Envenom Ations

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Envenomations

Eunice M. Singletary, MDa, Adam S. Rochman, MDa,Juan Camilo Arias Bodmer, MDb,Christopher P. Holstege, MDa,c,d,e,*

a

Department of Emergency Medicine, University of Virginia, Charlottesville, VA, USAbUniversidad de La Sabana, Bogota, ColombiacDepartment of Pediatrics, University of Virginia, University of Virginia Health System,

Charlottesville, VA, USAdDivision of Medical Toxicology, University of Virginia, Charlottesville, VA, USA

eBlue Ridge Poison Center, University of Virginia, Charlottesville, VA, USA

Numerous marine, crotalid, and arachnid animals in North America are

capable of envenomating humans. This article reviews these potential

envenomations and discusses the relevant approach to patients whomanifest toxicity. Appropriate therapy is discussed, and treatments that

may result in no benefit or potential harm are highlighted.

Marine envenomations

With steady growth in the numbers of diving enthusiasts and more than

12,000 miles of coastline in the United States, encounters with marine

animals are no longer considered unusual. Many marine animals have

developed systems for attack and defense that on accidental exposure tohumans result in envenomation. Most envenomations are not life-

threatening, often presenting only as a minor contact dermatitis.

Venomous marine organisms can be difficult to identify or may not be

seen at the time of envenomation. Knowledge of what venomous organisms

are found in local waters assists physicians with management of marine

envenomations. Marine animals responsible for envenomation can be

broken into two large groupsdinvertebrates and vertebrates. Venomous

invertebrates include jellyfish, anemones, and fire corals, whereas venomous

vertebrate marine animals include stingrays, lionfish, and catfish.

* Corresponding author. University of Virginia Health System, Po Box 800774, Charlottesville,

VA 22908-0774.

E-mail address: [email protected] (C.P. Holstege).

0025-7125/05/$ - see front matter 2005 Elsevier Inc. All rights reserved.

doi:10.1016/j.mcna.2005.07.001 medical.theclinics.com

Med Clin N Am 89 (2005) 11951224
mailto:[email protected]:[email protected]


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Invertebrates

Invertebrates most commonly implicated in envenomations include the

coelenterates, such as jellyfish, and the echinoderms, such as sea urchins.

Coelenterates are divided into three classes: Hydrozoa (hydroids, fire corals,

Portuguese man-of-war), Schyphozoa (true jellyfish), and Anthozoa (sea

anemones).

Schyphozoa and Hydrozoa

Scyphozoa found in North American waters include stinging nettles

(Chrysaora quineucirrha), which are commonly found in the Chesapeake

Bay during mid to late summer; the purple jellyfish (Pelagia noctiluca); thelions mane jellyfish (Cyanea capillata); and the chirodropid box jellyfish

(Chironex species). Chironex fleckeriis reputed to be the most lethal jellyfish

in the world, but it is more common in Australia and the South Pacific [1].

A related chirodropid, Chiropsalmus quadrumanus, was identified as the

culprit in a lethal envenomation of a 4-year-old boy at Galveston Island,

Texas, in 1990 [2].

The class Hydrozoa includes hydroids and stinging corals. Although both

cause various degrees of contact dermatitis, desquamative eruptions,

erythema multiforme, and anaphylaxis have been reported [35]. Themost dangerous of the hydrozoas is the Portuguese man-of-war (Physalia

physalis). Found in the Atlantic Ocean and the Gulf of Mexico during the

summer, the Portuguese man-of-war can cause fatal envenomations [6,7].

The portion of the animal that is visible above the surface of the water is the

pneumatophore, which is generally 10 to 30 cm in diameter and blue-to-

purple in color. The tentacles dangle from the pneumatophore.

Physalia species and the chirodropids are the only jellyfish in North

America known to result in human deaths. In Australia, the jellyfish species

Carukia barnesi(and similarly related species) cause the Irukandji syndromewith severe systemic and potentially life-threatening symptoms [8]. The

syndrome was first described in 1952 by Flecker [8] and named for the

Aboriginal tribe that inhabited the region where many of the stings

occurred. In 1966, using himself, his son, and another volunteer, Barnes [9]

identified the responsible small, peanut-sized, box jellyfish as a Carybdeid,

with one tentacle arising from each of four corners. The classic sequence of

symptoms begins within 5 to 45 minutes after a minor stinging pain at the

site of envenomation and includes low back pain; muscle cramps in the

limbs, abdomen, and chest; sweating; anxiety; restlessness; nausea; andheadache [10,11]. More severe symptoms include hypertension, pulmonary

edema, global heart dilation, and cerebral edema [10,12]. Fatalities have

followed development of severe hypertension and intracerebral hemorrhages

[13]. Reported treatments include the use of narcotic analgesics for pain,

muscle relaxants for spasm, and phentolamine for hypertension. Although

no antivenom is available, there is one report of dramatic resolution of

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agitation, sympathetic features, and pain after intravenous bolus and

infusion of magnesium sulfate [14]. Cardiopulmonary decompensation has

been described, and in one review there was an increase in troponin I levelsin 22% of 103 patients and varying degrees of systolic dysfunction or

hypokinesis on echocardiogram [15]. A symptom complex was described in

three divers who sustained envenomations in South Florida similar to the

Irukandji syndrome, suggesting the presence of small, previously undetected

Carybdeid jellyfish [16] in North America.

Venom of jellyfish. Jellyfish envenomate their prey through nematocysts.

Nematocysts are venom-containing stinging organelles located in specialized

epithelial cells called cnidocytes. The length of jellyfish tentacles variessignificantly, from a few millimeters to more than 40 m. Longer tentacles

frequently wrap around the legs of swimmers. Tentacles that have separated

from the jellyfish are still capable of stinging for weeks or months after

becoming detached, even if dried. Swimmers and snorkelers occasionally

may be stung by a detached tentacle, without any visible jellyfish in the area.

When a tentacle comes in contact with the epidermis of an unsuspecting

person, thousands of venom-filled nematocysts may fire simultaneously,

causing release of venom resulting in a jellyfish sting. Stings vary in

severity depending on the species of coelenterate, its size, the time of theyear, and the size and health of the victim.

Venoms are antigenic and toxic, causing a variety of reactions, including

rash, dermatonecrosis, neurotoxicity, cardiotoxicity, and hemolysis. Toxins

comprise a complex mixture of heat-labile polypeptides and proteins,

including catecholamines; histamine; hyaluronidase; fibrolysins; kinins;

phospholipases; and various hemolytic, cardiotoxic, and dermatonecrotic

toxins [17]. The venom is believed likewise to destabilize cell membranes

through interference with the sodium-potassium pump [18].

Envenomation from a jellyfish causes immediate pain that may bedescribed as a mild-to-moderate stinging or burning. Pain is followed by the

development of an erythematous rash, with linear papules or beaded streaks

for Portuguese man-of-war envenomations. The rash may be in the pattern

of the wrapped tentacles at the site of contact or develop more distantly. The

rash progresses to erythematous welts or vesicles within 2 hours and can last

24 hours or longer. Delayed skin changes include pigment changes, fat

atrophy, telangiectasias, scarring, keloids, or striae [1921]. Conjunctivitis,

chemosis, corneal ulcerations, and facial and lid edema all have been

described after envenomation to the eyes [19,22]. Tentacles still may beadherent on patient presentation.

For most jellyfish stings, symptoms are confined to localized pain and rash

that resolve over 24 hours. Multisystem reactions are seen more commonly

after envenomation by Chironex, Carybdeid, and Physalia species, with deaths

resulting from anaphylaxis or direct toxic effects. Gastrointestinal symptoms

include nausea, vomiting, and diarrhea. Headache, malaise, confusion,

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delirium, coma, seizures, paresthesias, and paralysis are potential neurologic

symptoms. Musculoskeletal complaints, which are prominent withCarybdeid

envenomations, include myalgias, muscle spasm, cramping, and paralysis.Cardiopulmonary effects include dysrhythmias, hypotension, cardiovascular

collapse, respiratory distress, bronchospasm, laryngeal edema, and respi-

ratory failure or arrest [1,23].

Management of jellyfish envenomation. Care for a jellyfish envenomation

begins at the scene. After treatment of life-threatening symptoms, de-

contamination should be initiated immediately. If specific decontamination

agents are not readily available, the skin can be rinsed with seawater or

saline solution to remove nematocysts. If a sting is suspected froma Chironex species, decontamination is initiated by flooding the envenoma-

tion site and any visible tentacles with 5% acetic acid (household vinegar)

for 10 minutes before attempting to remove any adherent tentacles. Vinegar

has been shown to inactivate undischarged nematocysts in cubozoan (box)

jellyfish and theoretically alters the pH of the protein toxin, making it less

bioactive [24]. For stings by all other jellyfish, decontamination can be

accomplished by liberal application of vinegar, baking soda, or a solution of

dilute (1/4 strength) household ammonia. Isopropyl alcohol may induce

further discharge of unfired nematocysts and is not recommended asa decontaminant. Vinegar and ammonia may be applied continuously by

applying soaked compresses. A paste made from unseasoned meat

tenderizer or papaya also has been reported to relieve significantly the

pain associated with jellyfish stings. Papain is believed to inactivate the

jellyfish venom by hydrolyzing the protein toxin [24]. If meat tenderizer is

used, it should be applied for no longer than 15 minutes. The other discussed

decontaminants should be applied until pain is relieved or for 30 minutes for

maximal benefit.

After decontamination, any remaining tentacles should be removed.Removal can be accomplished by fixing the area with shaving cream or

a baking soda slurry and then using a razor. At the scene, a paste of sand

and seawater can be used and the area scraped with a shell or a plastic credit

card [25]. After removal of the remaining tentacles, the decontaminant

should be reapplied for an additional 15 minutes.

Pain control, particularly for systemic reactions, may require parenteral

narcotics. There is evidence that hot water (4345C) immersion is more

effective than vinegar or papain meat tenderizer at relieving pain [23].

Jellyfish protein toxins are heat-labile, and heat immersion may penetrate theintracutaneous depths to inactivate the venom. If jellyfish sting victims

present to an emergency department within 60 minutes, a hot shower may be

useful for individuals with widespread stings. Smaller local reactions may

benefit from application of topical anesthetic ointments or sprays containing

benzocaine or 2.5% lidocaine. Topical hydrocortisone (1%) applied twice

daily may be beneficial for skin reactions. Tetanus prophylaxis should be



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wound. Some spines contain a blue-black dye that stain the wound or cause

temporary tattooing. This dye is absorbed over 1 to 2 days. Sea urchin venom

is poorly characterized, but similar to other marine venoms, it contains heat-labile, high-molecular-weight toxins, including steroid glycosides, hemoly-

sins, proteases, serotonin, and cholinergic substances [27].

Sea urchin envenomations may result in an immediate local reaction. This

reaction typically presents with swelling, puncture wounds, and burning pain

that is initially minor, but intensifies over 30 minutes and lasts several hours.

Multiple simultaneous wounds may result in greater envenomation, with

symptoms of muscle spasm, weakness, difficulty breathing, paresthesias,

ataxia, and syncope. Recommended treatment begins with hot water

immersion (43.345

C), which provides significant pain relief and theoreticalinactivation of the toxin. Visible spines, if easily accessible, should be

removed carefully using forceps. Care should be taken in spine removal

because they are brittle and may crumble in the wound. Surgical removal is

indicated for spines that penetrate or are in close proximity to a joint or

neurovascular structure [28]. Wounds should be irrigated copiously, and

tetanus prophylaxis should be administered when indicated. Prophylactic

antibiotics generally are not needed. Thin retained spines without symptoms

generally are absorbed or extruded, but a delayed secondary reaction

sometimes is seen. This reaction may present with induration and swelling oftenosynovitis or sarcoidal granuloma formation [29,30]. Treatment includes

a 7- to 14-day course of nonsteroidal anti-inflammatory drugs and, for more

severe reactions, oral prednisone.

Vertebrates

Venomous marine vertebrates include stingrays, scorpionfish, lionfish,

stonefish, and catfish. Three types of hazards are associated with venomous

marine vertebrates: (1) direct wound trauma, (2) pain and swelling fromvenom or trauma, and (3) subsequent tissue necrosis and infection.

Stingrays

The stingray is the most common cause of marine envenomations in the

United States. It is estimated that approximately 2000 stings occur annually

[31], with the Southern stingray (Dasyatis americana) being the main

offender in the East and the round stingray (Urolophus halleri) being the

main offender in the West. Stingrays are generally peaceful bottom dwellers.

Attacks occur most commonly when a swimmer inadvertently steps ona stingray buried in the sand, resulting in the stingray hurling its barbed tail

up in a defensive response and striking the foot or leg. Injuries also are

sustained to the hand or arm in the process of trying to remove the fish from

a stingray caught while fishing.

The stinging apparatus of a stingray consists of one or more barbs and

two ventrolateral venom-containing grooves encased in an integumentary



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sheath (Fig. 1). The barb is serrated and retropointed and can cause

significant lacerations and puncture wounds. A venom gland is located at

the base of the tail. An injury from a stingray is a traumatic puncture woundor laceration and an envenomation.

Venom of stingrays. Stingray venom is heat-labile and composed of

numerous toxic compounds, including phosphodiesterases, 58-nucleotidase,

and serotonin [31]. Vasoconstrictive properties of the venom cause

a cyanotic appearance around the wound along with subsequent poor

healing, necrosis, or infection. Symptoms of envenomation include

immediate, excruciating pain out of proportion for what might be expected

based on the wound appearance alone. The pain usually reaches maximumintensity in about 90 minutes and resolves over several hours. Potential

systemic symptoms include weakness, nausea, muscle cramps, vomiting,

peripheral vasoconstriction, cardiac dysrhythmias, respiratory depression,

seizures, and coma. Although fatalities are rare, intrathoracic and intra-

abdominal wounds have been reported and are associated with higher

morbidity and mortality [32,33].

Management of stingray envenomation. After stabilization of potential life

threats, the main goals of treatment are pain control, neutralization ofvenom, and wound care. Initial irrigation of the wound site should be

performed with cold normal saline to wash away existing venom, and the

resulting vasoconstriction may slow down further absorption of the venom.

The affected area should be immersed in hot water (4345C) for 30 to 90

minutes, which helps destabilize some of the venom and provides significant

pain control. Hot water immersion was shown to be effective at reducing

pain from venomous fish stings in 73% of cases in one series [34]. Parenteral

narcotics may be necessary for supplemental pain control. Any retained

fragments of the barb or its sheath should be de brided gently. Spines andbarb material are radiopaque, so plain radiography or ultrasound may aid

Fig. 1. Stingray. (Courtesy of Doug Kesling, NOAA-NURC/UNCW.)

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in identifying retained fragments. An anesthetized limb should not be placed

in hot water because of the risk of thermal injury. If indicated, tetanus

prophylaxis should be provided. Because of the risk of infection, primaryclosure of traumatic wounds should be avoided. Prophylactic antibiotics,

such as ciprofloxacin, doxycycline, or trimethoprim-sulfamethoxazole, are

recommended in patients with residual foreign bodies or if a patient is

immunosuppressed [34].

Scorpaenidae

Scorpaenidae are found worldwide in temperate, tropical, and sub-

tropical climates and include lionfish (Pterois), scorpionfish (Scorpaena),

and stonefish (Synanceia). All members of this family have 12 to 13 dorsalspines, 2 pelvic spines, and 3 anal spines. Spines are covered with a loose

integumentary sheath that is pushed down the spine when tissue is

punctured, compressing the two venom glands at the base of the spine

and allowing venom to pass up a groove in the spines into the wound. The

severity of envenomations seems to be mild for lionfish, more severe for

scorpionfish, and most severe or life-threatening for stonefish [35].

Most envenomations by Scorpaenidae in the marine setting occur outside

North American waters. In the United States, reported envenomations are

typically the result of encounters by home aquarists who keep lionfish intheir tanks [36]. Lionfish were introduced in the southeastern United States

in 1994, however, and have been spotted by divers from south Florida

northward as far as Long Island (Fig. 2). As of January 2004, lionfish

numbers seem to be increasing between Florida and North Carolina [37].

Physicians and the public need to be aware of the potential for interaction

with this venomous species in North American waters. Scorpionfish and

stonefish exposures occur most frequently outside United States waters from

wading with inadequate foot protection and inadvertently stepping on the

fish.

Fig. 2. Lionfish (Pterois volitans). (Courtesy of Doug Kesling, NOAA-NURC/UNCW.)



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Venom of Scorpaenidae. Venom from the Scorpaenidae, similar to other

marine venoms, comprises heat-labile, high-molecular-weight proteins with

antigenic properties. Scorpionfish and stonefish venom produces intensevasoconstriction, increased vascular permeability, and myotoxicity second-

ary to blockade of conduction in skeletal, involuntary, and cardiac muscles

[38,39]. After puncture by the spine of a lionfish, there is severe localized

pain, frequently accompanied by swelling. Systemic symptoms occurred in

13% of one series, without any fatalities [40]. Systemic symptoms included

nausea, diaphoresis, difficulty breathing, chest or abdominal pain, weakness,

hypotension, and syncope. Wounds are accompanied by swelling and

redness and in 4% by vesicles and 1% by tissue necrosis.

With lionfish envenomations, there is immediate excruciating pain thatmay radiate to the entire limb and regional lymph nodes. Similar to stingray

envenomations, pain peaks at about 60 to 90 minutes, but may last 12 hours

without treatment. Wounds are described as anesthetic, with surrounding

hypersensitivity. Scorpionfish envenomations also produce severe pain, but

less than envenomations from stonefish. Puncture wounds from scorpionfish

are surrounded by a ring of pallor and cyanosis, owing to the vaso-

constrictive properties of the toxin. Systemic effects include nausea, vomit-

ing, sweating, weakness, motor paralysis, respiratory depression, shock, and

possible cardiac arrest [31]. Symptom duration varies from days to weeksor months.

Management of Scorpaenidae envenomation. Similar to other marine

envenomations, initial resuscitation and stabilization is followed by wound

exploration and irrigation. The clinician needs to be prepared to treat an

allergic reaction at any time. Because venom is heat-labile, after initial

irrigation puncture wounds should be immersed in hot water (43.345C)

for 30 to 90 minutes or until pain is relieved. Limbs that have been

anesthetized with local or regional anesthetics are subject to thermal burns ifplaced into scalding water, so water temperature must be measured and

monitored carefully for patients receiving anesthetics before hot water

immersion. Parenteral analgesics may be used for additional pain relief.

Prophylactic antibiotics are unnecessary, and tetanus prophylaxis should be

offered when indicated. Wounds with vesicle formation are dressed with

topical antiseptics, such as silver sulfadiazine or bacitracin daily. Because

foreign bodies may be retained in 19.5% of marine animal injuries,

radiography or ultrasound is advised for suspected retained foreign bodies

in soft tissue [41]. Surgical removal of embedded spines is required withspines that penetrate or are in proximity to joints, nerves, or vessels.

Antivenom is available only for stonefish envenomation [42].

Catfish

More than 1000 species of freshwater and saltwater catfish exist

worldwide, and many are venomous to humans. Catfish possess axillary

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venom glands and one dorsal and two pectoral fin spines that inflict the

envenomation. Some species of catfish produce a proteinaceous toxic

epidermal secretion (crinotoxin). Catfish have retrousse barbs (tip turnedup) and can produce significant damage and be difficult to remove [41,43].

The heat-labile polypeptide venom is incompletely characterized, but is

believed to contain vasoconstrictive and dermatonecrotic factors [31].

Symptoms frequently include intense pain, paresthesias, and numbness that

may last 30 minutes to 48 hours. Erythema, hemorrhage, edema, cyanosis,

and lymphangitis also are common localized findings. Rare systemic effects

include fever, weakness, syncope, hypotension, and respiratory distress.

Death is rare. Puncture wounds frequently are followed by secondary

bacterial infections that may take months to resolve [4447]. Emergencytreatment of catfish envenomation is as described for stingrays.

Snake envenomations

More than 6000 people are reported to sustain snakebites annually in the

United States, with nearly half from poisonous species [48]. More than 100

people are reported to experience major morbidity and are likely to require

critical/intensive care. Although these cases are undeniably underreported,death seems to occur in only a few cases a year. Two families of poisonous

snakes are indigenous to North Americadthe crotalids (Crotalidae) and

elapids (Elapidae).

Crotalid

Crotalids are responsible for most snake envenomations in North

America. They may be distinguished from other species by their tri-

angular-shaped heads, infrared heat-sensing pits, elliptical-shaped pupils,and a single row of subcaudal scales. Three genera of crotalids inhabit the

United Sates: Crotalus (12 species), Sistrurus (2 species), and Agkistrodon (2

species) (Table 1). Although crotalids commonly are referred to as

rattlesnakes, this reference is inaccurate because the Agkistrodon species

(commonly called cottonmouth and copperhead) do not possess rattles.

Clinical presentation

The spectrum of clinical presentations from crotalid envenomations

ranges from asymptomatic to cardiovascular collapse and death. Thepresentation depends on the amount and properties of the venom injected,

the location of the bite, and the size and general health of the victim. The

components of snake venom vary not only with the different species of

snakes, but also with each snake itself depending on the season, nutritional

status, and age. It is impossible to predict accurately the extent of local

tissue damage a patient will develop after a snakebite. Bites from Crotalidae



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species that do not introduce venom (dry bites) have been estimated to

occur in 20% of exposures [49].

Tissue injury. Tissue damage at the site of the bite is the most common

complication after envenomation by North American snakes. Numerous

enzymes have been isolated from the venom of snakes (Box 1). The

mechanism of each of these enzymes is directed at the breakdown of specific

components of the tissue in which the venom has been injected, allowing thevenom to penetrate further. Hemorrhagic toxins have been isolated from

snake venom that cause damage to the capillary endothelial cells and the

basement membrane of vessel walls, allowing extravasation of erythrocytes

into the surrounding tissues [5052]. As a result, patients initially experience

edema at the bite site, which progressively spreads to adjoining tissues.

Ecchymosis also may develop and give the area around the bite a bluish hue.

In addition, hemorrhagic blebs may develop and become quite large (Fig. 3).

Lymphangitis and lymphadenopathy may progress secondary to lymphatic

spread of venom components, causing the clinician to assume incorrectly theoccurrence of secondary bacterial infection. Venom metalloproteinases

cleave protumor necrosis factor-a, releasing activated tumor necrosis

factor-a and initiating a cascade of endogenous inflammatory responses.

This uncontrolled response ultimately results in marked inflammation and

subsequent tissue necrosis [53,54]. Myotoxin A is one component that

causes direct necrosis of skeletal muscle [55].

Table 1

Crotalids of North America

Scientific name Common name LocationCrotalus adamanteus Eastern diamondback rattlesnake United States

Crotalus atrox Western diamondback rattlesnake United States, Mexico

Crotalus cerastes Mojave Desert sidewinder United States, Mexico

Crotalus horridus Timber rattlesnake United States

Crotalus lepidus Rock rattlesnake United States

Crotalus mitchelli Speckled rattlesnake United States, Mexico

Crotalus molossus Black-tailed rattlesnake United States, Mexico

Crotalus pricei Twin-spotted rattlesnake United States, Mexico

Crotalus scutulatus Mojave rattlesnake United States, Mexico

Crotalus tigris Tiger rattlesnake United States, Mexico

Crotalus viridis Western rattlesnake United States, Mexico

Crotalus viridis viridis Prairie rattlesnake United States

Crotalus viridis abyssus Grand Canyon rattlesnake United States

Crotalus viridis helleri Southern Pacific rattlesnake United States, Mexico

Crotalus viridis lutosus Great Basin rattlesnake United States

Crotalus viridis oreganus Northern Pacific rattlesnake United States, Canada

Crotalus willardi Ridge-nosed rattlesnake United States, Mexico

Agkistrodon contortrix Southern copperhead United States

Agkistrodon piscivorus Eastern/western cottonmouth United States

Sistrurus catenatus Massasauga United States, Mexico

Sistrurus miliarius Pigmy United States

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The presence of fang marks is considered essential to the diagnosis of

snakebite. Skin lesions may appear as one or more puncture marks or

scratches. Pain is frequently the initial complaint and usually begins at the

moment of envenomation or shortly thereafter. Duration of the pain seems

to depend on the severity of envenomation and may persist in lesser degrees

over several days. Nausea, vomiting, and diaphoresis are seen commonly

with mild-to-severe envenomations.

Box 1. Venom components

MetalloproteinasesArginine ester hydrolase

Thrombin-like enzyme

Collagenase

Hyaluronidase

Phospholipase A2Phospholipase B

Phospholipase C

Lactate dehydrogenase

PhosphomonoesterasePhosphodiesterase

Acetylcholinesterase

RNase

DNase

5#-Nucleotidase

Nicotinamide adenine dinucleotide nucleotidase

L-Amino acid oxidase

Myotoxin A

Fig. 3. Finger hemorrhagic blebs after copperhead (Agkistrodon contortrix) envenomation.

(Courtesy of Christopher P. Holstege, MD, University of Virginia.)



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When envenomation occurs, swelling usually begins within minutes of the

bite. Rapid progression may involve the entire extremity in 1 hour.

Untreated or inadequately treated with antivenom, the swelling mayprogress for days. The affected extremity may continue to show edema for

a few weeks after the initial recovery. Mild cyanosis at the site of injury is

a common finding and does not indicate a need for surgical intervention.

Tissue necrosis may follow cyanosis of the tissues or bleb formation over the

affected areas.

Differentiation of compartment syndrome from the grossly swollen

extremity without intracompartmental swelling may be difficult because the

latter may obscure pulse and present with significant induration (Fig. 4).

Direct measurement of intracompartmental pressures with a Stryker needleor similar instrument is essential to determine the presence of compartment

syndrome. In addition to direct tissue damage, rhabdomyolysis also has

been reported [5658]. Myonecrosis rarely may be associated with

compartment syndrome, but also has been reported in the absence of

elevated intracompartmental pressures.

Coagulopathy. After envenomation, coagulopathy has been reported in

36% to 50% of patients, depending on the species [59,60]. Venom-induced

thrombocytopenia, fibrinolysis, and disseminated intravascular coagulation(DIC) all have been reported (Table 2). Coagulopathy may be manifest as

gastrointestinal bleeding, epistaxis, hemoptysis, bleeding from wounds or

intravenous sites, or petechial rash.

Venom may damage capillaries by disrupting endothelial cells. Dilation

of the endoplasmic reticulum and perinuclear space is followed by swelling

and eventually bleb formation on endothelial cells with extension into the

capillary lumen. The cells subsequently rupture, releasing plasma and

erythrocytes into the extravascular space. Smaller blood vessels seem to be

more susceptible to the effects of hemorrhagic toxins, explaining the edemaand petechiae that accompany many bites. Some venoms contain thrombin-

like proteins, which slow the activity of fibrinogen. They also may contain

plasmin-like components, which produce proteolysis of fibrinogen and fibrin

[61]. Crotalus adamantus venom contains crotalase, a thrombin-like enzyme

that cleaves fibrinopeptide-A from the a chain of fibrinogen but does not

activate or clear platelets. It also fails to cleave the fibrinopeptide from the

b chain of fibrinogen, activate factor XIII, or complex with antithrombin

III. This can cause complete defibrination without producing DIC, as shown

by normal platelets, antithrombin III, factor XIII, and D-dimer [58,62].Platelet aggregation occurs as a result of capillary damage and possibly

the release of adenosine-5#-phosphate, which seems to be associated with

thrombosis [63]. This widespread thrombosis seems to lead to organ damage

and consumes platelets; this may explain venom-induced thrombocytopenia

and when combined with defibrination may look similar to DIC. It also may

be a contributing factor to DIC.

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Neuromuscular toxicity. Although uncommon, neuromuscular blockade

has been associated with Crotalus scutulatus scutulatus bites [57]. The

mechanism of paralysis seems to be associated with calcium channel

blockade in presynaptic neurons, which prevents the release of neuro-

transmitters at the motor end plate [64]. Less serious but more common

neurologic complaints include tingling or numbness of the tongue, mouth,

scalp, digits, or bite site. Facial and limb myokymia has been documentedafter Crotalus horridus envenomations [65,66].

Fig. 4. Arm edema and ecchymosis secondary to timber rattlesnake (Crotalus horridus)envenomation. (Courtesy of Christopher P. Holstege, MD, University of Virginia.)

Table 2

Coagulation abnormalities associated with snake envenomation

VIT DF DIC

Fibrinogen Normal Decreased Decreased

FSP Normal Increased Increased

Platelets Decreased Normal Decreased

PT Normal Prolonged Prolonged

PTT Normal Prolonged Prolonged

Overt bleeding No No Yes

RBC destruction No No Yes

Abbreviations: DF, defibrination; DIC, disseminated intravascular coagulation; FSP, fibrin

split products; PT, prothrombin time; PTT, partial thromboplastin time; RBC, red blood cell;

VIT, venom-induced thrombocytopenia.



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Treatment

Initial snakebite treatment is associated with numerous myths and

dangerous practices that can contribute to the morbidity of the patient. Themost important steps to ensure a good outcome include immobilization and

rapid transport of the victim for evaluation by trained medical personnel.

Many first-aid measures taught in the past are no longer recommended

[67,68]. Capture of the snake for identification may lead to another victim.

Thorough examination and proper observation dictate treatment regardless

of the species involved. Focus should be directed toward immediate access

to professional medical care. Performing incisions through the wound [69],

application of suction devices [70,71], electric shock therapy [7275],

tourniquets, cryotherapy, and heat application all should be avoided inthe management of North American crotalid envenomations [76].

In-hospital management. The bite area should be cleansed gently. Circum-

ferential measurement at several points along the affected limb should be

started shortly after the patients arrival and repeated at intervals until

progression has ceased. A useful technique to ensure consistent measure-

ment is to place a small mark on either side of the paper measuring tape.

The bitten extremity should be immobilized with a padded splint and an

elastic bandage wrapped gently but firmly from the distal to the proximalaspect of the limb. Elevation to a level above the heart may be achieved with

a pillow or other means. When elevated, the edema usually moves

proximally; this does not represent progression of toxicity if the edema of

the distal extremity decreases simultaneously. Neurovascular checks and

new measurements should be performed hourly until swelling subsides.

Analgesia. Pain control usually requires parenteral narcotic agents, such as

morphine, during the first 24 to 48 hours of therapy. Anti-inflammatory

agents should be used with caution, especially in patients with evidence ofcoagulopathy.

Infection and antibiotics. Numerous organisms have been found growing in

the mouths of snakes, including gram-negative rods (Enterobacter,

Pseudomonas, Aerobacter, Proteus), gram-positive cocci, Clostridium,

Salmonella, and fungi [7779]. Case series have shown the incidence of

infection to be low after snakebites [80,81]. Venom itself has been shown to

have antibacterial properties [82]. Currently, prophylactic antibiotics are not

recommended in all cases of snakebites. If a patient develops signs andsymptoms of infection that cannot be differentiated from the venoms

reaction itself, consideration should be given to instituting antibiotics to

cover the aforementioned organisms [83,84].

Excisional therapy. In the past, early surgical excisional therapy of the

envenomated area was advocated as the preferred method of managing

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snakebite victims [85]. It was believed that the bulk of deposited venom

would remain in the area of the bite, and that by excision of this tissue the

local toxicity would be eliminated [86]. These published reports were merelyphysicians personal experiences describing individual cases with no

controls. In a controlled animal model by Stewart and colleagues [87],

excisional treatment combined with antivenom therapy resulted in worse

muscle function compared with antivenom therapy alone. De bridement

without antivenom did not improve survival, decrease soft tissue edema, or

preserve function compared with controls. Excisional therapy is strongly

discouraged.

Fasciotomy. Appropriate use of fasciotomies in snakebite victims is a topicwrought with misconceptions. The literature is clear that fasciotomy should

not be performed unless elevated muscle compartment pressures are

documented. If muscle injury does occur after a snakebite, it is nearly

always the result of the myotoxins present in the snakes venom, not

elevated compartment pressures. Biopsy results in severe cases of snakebite

have revealed myopathy distant from the site of envenomation, supporting

myotoxin-induced necrosis rather than compartment syndrome [58,88].

Rarely can a snakes fang penetrate through the fascia and into the muscle

compartments. Clinically the snakebite extremity appears nearly identical toan extremity with a compartment syndrome. Victims have swelling, tense

skin, tenderness, paresthesias, and pain with passive motion secondary to

the local inflammatory reaction.

Past publications have advocated performing fasciotomies on all

snakebite victims with edematous extremities and touted an improved

outcome with this aggressive management [85,89]. These publications, often

inappropriately referenced in the support of fasciotomies, lack scientific

methods and are biased by individual physicians personal case reports.

Controlled animal studies have shown that fasciotomies are not beneficialafter snakebite [90]. Antivenom and fasciotomy performed before admin-

istration of venom did not prevent muscle necrosis compared with

antivenom alone [91]. Administration of antivenom after snake venom

injection decreases the elevation in compartment pressures and preserves

muscle function [87,92]. In addition, decreased muscle strength was

documented in animals receiving fasciotomy plus antivenom compared

with the antivenom-alone group, suggesting that fasciotomy is causing

further muscle damage [87]. Conservative therapy using antivenom without

fasciotomies in individual case reports and large case series has shown goodoutcomes for victims of snakebites [49,93]. Fasciotomies do have a role in

the management of snakebites [94,95]. When compartment pressures are

documented to be elevated greater than 30 mm Hg, and the patient already

has been treated adequately with antivenom, fasciotomy may be considered

[96]. Measurements can be taken easily with a wick catheter, slit catheter, or

needle manometer. In addition, other noninvasive techniques are beneficial



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in performing serial monitoring for elevated compartment pressure [97].

Pulse oximetry should not be used to assess compartment pressure [98].

Despite this literature, victims of snakebites continue to be mismanaged byphysicians too eager to decompress edematous tissues surgically.

Corticosteroids. Initially, corticosteroids were thought to be beneficial in the

treatment of snakebites and recommended as a standard of care [99].

Subsequent experimental studies failed to find benefit in their use, however

[100]. Steroids should not be routinely administered to victims of snakebites

but rather reserved for the treatment of serum sickness.

Blood products. Antivenom is the first choice of treatment for crotalidsnakebiteinduced coagulopathy. Blood products also may be indicated if

active hemorrhage is occurring or coagulation parameters are not correcting

at an acceptable rate. In the latter situation, an increased dose of antivenom

is frequently indicated. Blood products that may be beneficial in a limited

number of patients include fresh frozen plasma, cryoprecipitate, packed red

blood cells, platelets, and whole blood.

Fluid replacement. Hypotension may be caused by fluid loss owing to third

spacing, vomiting, hemorrhage secondary to coagulopathy, or vasovagaleffects. Crystalloid administration should begin immediately in these

patients. In the case of hypotension caused by extravascular fluid shifts or

hemorrhage, antivenom also is indicated. A common cause of prolonged

hypotension in snakebite victims is inadequate fluid resuscitation.

Antivenom. The most critical decision facing the clinician treating snakebite

victims is when to administer antivenom. For North American crotalid

envenomation, two antivenom products are available: a partially purified

polyvalent crotalid antivenom of equine origin (Wyeth-Ayerst Laboratories,Philadelphia, Pennsylvania) and a purified ovine polyvalent Fab immuno-

globulin fragment product (CroFab; Protherics, Brentwood, Tennessee).

There have been numerous reports of immediate hypersensitivity

reactions associated with the use of crotalidae antivenom polyvalent IgG

(Wyeth-Ayerst Laboratories). Incidence rates for immediate hypersensitivity

reactions associated with the use of this product range from 23% to 56%

[101]. This high reaction rate may be due in part to the large amount of

nonvenom neutralizing proteins within this partially purified horse

antivenom. In addition, this product contains the Fc portion of theantibodies, which may result in cross-linking on cell surface receptors and

lead to mast cell and basophil degranulation. Because of the high incidence

of hypersensitivity reactions to the Wyeth product, use of this product is

gradually diminishing in North America [102].

CroFab is a sterile, purified, lyophilized preparation of ovine polyvalent

Fab immunoglobulin fragments that has been approved for use in patients

1211ENVENOMATIONS


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with minimal or moderate North American crotalid envenomation. These

Fab fragments are obtained from the blood of sheep immunized with one of

the four following snake venoms: Crotalus atrox (western diamondbackrattlesnake), Crotalus adamanteus (eastern diamondback rattlesnake),

Crotalus scutulatus (Mojave Desert rattlesnake), and Agkistrodon piscivrus

(cottonmouth). The antivenom is prepared by fractionating the immuno-

globulin from the ovine serum, digesting it with papain, and isolating the

venom-specific Fab fragments on ion exchange and affinity chromatography

columns. These four different monospecific antivenoms are mixed, creating

the polyvalent CroFab.

CroFab is reported to have a lower risk of immediate hypersensitivity

reactions [103]. The product contains reduced amounts of the immunogenicFc portion of the antibody. In a review of the literature, a few cases of acute

allergic reaction have been reported with CroFab. The incidence of immediate

hypersensitivity reactions was reported as 19% in the original randomized

multicenter trial of this product[104]. Dart and McNally [101] reported a case

series of 42 patients who received CroFab in which 6 patients developed mild-

to-moderate allergic reactions. Five of these 6 reactions were associated with

an improperly purified lot of antivenom, however, containing higher amounts

of the Fc portion. Another case series from Dart and colleagues[105] reported

no acute reactions with 11 consecutive patients. Ruha and colleagues [106]described a case series of seven patients who received CroFab infusions of up

to 28 vials per case with no immediate hypersensitivity reactions noted.

Antivenom is less often administered with copperhead (Agkistrodon

contortix) envenomation. Because of the past high risk of hypersensitivity

reactions associated with the equine-derived product, it was reserved for

patients with marked systemic signs of toxicity. With the availability of the

less antigenic and safer Crotalidae polyvalent immune Fab (ovine),

antivenom treatment for copperhead bites is more commonly considered,

although its exact indications have not yet been delineated clearly [107,108].The major indications for antivenom therapy are as follows:

1. Rapid progression of swelling

2. Significant coagulation defect

3. Neuromuscular paralysis

4. Cardiovascular collapse

Attempts have been made to quantitate these signs and symptoms [109].

If in question, the most reliable means of determining the indication for

antivenom is through consultation with a regional medical toxicologist orpoison center. Patients who are asymptomatic or have minimal symptoms

should not be treated with antivenom. Instructions for mixing antivenom

are in the package insert. Full resuscitation capabilities should be available

during infusion of antivenom in the event that anaphylaxis develops.

Asymptomatic patients may be observed for 6 hours after the bite. If no

coagulopathy or symptoms develop, they may be released. There are a few



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reports of patients developing symptoms beyond 6 hours [110,111].

Although rare, the patient should be instructed to return if symptoms

develop, and a follow-up call should be made to the patient the followingday.

Disposition

Patients who remain asymptomatic for 6 hours and have normal

coagulation studies (fibrinogen, fibrin split products, platelets, prothrombin

time, partial thromboplastin time) may be released with instructions to

return if symptoms occur. Follow-up contact within 12 to 24 hours should

be made.

Symptomatic patients should be hospitalized and the need for antivenomtherapy should be determined. If symptoms have not progressed, and

coagulation studies are not altered significantly by 24 hours, the patient may

be released with follow-up arranged for the following day. The patient

should be instructed to return if symptoms recur.

The patient who has received antivenom therapy should be observed for

24 hours or until the progression of edema has stopped, coagulation studies

have been reversed to near-normal, and all signs of neuromuscular

impairment are gone. Wound management often requires repeated follow-

up visits. The patient should be instructed as to the appearance of serumsickness and should contact the physician if that occurs. Some clinicians

prefer to give the patient prescriptions for histamine blockers (ie,

hydroxyzine) and steroids at the time of dismissal so that there is less delay

in treatment when symptoms occur; this does not preclude the need for the

patient to contact the physician at the onset of symptoms.

Patients who have full-thickness tissue destruction may require referral to

an appropriate surgical consultant. This referral is best done during the

initial phase of treatment while the patient is hospitalized. Follow-up should

be arranged for outpatient management before discharge. Pain controlusually requires oxycodone or hydrocodone for 1 or 2 weeks after discharge.

After that time, nonsteroidal anti-inflammatory drugs may be substituted.

Arachnids

Brown recluse

Description

The brown recluse spider, also known as the fiddleback or violin spiderowing to the dark violin-shaped coloring on its cephalothorax, is 1 of 13

brown spiders in the family Loxoscelidae found in the United States. They

are light tan to gray in color and are on average 9 mm long with a leg span

of approximately 25 mm. They are unique from most other spiders because

they possess three sets of eyes compared with most other spiders, which

possess four (Fig. 5).

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The brown recluse is distributed throughout the southeastern and

midwestern United States, but is most concentrated in Kansas, Arkansas,

Oklahoma, and Missouri [112]. They inhabit outdoor and indoor areas, but

are commonly found within human habitats, such as basements, storage

sheds, under piles of wood and rock, and infrequently used drawers.

Although these spiders are not aggressive, brown recluse bites can occur

because of the close proximity of their habitat with humans. Common

scenarios include reaching into an infrequently used drawer, picking up

wood from a stored pile, or putting on old clothing where the spider is

located. In most instances, the bite is painless and goes unnoticed for hours,

making diagnosis difficult.

Venom

The venom of brown recluse spiders is composed of at least nine different

enzymes; the most significant is thought to be sphingomyelinase D2

[113,114]. In conjunction with host factors and its accompanying enzymes,

sphingomyelinase D2 causes local endothelial damage, neutrophil and

platelet aggregation, and factor activation leading to small vessel occlusion

and eventual tissue necrosis. Sphingomyelinase D2 also causes calcium-

Fig. 5. Brown recluse spider. (Courtesy of Sue Kell, University of Virginia.)

Fig. 6. Black widow spider. (Courtesy of Christopher P. Holstege, MD, University of Virginia.)



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dependent erythrocyte lysis and is responsible for the hemolytic anemia that

can be seen after brown recluse bites [115].


The presentation of a brown recluse bite ranges from a mild local skin

reaction to severe systemic illness. The varying severity of peoples reactions

is thought to depend on the amount of venom injected, location of the bite,

and inclusion of gastric contents with the venom [116118]. Initially the bite

is painless, but within 6 hours patients may develop pain, erythema, and

pruritus at the site of the bite. A small blister with a blue discoloration may

develop surrounded by a ring of erythema. Over the next 2 to 3 days, the

blister may enlarge and can be become necrotic. An escar can develop thatwith time sloughs off, leaving an ulcer. The ulcer varies in size from 1 cm to

30 cm and can become large enough to require skin grafting.

A small percentage of patients develop systemic symptoms, referred to as

loxoscelism. Systemic symptoms typically begin 2 to 3 days after the bite.

Symptoms are flulike and may include fever, chills, nausea, vomiting,

arthralgias, convulsions, and rash [119,120]. Rarely, patients develop severe

systemic illness, such as hemolytic anemia, DIC, thrombocytopenia, and

kidney failure [113]. A study by Wright and colleagues [121], evaluating the

clinical presentations of suspected brown recluse bites to their institution,found that only 14% of patients presented with systemic symptoms, and

only 5% of patients were sick enough to warrant hospitalization.

The diagnosis of brown recluse spider bite is overused for necrotic skin

wounds of uncertain etiology [122126]. Misdiagnoses are common [127].

Clinicians should be careful not to fall into the trap of diagnosing all

necrotic skin lesions as brown recluse spider bites.

Treatment

Most brown recluse spider bites cause minor local reactions and healwithout medical treatment in several weeks [128]. Patients who present with

minor lesions should have their wound cleansed thoroughly, given tetanus

vaccine if necessary, instructed to elevate the affected extremity, and be

given analgesics. For bites with larger skin necrosis or systemic symptoms,

a variety of treatment modalities have been advocated with varying success;

however, all remain controversial.

Treatments that have been advocated include early surgical excision,

steroids, dapsone, hyperbaric oxygen, topical nitroglycerin, and brown

recluse antivenom. Early surgical excision was theorized to help decreasewound propagation and the need for skin grafting through early curettage

of the necrotic area around the bite. Studies have now shown that early

surgical excision has been associated with increased scarring and skin graft

rejection and is no longer recommended [113,129131]. Delayed skin

grafting, if needed, is best done after wound stabilization, which usually

occurs in 6 to 10 weeks [132,133].

1215ENVENOMATIONS


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Intralesional and systemic steroids do not seem to affect lesion size and

are not recommended for wound protection [134,135]. Steroid use has been

proposed, however, to be kidney protective in patients who are undergoinghemolysis and subsequently experience hemoglobinuria [136].

Dapsone, a drug that suppresses neutrophil diapedesis, is thought to

work by preventing neutrophil infiltration into the wound and its

subsequent inflammatory response. Studies of dapsone suggest little, if

any, benefit [137,138]. Side effects of dapsone use include hemolysis,

agranulocytosis, aplastic anemia, methemoglobinemia, sore throat, pallor,

jaundice, and hyperbilirubinemia.

Hyperbaric oxygen also has been used with mixed results. The exact

mechanism of preventing wound propagation is unknown, but theoriesinclude inactivating free radicals; sequestering neutrophils in the lung,

limiting their response to the wound; and production of fibroblasts

[139,140]. Clinical trials have produced mixed results, and it is unknown

whether hyperbaric oxygen is helpful [141,142].

The use of topical nitroglycerin and brown recluse antivenom has been

shown to decrease wound size in certain studies, but comparison studies

have found no change in wound size compared with controls [143145].

These treatment modalities must be applied with care until more research

has been done.

Latrodectus

Description

Latrodectus species (black widow) are present throughout much of North

America except for the northern reaches. The female spider is responsible

for the characteristic toxicity and is shiny black in color with a red hourglass

of varying size on its ventral abdomen (Fig. 6). Its webs are disorganized,

appear abandoned, and are often found near human habitation.

Venom

The venom of the black widow containsa-latrotoxin. This toxin binds to

multiple sites, resulting in the unregulated opening of cation channels and

the subsequent influx of calcium [146,147]. Elevated cytosolic calcium causes

unregulated release of neurotransmitters [148]. As a result, neurotransmit-

ters, such as acetylcholine and norepinephrine, are increased. This increase

in neurotransmitters results in activation of the sympathomimetic and

cholinergic systems and causes increased stimulation at the neuromuscularjunction.


Initially a pinprick sensation may be felt at the bite site. The initial pain

may go unnoticed, however. Locally a small circle of erythema or induration

may be seen at the bite site. Within the ensuing hours, systemic signs and



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symptoms may develop, progress, and last for days [149]. Muscle cramping

is a characteristic finding associated with black widow envenomation [150].

The cramps my be mild and remain localized to the site, or the cramps caninvolve all muscle groups diffusely and become severe and unrelenting [151].

The worst cases may develop opisthotonus posturing and abdominal

rigidity. Nausea, vomiting, headache, palpitations, hypertension, tachycar-

dia, diphoresis, priapism, facial edema, renal failure, and anxiety all may be

seen clinically [152154]. The diagnosis of black widow envenomation is

made solely on the clinical presentation; no clinical laboratory tests are

available to confirm the diagnosis [155].

TreatmentWounds should be cleansed, and if needed tetanus prophylaxis should be

administered. Patients should be monitored for at least 6 hours. In patients

manifesting muscular spasms, opioid analgesics orally or intravenously

should be considered. Antispasmodics, such as diazepam, also may provide

additional relief. Methocarbamol and dantrolene have been used for

treatment, with mixed results [156158]. Intravenous calcium initially was

touted to be efficacious to alleviate the pain associated with cramps, but

subsequent studies have not found it to be of significant benefit [149,156].

Latrodectus mactans antivenom (equine-derived) is rapidly effective atrelieving the clinical effects associated with toxicity [159161]. Its use is

limited, however, to patients manifesting significant toxicity not relieved by

conventional therapy or patients with health problems that place them at

increased risk for complications. The antivenom has an associated risk of

anaphylaxis and, if used, should be administered in a hospital with full

resuscitation capabilities [151].

Summary

Numerous types of envenomations may be encountered by health care

workers depending on where in North America they work. Clinicians should

be familiar with the animals in their region that may lead to envenomation.

A rational approach with use of poison center or medical toxicology

consultation services ensures that cases are managed appropriately.

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