Snakebite: Introduction - The Merck Veterinary Manual

Snakebite: Introduction

Venomous snakes fall into 2 classes: 1) the elapines, which include the cobra, mamba, and coral snakes; and 2) the 2 families of viperines, the true vipers (eg, puff adder, Russell’s viper, and common European adder) and the pit vipers (eg, rattlesnakes, cottonmouth moccasin, copperhead, and fer-de-lance). Poisonous North American snakes include pit vipers and coral snakes.

Elapine snakes 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. Viperine snakes have long, hinged, hollow fangs; they strike, inject venom (a voluntary action), and withdraw. Many bites by vipers reportedly do not result in injection of substantial quantities of venom. Viperine venom is typically hemotoxic, necrotizing, and anticoagulant, although a neurotoxic component is present in the venom of some species, eg, the Mojave rattlesnake ( Crotalus scutulatus scutulatus ).

Fatal snakebites are more common in dogs than in any other domestic animal. 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. Because of their size, 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.

Diagnosis:

In many instances, the bite has been witnessed, and diagnosis is not a problem. However, many conditions thought by the owner to be snakebites are actually fractures, abscesses, spider envenomations, or allergic reactions to insect bites or stings. When possible, owners should be instructed to bring the dead snake along with the bitten animal; they should be warned not to mutilate the snake’s head because identification may depend on the morphology of the head. Many bites do not result in envenomation, or are made by nonpoisonous snakes.

Typical pit viper 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. Frequently, the epidermis sloughs when the overlying hair is clipped or merely parted. Hair may hide the typical fang marks. Sometimes, only one fang mark or multiple punctures are present. In elapine snakebites, pain and swelling are minimal; systemic neurologic signs predominate.

Treatment:

Intensive therapy should be instituted as soon as possible because irreversible effects of venom begin immediately after envenomation.

Animals bitten by an elapine may be treated with antivenin (which may be available on an as-needed basis through larger human hospital emergency rooms) and supportive care, including anticonvulsants if necessary. A polyvalent antivenin (horse-serum origin) against North American pit vipers is readily available and should be used in all cases of substantial pit viper envenomation.

The progression of events after pit viper envenomation can be divided into 3 phases: the first 2 hr, the ensuing 24 hr, and a variable period (usually ~10 days) afterward. The first 2 hr is the acute stage in which untreated, severely envenomized animals usually die. If death does not occur during this period, and the untreated animal is not in shock or depressed, the prognosis usually is favorable. The acute phase can be prolonged for several hours by use of corticosteroids and, if they are administered, prognostication should be withheld. If the animal is active and alert after 24 hr, death due to the direct effects of the venom is unlikely. The third phase is a convalescent period in which infection (possibly anaerobic) may be of concern. If necrosis has been extensive, sloughing occurs and may be so severe as to involve an entire limb.

An attempt to estimate the severity of envenomation should be made. Although not infallible, it is prudent to consider the size of the snake both as an indicator of the quantity of venom injected, and as it relates to the size of the victim. In dogs and cats, mortality is generally higher from bites to the thorax or abdomen than from bites to the head or extremities. However, this may relate to the size and vulnerability of the victim because smaller animals are more likely to be bitten on the body. Sensitivity to the venom of pit vipers varies among domestic animals. In decreasing order, sensitivity is reportedly horse, sheep, goat, dog, rabbit, pig, and cat. If there has been a previous bite, the victim may have developed some degree of active humoral immunity and be less vulnerable to the toxic effects of the venom.

Treatment for pit viper envenomation should be directed toward preventing or controlling shock, neutralizing venom, preventing or controlling disseminated intravascular coagulation, minimizing necrosis, and preventing secondary infection. Any dog or cat presented within 24 hr of a snakebite showing signs of pit viper envenomation requires intensive treatment, starting with IV fluids to combat hypotension. The use of corticosteroids has been questioned, principally because they alone do not alter the ultimate outcome. They do, however, prolong the clinical course and therefore allow more time in which to institute curative measures. Rapid-acting corticosteroids may help to control shock, protect against tissue damage, and minimize the likelihood of allergic reactions to antivenin. Antivenin is highly beneficial because its action is the only direct and specific mechanism for neutralizing snake venom. Smaller animals probably receive a larger dose (per unit body wt) of venom than more massive animals and, accordingly, require proportionally larger doses of antivenin. Up to 100 mL of antivenin may be necessary for small dogs bitten by a large snake; 5-10 mL may be injected into the tissues around the bite, and the remainder given IV. The efficacy of antivenin is diminished if the bite occurred >24 hr previously. In the event of an anaphylactoid reaction to the heterologous (horse) serum components in antivenin, 0.5-1 mL of 1:1,000 epinephrine should be administered SC. If disseminated intravascular coagulation occurs, appropriate treatment, including blood products and heparin sodium (in mini dose at 5-10 U/kg/hr or low dose at 50-100 U/kg, tid), should be administered SC.

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 rattlesnakes’ mouths. Antibiotics should be continued until all superficial lesions have healed.

Tetanus antitoxin also should be administered; other supportive treatment (eg, blood transfusion in the case of hemolytic or anticoagulant venoms) is administered as needed. In most cases, surgical excision is impractical or unwarranted. Antihistamines have been reported to be contraindicated, but diphenhydramine hydrochloride is frequently given along with antivenin to treat snakebite in humans.

Other procedures to neutralize venom (high-voltage, low-amperage electric shock and trypsin) have not proved effective in controlled studies.