An estimated 1.5 to 3 million bites and possibly greater than 100,000 deaths occur each year in the world from venomous snakes.¹ The American Association of Poison Control Centers reports an average of 6000 bites each year, approximately 2000 of them by venomous snakes. Because of underreporting, the true number of snakebites is possibly as high as 45,000 per year in the United States, with 7000 to 8000 by venomous snakes.² The major venomous snakes of the world can be divided into three groups: Viperidae (vipers and pit vipers), Elapidae (includes Hydrophiinae, or sea snakes; see chapter 213, titled “Marine Trauma and Envenomation”), and the diverse group of non–front-fanged colubrid snakes (former family Colubridae, now split into several families).

In the United States, most snakebites occur in the warm summer months, when snakes and victims are most active. In the past, it was estimated that mortality from venomous snakebite approached 25%. Because of the availability of antivenom and advances in emergency and critical care, mortality rates today are <0.5%; approximately five deaths occur per year.³

Except for bites by imported species, North American venomous snakebites involve the pit vipers (Crotalinae subfamily of Viperidae) or coral snakes (Elapidae family). The crotaline snakes are represented by the rattlesnakes (Crotalus species), pygmy rattlesnakes, and massasauga (Sistrurus species), as well as the copperheads and water moccasins (Agkistrodon species). Venomous snakebites from imported exotic species are infrequent but may occur in zoo personnel as well as in amateur herpetologists. A regional poison control center can provide information on snake identification, expected toxicity, and location of antivenom.

The crotaline snakes are called pit vipers because of bilateral depressions or pits located midway between and below the level of the eye and the nostril (Figure 212-1). The pit is a heat receptor that guides strikes at warm-blooded prey or predators. Crotaline snakes are also distinguished by the presence of two fangs that fold against the roof of the mouth, in contrast to the coral snakes, which have shorter, fixed, erect fangs. Within the pit viper group, the rattle distinguishes the rattlesnake from other crotaline snakes. The mistaken belief that rattlesnakes always rattle before striking has persisted for centuries. In truth, many strikes occur without a warning rattle.

Crotaline venom is a complex enzyme mixture that causes local tissue injury, systemic vascular damage, hemolysis, fibrinolysis, and neuromuscular dysfunction, resulting in a combination of local and systemic effects. Crotaline venom quickly alters blood vessel permeability; this leads to loss of plasma and blood into the surrounding tissue, which causes hypovolemia. Crotaline venom activates and consumes fibrinogen and platelets, causing a coagulopathy. In some species, specific venom fractions block neuromuscular transmission, which leads to cranial nerve weakness (e.g., ptosis), respiratory failure, and altered sensorium.

Up to 25% of crotaline snakebites are dry bites: venom effects do not develop. The manifestations of crotaline envenomation involve a complex interaction of the venom and the victim. The species and size of the snake, the age and size of the victim, the time elapsed since the bite, and characteristics of the bite or bites (location, depth, and number; the amount of venom injected) all affect the clinical evolution. The severity of envenomation following a crotaline bite is therefore variable. An initially minimal bite may evolve into a more serious bite and require large amounts of antivenom.

The cardinal manifestations of crotaline envenomation are the presence of one or more fang marks, localized pain, and progressive edema extending from the bite site.² Other early symptoms and signs are nausea and vomiting, weakness, oral numbness or tingling of the tongue and mouth, dizziness, and muscle fasciculation. Systemic effects include tachypnea, tachycardia, hypotension, and altered level of consciousness. In general, local swelling at the bite site becomes apparent within 15 to 30 minutes, but in some cases, swelling may not start for several hours. In severe cases, edema can involve an entire limb within an hour. In less severe cases, edema may progress over 1 to 2 days. Edema near an airway or in a muscle compartment may threaten life or limb without causing systemic effects. Rapid onset of angioedema may occur.

Progressive ecchymosis may also develop because of leakage of blood into subcutaneous tissue. Ecchymoses may appear within minutes or hours, and hemorrhagic blebs may be seen within several hours. Hemoconcentration often develops as a result of fluid extravasation into subcutaneous tissue, followed by a decrease in hemoglobin level over several days as intravascular volume is restored.

The diagnosis of snakebite is based on the presence of fang marks and a history consistent with exposure to a snake (e.g., walking through a field). Snake envenomation involves the presence of a snakebite plus evidence of tissue injury. Clinically, the injury may be manifest in three ways: local injury (swelling, pain, ecchymosis), hematologic abnormality (thrombocytopenia, elevated prothrombin time, hypofibrinogenemia), or systemic effects (e.g., oral swelling or paresthesias, metallic or rubbery taste in the mouth, hypotension, tachycardia). Abnormalities in any one of these areas indicate that venom effect is developing. The absence of any of these manifestations for a period of 8 to 12 hours following the bite indicates a dry bite.

FIRST AID

First aid measures should never substitute for definitive medical care or delay the administration of antivenom (Table 212-1). Take all patients bitten by a pit viper to a healthcare facility. Avoid dangerous first aid treatments such as suction and incision. Do not use Snake Bite Kit and similar products because they contain cups that produce little suction and seal poorly on digits. The blade in the kit, or any method of incision, can injure digital nerves, arteries, and tendons. The Sawyer Extractor (Sawyer Products, Inc., Safety Harbor, FL) suction pump is said to remove venom without incision, but safety and efficacy of the product are questioned.⁴ Electric shock treatment of the bite site is dangerous and ineffective and can cause electrical injuries. Ice water immersion worsens the venom injury.

Do not use tourniquets because they obstruct arterial flow and cause ischemia. Constriction bands may be useful, especially when immediate medical care is not available. A constriction band is an elastic bandage or Penrose drain, thick rope, or piece of clothing wrapped circumferentially above the bite, applied with enough tension to restrict superficial venous and lymphatic flow while maintaining distal pulses and capillary filling. Apply the band snugly but loose enough to avoid arterial compromise. A constriction band can delay venom absorption without causing increased swelling.⁵

PREHOSPITAL MANAGEMENT

In the prehospital phase, immobilize the limb, establish IV access in another limb, administer oxygen, and transport the victim to a medical facility. Do not remove tourniquets or constricting bands until antivenom is available.

Institute advanced life support measures as indicated. If the patient is hypotensive, rapidly administer IV isotonic fluids. Continue to immobilize the limb in a neutral position during transport to reduce further venom absorption. Consult with a physician or poison control center familiar with the management of snake envenomation for most cases.

ED MANAGEMENT

Antivenom is the mainstay of therapy for venomous snakebites^2,6 (Table 212-2). Antivenom is composed of heterologous antibodies derived from the serum of animals immunized with the appropriate snake venoms. The antibodies bind and neutralize the venom molecules.

Crotalidae Polyvalent Immune Fab (Ovine) (FabAV) is used in the United States; equine-derived products (Antivenom [Crotalidae] Polyvalent; see below) are no longer available. FabAV is produced by immunizing herds of sheep with one of four crotaline snake venoms: eastern diamondback (Crotalus adamanteus), western diamondback (Crotalus atrox), Mojave (Crotalus scutulatus), or cottonmouth (Agkistrodon piscivorus). The immune serum is harvested from each group and then digested with papain to produce antibody fragments (Fab and Fc). The more immunogenic Fc portion of the antibody is eliminated during purification. The four individual monospecific Fab preparations are combined to form the final antivenom product.

Treat all patients with bites who develop progressive signs and symptoms with antivenom promptly. Progression is defined as worsening of local injury (e.g., pain, ecchymosis, or swelling), abnormal results on laboratory tests (e.g., worsening platelet count, prolonged coagulation times, or decreased fibrinogen level), or systemic manifestations (e.g., unstable vital signs or abnormal mental status) (Table 212-3).