The arthropods make up the largest phylum in the animal kingdom.
All arthropods have an exoskeleton with jointed appendages. The
phylum is divided into two subphyla: the Chelicerata, which includes
spiders, scorpions, ticks, mites; and the Mandibulata, which includes
More than 100,000 species of spiders (class Arachnida) are known
to exist. All are carnivorous and have fangs and venom that they
use to immobilize and kill their prey. The risk of serious bites
is small, because in most species, the fangs are too short and fragile
to penetrate human skin, and the venom is mild. Contrary to common
belief, most spiders are harmless and shy.
Two species of Loxosceles have caused envenomation
in the Western Hemisphere. Loxosceles reclusa is
found primarily in the southern and midwestern states. L.
laeta is found in South and Central America. These small
spiders (1–1.5 cm long) are characterized by a brown violin-shaped
mark on the dorsum of the cephalothorax. They establish nests indoors,
especially in closets and basements, and bite when disturbed. The
venom contains a cytotoxic factor related to hyaluronidase.
Initially, the bite appears innocuous, but the site can become
painful within hours. Because the bite is often unnoticed at first,
there is sometimes a delay in seeking medical attention. The spectrum
of reaction ranges from minor local reaction to severe necrosis.
Mild to moderate pain, generally 2 to 8 hours after the bite, characterizes the
local reaction, which varies with the amount of venom injected.
At the site of the bite, erythema develops with a central blister
or pustule. A bulla may develop, and concentric areas of ischemia
and erythema may appear. During the ensuing 24 to 48 hours, the
lesion becomes cyanotic and ulcerates. The necrotic ulcer slowly
expands and can reach 10 to 20 cm in diameter during the subsequent
weeks to months. Scar formation is rare if there is no clinical
evidence of necrosis within 72 hours of the bite. Systemic reaction
is usually noted 24 to 48 hours after the bite, and includes fever,
chills, malaise, weakness, nausea, vomiting, joint pain, morbilliform eruption
with petechiae, intravascular hemolysis, hematuria, and renal failure.6,7
Unless the spider is available for identification, definitive
diagnosis cannot be made. Envenomation outside of endemic areas
is rare.8 Currently there is no specific serologic,
biochemical, or histologic test to diagnose envenomation approved
for use in humans. Serious complications are rare, and the vast
majority of victims will heal with supportive care. If large areas
of necrosis have become demarcated, surgical excision and skin grafting
may be required, but grafting is usually not needed. Administration
of steroids or heparin does not seem to alter the extent of necrosis.
The use of dapsone should be limited to adults with proven brown
recluse bites because of the possibility of methemoglobinemia. Antivenin
is not commercially available. If systemic manifestations occur,
vigorous supportive care is needed, as well as laboratory monitoring
for evidence of hemolysis and renal failure.7
Latrodectus mactans is the leading cause of death
from spider bites in the United States. The female is shiny black
with a brilliant red hourglass mark on the abdomen. The average
width of the abdomen is 6 mm, and the overall length (with legs
extended) is 40 mm. The male may have a similar mark, but is not
a threat because it is only one-quarter the size of the female,
and its fangs cannot penetrate human skin. The webs are usually
found in out-of-the-way places such as vacant rodent burrows, hollow
stumps, or dark corners of barns, privies, and garages. The female
is not aggressive unless guarding her egg sac or provoked. The venom
is a complex protein that includes a neurotoxin that stimulates myoneural
junctions, nerves, and nerve endings.
The bite of the female black widow spider resembles a pinprick,
sometimes with slight swelling. Immediately after the attack, the
victim experiences local sharp, throbbing pain that increases in
intensity for several hours, by which time vascular spread has occurred.
One to 8 hours after the bite, cramping pain is felt in the abdomen,
flanks, thighs, and chest. Nausea and vomiting are often reported
in children. Respiratory distress is not unusual. Chills, urinary
retention, and priapism have been reported. There is an overall
4% to 5% mortality rate, with death resulting
from cardiovascular collapse.
Symptoms generally are more severe in children and the elderly.
A child who presents with severe pain and muscle rigidity after
a spider bite should be considered a potential Latrodectus bite
victim.9 In children who weigh less than 40 kg,
treatment with Latrodectus antivenin (Merck), if
available, should be administered as soon as a bite is confirmed.
After skin testing for sensitivity to horse serum, the usual dose
is 2.5 mL (1 vial) in 50 mL of saline administered by slow intravenous
injection. For children who weigh more than 40 kg, administration
of antivenin is not as urgent, but indications for its use include
patients under age 16 years, respiratory difficulty, or marked hypertension.
Antivenin is usually effective within 30 minutes and may be repeated
once (maximum dose: 2 vials) within 2 hours if necessary. Serum
sickness is a possible side effect but is uncommon. Muscle relaxants
such as diazepam have been advocated, but they are variably effective
and the effects are short lived. Analgesia may be achieved with
morphine. A monoclonal antibody fragment has been used in mice to
neutralize alpha-latrotoxin, a neurotoxic component of the black
widow spider venom.9,10
Tarantulas, although fearsome in size and appearance, do not
bite unless provoked. The venom is mild, and envenomation is not
a problem. The wolf spider (Lycosa spp) and the jumping
spider (Phidippus spp) also have been implicated
in bites. Like the tarantula, they have a mild venom that causes
only local reactions. Bites from all three of these spiders should
be treated with local wound care.
There are many scorpion species that accidentally sting humans.
Only a limited number are dangerous to man. In Mexico, for example, where
scorpions have been responsible for 82% of 24,627 deaths
from poisonous animals over a 10-year period, more than 80% of
these fatalities have occurred in children under age 5 years, and
94% in children under age 10 years. In the southwestern
United States, the bark scorpion, or Centruroides sculpturatus (C.
exilicauda) is the only native, lethal inhabitant. The
animal has two pinching claws and a tail or pseudoabdomen that ends
in a telson. The telson houses a pair of poison glands and a stinger.
Scorpions are nocturnal; during the day they may crawl into sleeping
bags and unoccupied clothing.
The scorpion’s venom contains a local cytotoxin and
a neurotoxin that also have hemolytic properties. The general neurotoxicity
is excitatory, affecting the autonomic and skeletal neuromuscular
system. Following a sting there is an immediate sharp pain. Common
symptoms include restlessness, hyperactivity, roving eye movements,
and respiratory distress. Other associated signs may include convulsions,
drooling, wheezing, hyperthermia, cyanosis, and respiratory failure.
Pulmonary and gastrointestinal hemorrhage may occur. Death occurs because
of respiratory paralysis, pulmonary edema, or intractable hypotension
and shock. A history of a sting may not be elicited, making the
diagnosis difficult. There is no laboratory test for confirmation
Treatment should be initiated as soon as possible. General supportive
care is critical. Cryotherapy of the site of sting has been advocated to
reduce swelling and local induration. Continuous intravenous benzodiazepines
may be necessary up to 24 hours to mitigate symptoms in severe envenomation.11 In
Central Arizona, a locally manufactured scorpion antivenin was available
for severe envenomation for many years, but production ceased in
2001, depleting stockpiles of antivenin in 2004, and leading to greater
numbers of admissions to pediatric intensive care units.12,13
Both tick bites and tick-borne diseases have become more frequent,
especially along the East Coast of the United States. Ticks are
blood-sucking ectoparasites in all of their stages, and they can
be recognized easily by the organization of their mouthparts and
body. They are subdivided into two major groups: (1) the argasids,
or soft ticks; and (2) the ixodids, or hard ticks.
Ticks are widespread in nature and may transmit numerous infectious
diseases including spirochetes, viruses, rickettsiae, bacteria,
and protozoa. In addition, they cause mechanical injury at the bite
wound. Occasionally, they may release toxic substances of their
own, as in the case of the tick-induced paralysis. Ticks attach to
their host by their highly specialized mouthparts, and they may
engorge themselves with blood for days or weeks before dropping
off. During this period, they may become so enlarged that they resemble
a pedunculated wart or fibroma. The North American deer tick, Ixodes scapularis, is
minute and may go unnoticed. After a tick bite and detachment, a
granuloma may form at the bite wound. This generally resolves during
the subsequent few months.
Tick paralysis most often is reported in children, in whom almost
all fatalities occur. Approximately 20 species of ticks, in the
genera Dermacentro, Amblyomma, Rhipicephalus, Ixodes, Ornithodoros,
Haemaphysalis, and Argas, have been implicated.
In North America, tick paralysis in humans is usually associated
with species of Dermacentor and Amblyomma. Symptoms
may begin with motor weakness and progress as an ascending, flaccid,
motor paralysis, which often is mistaken for Guillain-Barre syndrome
or poliomyelitis. Sensory involvement is uncommon. Symptoms of paralysis
may become evident 4 to 7 days after the bloodsucking starts, although
symptoms occurring after only 1 day have been reported. The ascending paralysis
may progress in a matter of hours to involve the cranial nerves.
Patients may die of respiratory failure or aspiration pneumonia. Laboratory
data, including cerebrospinal fluid are usually normal, but lymphocytic
pleocytosis has been reported. It is believed that the gravid female
tick secretes in her saliva a neurotoxin that blocks the release
of acetylcholine at neuromuscular junctions. If not too far advanced,
removing the tick is associated with prompt, and often dramatic,
reversal of the symptoms.14 Patients are usually
afebrile. A tick may be found after careful examination. It is important
to search the scalp, axilla, and pubic regions to locate the ticks.
Ticks normally should be removed manually by gentle traction
using blunt forceps or tweezers. The tick should be grasped as close
to the skin surface as possible and pulled upward with a steady,
even pressure. A twisting or jerking motion may cause the mouthparts
to break off. The entire tick, including the mouthparts, must be
removed. If the mouthparts are left behind, they usually cause a
severe granulomatous lesion that may not heal for months. Squeezing
or crushing the body of the tick may facilitate inoculation of infective
agents into the host. Ticks can be controlled with synthetic permethrin
or pyrethroid sprays. Dogs should wear tick collars that are changed
every 30 to 60 days. Clothing can be impregnated with tick repellents such
as dimethylphthalate, diethyltoluamide, or indalone. Dogs should
be inspected every day to prevent infesting the home.
Centipedes (class Myrapoda) are wormlike arthropods possessing
many repetitive body segments, each of which has one pair of segmented legs.
Immediately below the mouth are modified legs of the first body
segment (ie, the maxillipeds), which are powerful poison claws used to
attack and kill prey. Although centipedes are greatly feared for
their appearance, they rarely bite. However, bites can be extremely
painful. The toxin causes only local reaction. The pain usually
diminishes rapidly and may require nothing more than a cold compress
and local wound care. Injection of local anesthetic at the wound
site is used for extreme pain. More generalized reactions, such
as nausea, vomiting, and dizziness, are rare. General supportive
care is warranted in these cases. A single death in a 7-year-old
child has been reported.
The stings of bees, hornets, yellow jackets, wasps, and fire
ants introduces a venom that in nonsensitized individuals causes
immediate pain, induration, and redness lasting several hours or
longer. Serious allergic reactions including death may occur, especially
in those who are previously sensitized. Hymenoptera are responsible
for 50% of human deaths from venomous bites and stings.
Although higher levels are reported in adults than in children, only
approximately 8% develop an allergic reaction following
a repeat sting. It is not clear whether subsequent experiences are
associated with progressively more severe reactions. Stings may
cause a profound systemic reaction with nausea, vomiting, hypotension,
loss of consciousness, and death. However, in most cases, individuals
who have had local reactions continue that pattern with each sting. Systemic
reactions occur more frequently in individuals who have had multiple
The venoms of the bee, hornet, yellow jacket, and wasp contain
protein antigens that can elicit an immunoglobulin (IgE antibody)
response in those persons who are stung. In addition, venoms contain
various biogenic amines, phospholipase, phosphatase, and hyaluronidase.
The barbed stinger of the bee remains in the victim’s skin.
The wasp, in contrast, may sting many times. Reactions may be grouped
by severity. Local reaction to a sting results in pain, erythema
and swelling. Large reactions consist of more extensive erythema
and edema. Systemic allergic reactions may be grouped using the
- Group I: generalized urticaria or erythema, itching, malaise,
- Group II: angioedema or two or more of the following: chest
or throat tightness, nausea, vomiting, diarrhea, abdominal pain,
- Group III: dyspnea, wheezing, or stridor, or two or more of
the following: dysphagia, dysarthria, hoarseness, weakness, confusion,
or feeling of impending disaster
- Group IV: hypotension, collapse, loss of consciousness, cyanosis,
The barbed honeybee stinger with venom sac is avulsed and often
remains in the victim’s skin. It must be removed if possible;
delays in removal are likely to increase the dose of venom received. Treatment
is based on the severity of the allergic reaction. Local reactions
require only cold compresses at the site of sting. More severe local
reactions are treated with diphenhydramine or loratadine orally
for several days and oral steroids are often added. Group I through
group III reactions are treated with subcutaneous injection of epinephrine
1:1000 (0.01 mL/kg, 0.3 mL max). It may be necessary to
repeat epinephrine twice at 10-minute intervals to arrest the symptoms,
followed by oral antihistamines. H2-blockers such as ranitidine
or famotidine may provide additional benefit for group I and II
patients. Group II and group III patients should be admitted for
observation for 24 hours.16 Group IV reactions
may require intubation if upper-airway obstruction is present. Hypotension
should be treated with a fluid bolus of saline or lactated Ringer
solution. Intravenous epinephrine may be indicated if hypotension
fails to respond to subcutaneous epinephrine and fluid bolus.17 In
addition, intravenous steroids are indicated.
Children who have had a group II, III, or IV reaction merit follow
up by an allergist, if possible and should be considered for hyposensitization.
Because immunotherapy may reduce the risk of anaphylaxis to approximately
3%, many advocate that venom-sensitized patients undergo
immunotherapy. Allergic individuals who have not had immunotherapy
should be advised to carry an anaphylaxis emergency treatment kit.
Parents should receive information regarding the avoidance of situations
and behaviors that would attract stinging insects.
Ant stings frequently occur in the southern United States and
are caused by various species of fire ants of the genus Solenopsis. Multiple
stings and mass attacks can cause severe reaction. Harvester ants
(ie, Pogonomyronex) attack humans readily and cause
painful stings. The venom differs from the venom of other Hymenoptera
in that it is an alkaloid with a direct toxic effect on mast cells.
There is no cross-reactivity with other members of the order. Severe
and fatal reactions have been reported in farm animals; fortunately,
these are rare in humans. The fire ant bites with well-developed
jaws and then uses its head as a pivot to inflict multiple stings.
Immediately after a sting, an erythematous wheal appears, which
vesiculates after a few hours. A pustule forms within 24 hours;
in several days to a week this ruptures, encrusts, and finally forms a
small fibrous nodule or scar. Pain can persist for 3 to 10 days.
Systemic reactions can occur, especially if there are multiple stings.
Treatment is symptomatic. Local care, such as ice applied to the
reactive area, and frequent cleansing of the lesions to prevent
secondary infection is all that is usually required. Systemic therapy
does not appear to prevent pustule formation. Antihistamines are
useful for pruritus. Systemic reactions are rare and should be treated
similarly to other Hymenoptera reactions.
Although only 15% of the 120 snake species found in
the United States are venomous, poisonous snakes bite an estimated
8000 persons annually. Predictably, the pediatric population, especially
males ages 5 to 19 years, accounts for a disproportionately large
number of these victims, and males are more likely than females to
sustain bites that require antivenin. The highest incidence occurs
in the Southeast and Southwest between April and October. If treated
properly and early, these injuries have a remarkably low mortality
and morbidity. Only 10 to 15 deaths are reported per year, but the
morbidity in limb dysfunction and other complications, though unknown,
is undoubtedly higher.
Snake venoms are an evolutionary adaptation for obtaining food.
As such, venoms are complex mixtures of potent enzymes, primarily proteinases
and low-molecular-weight peptides that possess toxic properties.
Certain components are intended to immobilize prey, whereas other
components are digestive enzymes that penetrate throughout the prey’s
tissues. Crotalid venom is often a combination of necrotizing, hemotoxic,
neurotoxic, nephrotoxic, and/or cardiotoxic substances.
Elapid venom contains neurotoxic and cardiotoxic components. Mojave
rattlesnake venom contains primarily neurotoxic compounds that are
related to phospholipase A and bind the nicotinic acetylcholine
receptors, thus preventing the depolarizing action of acetylcholine.
Proteolytic enzymes aided by hyaluronidase cause much of the local
tissue destruction. Many of the venoms induce increased endothelial
permeability and venous pooling, thus decreasing intravascular volume.
Transient hemoconcentration may be present as a result of plasma
extravasation. Respiratory failure may occur because of pulmonary
edema. Hemotoxic effects include hemolysis and fibrinolysis. Thrombocytopenia
is frequently present. Elapid snake venoms may cause considerable necrosis
in addition to exhibiting neurotoxicity.
The venom enzymes typically found in crotalid and viperid venoms
are esterases with procoagulant and bradykinin-releasing activities. They
cause intravascular clotting either by a thrombinlike action (pit
vipers) or by activation of factor X (eg, Russell viper). The thrombinlike
activity of many North American pit viper venoms differ, however,
from that of thrombin in that other clotting factors are not usually
activated and the resulting microclots are friable, unstable, and
readily lysed by the activation of the plasminogen–plasmin
system. This results in defibrination and a clinical picture resembling
disseminated intravascular coagulation in which the defibrinating
agent is presumed to be thrombin. Snake venom procoagulants, however,
do not usually cause platelet aggregation, nor do they activate
and destroy factors V and VIII. Inhibition by heparin is incomplete
or does not occur. The defibrination produced is readily corrected
The poisonous snakes indigenous to the United States are members
of the Crotalidae (pit viper) or Elapidae families. The Crotalidae contain
three genera: Crotalus, or large rattlesnakes,
with about 30 species including the Eastern and Western diamondback,
timber, prairie, and pacific rattlesnakes; Sistrurus, or ground
rattlers, which include the massasauga and the pygmy rattlesnake;
and Agkistrodon, or moccasins, which include the
cottonmouth and copperhead. The pit vipers have several characteristic
features that distinguish them from nonvenomous snakes: (1) the
pit from which their name originates contains heat-sensitive organs
that assist in the localization of prey and are located on each
side of the head between the eye and nostril; (2) their pupils are
elliptical and vertically oriented in contrast to the round pupil
of harmless snakes; (3) they have two, 5- to 20-mm-long curved fangs
or hollow maxillary teeth that are folded posteriorly against the
palate and advance forward when the pit viper strikes; in larger
snakes, they may be spaced as widely as 3 cm; (4) a relatively more
triangular head than that of most nonvenomous snakes; and (5) a
single-row scute, or scales, on the ventral portion, caudad to the
anal plate, as opposed to the double-row seen in nonpoisonous snakes. Physicians
who might treat snakebite victims should become familiar with the
particular species in their areas.
The effects of a pit viper bite depend on the characteristics
of both victim and snake. The victim’s size and state of
health influence how the toxins are tolerated; the characteristics
of the wound inflicted by the bite and its location affect venom
absorption. Fang penetration of a vessel or subfascial compartment
ensures a more rapid absorption and serious systemic effects. Likewise,
a bite on the head, neck, or trunk (3% of snakebites) hastens
systemic absorption. Approximately one third of snakebites involve
the upper extremity and cause higher long-term functional morbidity
than do lower-extremity wounds.
The snake’s size, the amount of venom injected, and
the potency of the particular species’ venom also influence
the bite’s outcome. Thus, long, healthy fangs or full stores
of venom add to its toxicity.
Local pain after a crotalid envenomation is typically intense.
A sensation of burning occurs almost immediately (within 5 to 10
minutes). The pain increases as edema develops and is dependent
on the size of the venom inoculate. Victims of a significant rattlesnake
bite often complain within minutes of perioral numbness and paresthesias
extending to the scalp and periphery. These paresthesias may be
accompanied by a metallic taste in the mouth. Nausea, vomiting,
weakness, chills, sweating, and syncope are also frequent. A copperhead
or pygmy rattlesnake envenomation usually produces less-localized
symptoms, and systemic consequences are often minimal, unless the
victim is a small child, there are multiple bites, or a larger-than-average
snake is involved.18 The effects of the water moccasin’s
envenomation are more variable. Severe pain and swelling are absent
after Mojave rattler bites, although, as in other crotalid bites,
the patient may complain of paresthesia in the affected extremity.
Within several hours, neuromuscular symptoms, such as diplopia,
swallowing difficulty, lethargy, nausea, and progressive weakness
The wound should be inspected for fang punctures, and if two
are present, the distance between them should be noted. In general,
less than an 8 mm inter fang distance suggests a small snake; 8
to 12 mm suggests a medium-sized snake; and greater than 12 mm suggests
a larger snake. Fang wounds by small snakes such as the pygmy rattler
may be extremely subtle. There may be bloody serosanguineous fluid
dripping from the fang punctures. Depending on the time to presentation,
the fang marks may be hidden within hemorrhagic blebs and edema.
Occasionally, only one puncture or two simple scratches are present.
In these wounds, there is still the potential for envenomation.
However, 10% to 20% of known rattlesnake strikes
do not inject venom. Other etiologies for puncture
wounds also must be kept in mind, notably rodent bites or thorn wounds.
Nonpoisonous snakes sometimes leave an imprint of their two rows
of teeth, but the wounds lack fang puncture marks.
Progressive swelling usually develops over the next 8 hours and
may continue to some degree for an additional 24 hours, depending
on the size of the inoculum. In a severe diamondback rattlesnake
bite, an entire extremity may be swollen within 1 hour. The swelling
looks impressive and the skin may feel tense and look shiny. Subfascial
compartmental pressures are generally not increased, and compartment
syndromes requiring fasciotomy are rare. Bluish discoloration of
the bitten part is common, and ecchymoses, blebs, and blisters may
develop. Local ecchymoses and vesicles usually appear within the
first few hours, and, commonly, by 24 hours hemorrhagic blebs are
present. Lymph node enlargement or lymphadenitis also may become
apparent. Without appropriate therapy, these local manifestations
progress to necrosis and may extend throughout the bitten extremity.
However, local necrosis may occur even in optimally treated patients.
Other systemic signs are dependent on the species and the amount
of venom injected. Tachycardia and decreased capillary perfusion may
be seen. In severe cases, hypotension and shock develop. Increased
respiratory effort may be the result of metabolic acidosis or from pulmonary
edema, and may progress to respiratory failure. Oliguria may be
secondary to shock or renal failure. Hemoglobinuria and hematuria
are the result of the bleeding diathesis, which can develop. Hemoglobinuria
cannot be the result of the bleeding problem alone. Neurologic signs
include fasciculation, weakness, paralysis, and convulsions.
Therapy for poisonous snakebites remains controversial. Because
snakebites are uncommon, few physicians have extensive experience,
and controlled studies are infeasible. In spite of this, certain
tenets of management are not in question. As in all medical emergencies, the
airway, breathing, and circulation of the patient must be assessed
and guaranteed before attending to the snakebite. The first priority
of prehospital care of the snakebite victim is rapid transport to
a medical facility.
It is important to reassure the patient and avoid agitation.
The affected extremity should be stripped of any jewelry or clothing
and immobilized in a position of function below the level of the
heart. Tight tourniquets are not recommended. However, a constriction
band that obstructs lymph and venous flow can be valuable when a
transport longer than 30 to 60 minutes is anticipated. The band
should be at least 2 cm wide, made of nonstretchable material, and placed
5 to 10 cm proximal to the wound. Only the lymphatics and superficial
veins need to be occluded, and good distal arterial pulses should be
preserved (band loose enough to admit a finger). Observation for
adequate perfusion is necessary because of progressive edema; the constriction
band should be shifted to remain proximal to the swelling. The band
must be applied initially within 1 hour of a pit viper bite. (Note
that constriction bands are not recommended in coral snake envenomation.)
Incision and suction cannot be recommended. A study of a suction
device (Sawyer Extractor pump) in a simulated snakebite in human
volunteers demonstrated that the pump removed bloody fluid but almost
no mock venom, and is unlikely to reduce the total body burden in
the field.19 In the rare situation in which skilled
personnel and supplies are at the scene and a long transport is
expected, it is reasonable to allow one or two attempts at intravenous
access. Many also suggest capturing or killing the snake for later
verification; however, an inexperienced person should be extremely
cautious and not risk a second bite. If the snake arrives in the
emergency department or office, treat it with respect. Snakes that
appear to be dead have been known to bite, and decapitated snake
heads can bite reflexively for up to 1 hour.
In the past, the use of ice to cool the bitten area was advocated.
However, cryotherapy should never be used in snakebite
because frostbite is easily produced in a limb with circulation
already impaired by the action of the venom. Cooling does not slow
the action of the venom. Recently, the use of electric shock therapy
has received a great deal of publicity in the lay press. The use
of high-voltage, low-current shocks in experimental studies has
failed to demonstrate any beneficial effects and should not be used.20
Following arrival in the emergency department the key steps to
management of snakebite include: (1) establish a baseline of physical
findings and physiologic parameters; (2) grade the level of envenomation
(see Table 122-1); (3) administer antivenin
if indicated; and (4) provide other supportive and therapeutic measures.
Table 122-1. Crotalidae
(Pit Viper) Envenomation Grading System (AAPCC) ||Download (.pdf)
Table 122-1. Crotalidae
(Pit Viper) Envenomation Grading System (AAPCC)
|Grade of Envenomation||Local Findings||Systemic Findings||Laboratory Abnormalities|
|None||Little or no pain; no swelling after 4 hours||None||None|
|Mild||Pain, tenderness, and swelling within 10 cm of the bite;
possible slight bluish discoloration around the bite||None||None|
|Moderate||Same as in mild envenomation, with progressive swelling; may
have bluish discoloration of entire limb||Nausea, vomiting, weakness, perioral and scalp paresthesias,
and fasciculation||Thrombocytopenia, hypofibrinogenemia, and hemoconcentration|
|Severe||Rapidly progressing pain and swelling; development of vesicles/bullae
and ecchymoses||Same as in moderate envenomation, with hypotension, shock, bleeding
diathesis, and respiratory distress||Thrombocytopenia, hypofibrinogenemia, anemia, and metabolic
A brief history should be obtained and an initial physical examination
including vital signs, an inspection of the bite site for fang and/or
tooth marks, and evaluation of current neurologic status should
be done. Next, the circumference of the injured extremity at the
leading point of edema and 10 cm (4 inches) proximal to this level should
be measured every 30 minutes for 6 hours and then at least once
every 4 hours for a total of 24 hours. If the history and physical
examination on arrival in the emergency department are consistent
with a venomous snakebite, immediate laboratory evaluation (detailed
below) and intravenous access are indicated. Aggressive supportive
medical care must be available if signs of major system dysfunction
are present. Any prehospital care (eg, extremity immobilization)
should be rechecked. If an occluding tourniquet is present, it should
be removed after placing a more proximal constriction band, staying
well prepared to respond to a systemic release of venom.
Therapy is based on the clinician’s overall grading
of venom toxicity. Local and systemic manifestations, as well as
laboratory findings, weigh heavily in this judgment. A complete blood
count, coagulation studies, platelet count, urinalysis, and blood
crossmatching should be obtained on all patients with suspected
venomous snakebite. In moderate or severe poisoning, serum electrolytes,
blood urea nitrogen, creatinine, fibrinogen, and arterial blood
gases are indicated because of the findings described below. The
laboratory studies may need to be repeated every 6 hours to ensure
that no significant changes occur. The clinical pattern may change
dramatically as the venom’s effects unfold. Frequent reassessment
The Scientific Review subcommittee of the American Association
of Poison Control Centers has suggested a grading system. The grading system
applies only to pit viper bites (Table 122-1).
Antivenin is highly effective in the management of crotalid snakebite.
The currently available antivenin is CroFab (Crotalidae Polyvalent Immune
Fab Ovine: Protherics, Inc.), which contains purified Fab fragments
specific to pit viper species. An equine IgG antivenin (Antivenin
Crotalidae Polyvalent, Wyeth Laboratories), used in the past for
rattlesnake, water moccasin, and copperhead envenomations, is highly
antigenic. The purified Fab product is safe in children as well
as adults, and is as efficacious as the older IgG antivenin, but
is associated with fewer allergic reactions, although the shorter
half-life of the Fab antivenin may allow recurrence of venom effects.
CroFab is indicated for progressive venom injury, including worsening
local injury, coagulopathy, or systemic effects. Early use within
6 hours of snakebite is recommended to prevent or correct abnormalities
that result from envenomation.21-24
Wound care includes irrigation, cleansing, a loose dressing,
and tetanus prophylaxis if the patient is judged to lack immunity.
The affected extremity should be maintained just below the level of
the heart and in a position of comfort. Cotton padding between swollen
digits is useful. As in any animal-inflicted wound, secondary infection is
a risk. Broad-spectrum prophylactic antibiotics may be indicated.
Analgesics for pain should be given. Surgical excision of the wound,
routine fasciotomy, and application of ice are not indicated. Fasciotomy
should be reserved for the very rare case of a true compartment
syndrome. Proteolytic enzymes or inappropriate therapy, not compartmental
pressure, usually cause necrosis. Superficial débridement
may be required at 3 to 6 days. Physical therapy is beneficial during
the healing phase.
The major goal of supportive care is correction of the intravascular
volume depletion that results from increased venous capacitance,
interstitial edema, and hemorrhagic losses. Moderate or severe envenomation
requires placement of two intravenous catheters for separate but
simultaneous antivenin therapy and volume replacement. Shock usually
develops between 6 and 24 hours after the snakebite but may present within
the first hour in severe envenomation. Signs of hypovolemia deserve
aggressive therapy. Central vascular monitoring and accurate urine
output measurements are desirable for optimal therapy. Normal saline
or lactated Ringer solution (20 mL/kg), followed by fresh
whole blood or other blood components, frequently corrects the hypovolemia.
Vasopressors are usually needed only transiently in the most severe
cases. A bleeding diathesis is best managed with fresh whole blood,
or blood-component therapy, in addition to antivenin. With life-threatening
bleeding, platelets and cryoprecipitate should be considered. Abnormal
clotting tests, including fibrinogen concentration and platelet
and blood counts, should be reevaluated every 4 to 6 hours. Respiratory
support also is frequently required when shock has developed. Renal
failure is another potential problem in this setting.
The family Elapidae, which includes cobras and mambas, is represented
by two species of coral snake, the eastern (Micrurus fulvius)
and the Arizona (Micruroides euryxanthus). M. fulvius is
responsible for the majority of human envenomation and is found
in most of the southeastern states. M. euryxanthus is
indigenous only to Arizona and New Mexico. The relatively passive
coral snake is responsible for only 10 to 15 snakebite cases per
year in the United States. Coral snakes are 2 to 3 feet long and
do not share the pit viper’s distinctive physical characteristics.
Unlike nonpoisonous snakes, the coral snake does have two small maxillary
fangs. A small amount of highly toxic venom is produced. The snout
of the coral snake is always black and is followed by brightly colored
transverse bands of yellow, red, and black.
Symptoms seen after coral snakebite differ from those seen after
the bite of pit vipers. The signs and symptoms reflect the neurotoxic
nature of the venom. The bite may have 1 or 2 punctures, at most
7 to 8 mm apart, as well as other small teeth marks, as opposed
to the one or two fang marks of pit viper bites. There is usually
only mild pain and little, if any, swelling. Local necrosis does
not occur. Systemic symptoms are delayed and occur over several
hours. Initial symptoms include generalized malaise and nausea,
vomiting, and paresthesias in the bitten part. Fasciculations and
weakness develop insidiously. The patient may complain of diplopia
and may have difficulty talking or swallowing. Physical examination reveals
bulbar dysfunction and generalized weakness. Paralysis of skeletal
muscles follows, beginning with the limb girdles and progressing distally.
Respiratory failure may ensue. Paralysis persists for 3 to 4 days
followed by recovery, although minor effects may linger for several weeks.
An elapid (Micrurus fulvius) antivenin (Wyeth)
went out of production in 2006. Other elapid antivenins are under
investigation. There is no antivenin available for the Arizona coral
snake (Micruroides euryxanthus). Additional supportive
care measures as outlined in the management of pit viper bites should
The clinician confronted with an exotic snakebite or a clinician
inexperienced in snakebites should consult a local medical herpetologist
or a regional poison control center of the American Association
of Poison Control Centers (1-800-222-1222). Report all illegally
possessed reptiles to the police or to the appropriate fish and