An estimated 3 million bites and 150,000 deaths occur each year
from venomous snakes in the world.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 U.S., with 7000 to 8000 by venomous
snakes.2 The major venomous snakes of the world
can be divided into three groups: Viperidae (vipers), Elapidae,
and Hydrophiinae (sea snakes, see Chapter 207, Trauma and Envenomations from Marine Fauna).
Approximately 20 of the 120 snake species indigenous to North
America are venomous. Most bites 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 5 to 10 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).
Poisonous 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 206-1). 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 venom poisoning
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 poisoning following
a crotaline bite is therefore variable. An initially minimal bite
may evolve into a more serious bite and require large amounts of
The cardinal manifestations of crotaline venom poisoning 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 of envenomation are nausea and vomiting, weakness,
oral numbness or tingling of the tongue and mouth, dizziness, and
muscle fasciculation. Envenomation may produce systemic effects
with 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 even when no systemic effects are present. 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
First aid measures should never substitute for definitive medical
care or delay the administration of antivenom (Table
206-1). All patients bitten by a pit viper should be taken
to a health care facility. First aid treatments
such as suction and incision are dangerous and should not be done. Snake
Bite Kit and similar products should not be used because they contain
cups that produce little suction and seal poorly on ...