkistrodon piscivorus], and copperhead [A cortotrix]). Elapids are generally restricted to southern edges of the USA, whereas crotalids are 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 most snakebite-related deaths in people and domestic animals in the USA. Although Australia is home to a large number of venomous snakes from the families Colubridae, Hydrophiidae, and Elapidae, the most clinically significant venomous species are elapids, particularly the black (Pseudechis), brown (Pseudonaja textilis), Taipan (Oxyuranus sp), and tiger (Notechis scutatus) snakes.
Crotalids have long, hinged, tubular 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). North American elapids have short fangs that deliver a neurotoxic venom that paralyzes the respiratory center. Except fordeath adders (Acanthophis spp), the venom delivery system of which resembles that of crotalids, Australian elapids tend to have relatively short, grooved to tubular fangs. The venoms of Australian elapids may have neurotoxic, myotoxic, procoagulant, anticoagulant, and/or hemolytic properties; pronounced cardiovascular abnormalities have been associated with envenomation by tiger and brown snakes.
Fatal snakebites are more common in dogs than in other domestic animals. Because of 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 are 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 (see Spiders and Scorpions), 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, because this may hinder proper identification. Some bites do not result in envenomation or have been made by nonvenomous snakes. In Australia, venom detection test kits have been developed to detect the various snake venoms and determine the appropriate antivenom to use, but these appear to be infrequently used for veterinary patients.
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. Neurologic signs, including muscle fasciculations, are possible if neurotoxic crotalid venom is involved. In elapid snakebites, pain and swelling are minimal, and systemic neurologic signs predominate. Signs of coral snake envenomation include tetraparesis, ptyalism, tachypnea, shallow/abdominal breathing, depressed gag reflex, ataxia, muscle fasciculation, decreased spinal reflexes, and quiet mentation. Australian elapid bite victims may show collapse, vomiting, ptyalism, tremors, tachypnea, urinary and/or fecal incontinence, tetraparesis, hemolysis, coagulopathy, rhabdomyolysis, swelling at the bite site, renal failure, and/or delayed immune-mediated hemolytic anemia (red-bellied black snake).
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; however, prolonged use of corticosteroids is not recommended. Monitoring for the development of echinocytes or coagulopathy is recommended, because these are often early signs of severe envenomation.
Antivenom is the only direct and specific means of neutralizing snake venom. Antivenoms available against North American pit vipers include equine-derived polyvalent antivenin, ovine-origin polyvalent F(ab) fragment antivenin, and equine-origin polyvalent F(ab)2 fragment antivenin. The F(ab) antivenins use the F(ab) components of the immunoglobulin molecule, resulting in an antivenin that has lower risk of allergic reaction, faster reconstitution, and potency similar to that of the polyvalent immunoglobulin. Antivenom is most effective if administered in the first 6 hr after the bite, although improvement in clinical condition may be seen after antivenin administered ≥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, with or without antihistamines such as diphenhydramine, should be administered SC. In severe envenomations, multiple vials of antivenom/antivenin may be required, although this is frequently cost-prohibitive in veterinary patients.
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, disseminated intravascular coagulation, 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 to manage hypovolemia; however, colloids should be used with caution because of their potential to leak out of damaged vessels and pull fluids into tissue beds.
Several potential pathogens, including Pseudomonas aeruginosa, Clostridium spp, Corynebacterium spp, and staphylococci have been isolated from the mouth of rattlesnakes. However, the incidence of wound infection after snake bites is low, and many clinicians use antibiotics only when significant tissue necrosis is present. Broad-spectrum antibiotics such as amoxicillin/clavulanate or cephalosporins are preferred.
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 to manage fractious patients and may possibly assist in minimizing risk of allergic reactions to antivenin.
Animals bitten by elapids may be treated with supportive care as needed (IV fluids, ventilatory support, anticonvulsants, etc) and antivenom/antivenin, if available. Ventilatory support is frequently required for 6−8 hr in animals experiencing Australian elapid envenomation; additional vials of antivenom can reduce ventilator time. Antivenom against coral snake venoms is no longer being manufactured in the USA, although some practitioners have received special permission to import coral snake antivenom from Mexico. In Australia, several antivenoms/antivenins are available for use in veterinary patients. A polyvalent antivenin is available for use when the identity of the snake cannot be ascertained, and many clinicians prefer to use the polyvalent antivenin for all envenomations. Additionally, animals bitten by Australian elapids should be monitored for development of coagulopathy, hemolysis, renal injury, cardiovascular abnormalities, or rhabdomyolysis; appropriate treatment should be instituted as needed. As with crotalid bites, broad-spectrum antibiotics may be indicated if there is 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 the institution of treatment. Animals that survive elapid bites generally make 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 July 2013 by Sharon M. Gwaltney-Brant, DVM, PhD, DABVT, DABT