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Goldfrank's Toxicologic Emergencies, 11e

Chapter 119: Native (US) Venomous Snakes and Lizards Anne-Michelle Ruha; Anthony F. Pizon

EPIDEMIOLOGY

Snakes

More than 3,000 species of snakes are identified worldwide, with nearly 800 species considered venomous.All venomous species are classified taxonomically into one of 4 general groups. These include the familiesViperidae, Elapidae, and Colubridae, as well as the Atractaspidinae, a subfamily of the Lamprophiidae family.The United States is home to nearly 30 species and subspecies of venomous snakes (Table 119–1), with manymore found throughout Mexico. All belong to either the Crotalinae subfamily of Viperidae or the Elapidaefamily.

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TABLE 119–1

Medically Important Snakes of the United States

Genus Species Common Name

Crotalinae    

Crotalus adamanteus Eastern diamondback rattlesnake

atrox Western diamondback rattlesnake

cerastes

cerberusSidewindera

Arizona black rattlesnake

horridus Timber rattlesnake

lepidus Rock rattlesnakea

mitchellii Speckled rattlesnakea

molossus

oreganusBlack-tailed rattlesnakea

Western rattlesnakea

pricei Twin-spotted rattlesnakea

ruber Red diamond rattlesnakea

scutulatus

stephensiMojave rattlesnakea

Panamint rattlesnake

tigris Tiger rattlesnake

viridis Prairie rattlesnakea

willardi Ridgenose rattlesnakea

Sistrurus catenatus Massasaugaa

miliarius Pygmy rattlesnakea

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aSubspecies identified for this species.

Genus Species Common Name

Agkistrodon contortrix Copperheada

piscivorus Cottonmoutha

Elapidae

Micrurus fulvius Eastern coral snake

Micrurus tener Texas coral snakea

Venomous snakes possess glands that are associated with specialized teeth, or fangs, which allow delivery ofvenom for the purpose of prey immobilization or defense. Fangs are located in the front of the mouth in mostvenomous species. In addition to fangs, venomous snakes have rows of small teeth that may causeadditional injury during a bite.

The majority of snake species in North America are rear-fanged, nonvenomous members of the Colubridaefamily. Bites by these species, which include corn snakes, gopher snakes, and garter snakes, are usuallyharmless. Colubrids do not possess venom glands, but some produce secretions from Duvernoy’s glands thatcontain toxins similar to those found in the venom of venomous species. Although the vast majority of bitesby nonvenomous colubrids do not produce symptoms, rare cases of envenomation are documented

following a bite by a nonvenomous species.62

Venomous snakes are found throughout most of the United States. They are much more common in thesouthern and western states than in the northern states. Though venomous species are not endemic toMaine, Alaska, or Hawaii, bites are reported in every state except for Hawaii. The true number of bites thatoccur each year is not accurately known, but an average of 5,000 native venomous snakebites are reported to

US poison control centers annually.49 Mortality is rare in the United States, with fewer than 10 deaths peryear reported. Epidemiologic data on snakebites in Mexico is poor, but the number of bites and deaths isthought to be higher. Internationally, snakebites are an important and common cause of morbidity andmortality (Special Considerations: SC10).

The majority of snakebites in the United States occur between April and September, with the peak numberreported in July. Men comprise 75% of snakebite victims and children represent about 10% to 15% of

reported cases.49 Most victims are bitten on an extremity, although bites to the torso, face, and tongue alsooccur. Bites o�en occur when an individual is purposely handling a known venomous snake. Herpetologists,those who capture and keep wild snakes, and religious snake handlers are at highest risk. Occasionally

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people are envenomed a�er killing and decapitating a rattlesnake. This is likely due to persistent reflexes inthe venom apparatus.

Snake handlers and collectors are at risk for multiple bites during their lifetime. There is no convincingevidence that immunity develops as a result of repeated envenomation. Victims of repeat bites actually havea greater risk for anaphylaxis because of prior sensitization and the development of IgE antibodies to

venom.45

Snake enthusiasts o�en keep nonnative (exotic) species as pets. Approximately 30 to 50 bites from a large

variety of exotic venomous snakes are reported to poison control centers each year.51

Pit Vipers

The majority of native venomous snakes are members of the Crotalinae subfamily of Viperidae. Thesecrotaline species are variably referred to as crotalids, New World vipers, or pit vipers. The term “pit viper”describes the presence of a pitlike depression behind the nostril that contains a heat-sensing organ used tolocate prey. Native pit vipers include the rattlesnakes (genera Crotalus and Sistrurus) and the cottonmouthsand copperheads (genus Agkistrodon). These pit vipers can be distinguished from native nonvenomousspecies by a triangular-shaped head, vertically elliptical pupils, and easily identifiable fangs (Fig. 119–1).Crotalinae have front, mobile fangs that are paired, needlelike structures that can retract on a hingelikemechanism into the roof of the mouth. Rattlesnakes have the longest fangs, reaching 3 to 4 cm. Pit vipers arealso identifiable by their scale patterns. Their undersurface has a single row of plates or scales, as opposed tothe double row found on nonvenomous species. Rattlesnakes may or may not have rattles, depending onmaturity. A rattling sound is o�en, but not always, heard before a strike. Copperheads and cottonmouths donot have rattles, but shake their tales similarly to rattlesnakes. Cottonmouths, which are also commonlyknown as water moccasins, are semiaquatic and have a distinct white mouth. Copperheads are known fortheir reddish-brown (copper) heads and dark hourglass-shaped bands contrasting with a lighter backgroundon their bodies (Fig. 119–2).

FIGURE 119–1.

Pit vipers have a triangular-shaped head, vertically elliptical pupils, and heat-sensing pits behind the nostril.

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FIGURE 119–2.

Copperhead (Agkistrodon contortrix). (Used with the permission from Michelle Ruha, MD.)

Of crotalid bites for which the type of snake is reported, about half are rattlesnake species, and theremainder copperheads and cottonmouths. Rattlesnakes are found throughout most of the United States,but encounters are most common in western and southern states. Rattlesnakes account for the greatestmorbidity among the various types of pit vipers. Deaths following snakebite are almost always due to

rattlesnakes, although rare deaths are reported from copperhead bites.41 Copperhead bites are most o�en

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reported in the eastern and southeastern United States, although they also occur in the northeast.Cottonmouths are found mainly in the southeastern United States.

Coral Snakes

Coral snakes (genera Micrurus and Micruroides) represent the Elapidae family in North America. Thesebrightly colored snakes typically have easily identifiable red, yellow, and black bands along the length oftheir bodies. In the United States, coral snakes and the similarly colored nonvenomous scarlet king snake areo�en confused. Coral and king snakes can be distinguished by their color patterns. Whereas coral snakeshave black snouts, king snakes have red snouts. Both species have red, yellow, and black rings, but indi�erent sequences: the red and yellow rings touch in the coral snake but are separated by black rings in kingsnakes (“Red on yellow kills a fellow; red on black, venom lack”) (Fig. 119–3). This general rule for identifyingcoral snakes does not apply to Mexican species, some of which have di�erent color patterns.

FIGURE 119–3.

Coral snake with characteristic black snout and red bands bordered by yellow bands. (Used with permissionfrom Banner Good Samaritan Medical Center Department of Medical Toxicology.)

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Elapids possess front-fixed fangs. The fangs of coral snakes are small, and discrete fang marks may not beobvious a�er envenomation. Coral snakes o�en latch on to a victim or “chew” for a few seconds in anattempt to deliver venom. A history of this activity may help identify a coral snakebite when the o�endingreptile cannot be located.

Coral snakes are responsible for approximately 2% of bites reported to US poison control centers.49 Micrurusspecies are found in 11 southeastern states, where up to 100 bites are reported per year. Micrurus fulvius (theEastern coral snake) is responsible for the greatest morbidity and mortality, whereas M. tener (the Texas coralsnake) seems to be less dangerous. The Sonoran coral snake (Micruroides euryxanthus) does not produce

envenomation necessitating medical intervention.61

Lizards

There are 2 species of lizard that are known to produce envenomation in humans. These are the Gila monster(Heloderma suspectum) (Fig. 119–4), which is native to the desert southwestern United States, and thebeaded lizard (H. horridum), which is found in Mexico. Both species are members of the Helodermatidaefamily. Bites by the Gila monster and beaded lizard are extremely uncommon, even in areas where the lizardsare endemic. These lizards are slow moving, nocturnal, and thick bodied. Adults reach a maximum length of60 cm and are generally shy, so bites are relatively rare and usually occur as a result of handling. Bites almostalways occur from captive animals, whether found in the wild or kept in a zoo or personal collection. Gilamonsters are known for their forceful bites. They can hang on and “chew” for as long as 15 minutes, and theymay be di�icult to disengage. The great majority of reported cases have involved adult men.

FIGURE 119–4.

A) Young Gila monster (Heloderma suspectum). (Used with the permission from Steven Curry, MD.) (B)Beaded lizard (Heloderma horridum). (Used with the permission from Michelle Ruha, MD.)

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The helodermatid lizards have a less e�ective venom delivery system than venomous snake species. Thelizards possess paired venom glands that are located on either side of the anterior lower mandible. Venomducts carry the venom from the glands to the base of grooved teeth. When a tooth produces a puncture

wound, the venom travels by capillary action into the grooves and then into the wound.47

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PHARMACOLOGY

Snakes

Snake venom is a complex mixture of proteins, peptides, lipids, carbohydrates, and metal ions. Venomcontains a variety of enzymes including phospholipases A2 (PLA2s), metalloproteinases (SVMPs), serine

proteases, acetylcholinesterases, L–amino acid oxidases, and hyaluronidases. Nonenzymatic proteins

include 3-finger toxins (3FTXs), sarafotoxins, disintegrins, and C-type lectins among others. The content andpotency of venom in any given snake varies depending on age, diet, and geography. Thus, an adult snake

may have significantly di�erent venom composition than a young snake of the same species.59

Snakes typically produce about 100 to 200 mg dry venom in a single milking, although some produce several

hundred mg to over 1 g.59 Many venom components are pharmacologically active and target receptors, ionchannels, enzymes, or other proteins in mammals. The actions of only a fraction of snake venomcomponents are fully understood. Identification of individual snake venom toxins, understanding ofpharmacologic mechanisms, and potential medicinal uses for venom are areas of ongoing research.

Lizards

Helodermatid venom contains a complex mixture of components similar to those of snake venoms, including

numerous enzymes such as hyaluronidase, phospholipase A2, and serotonin.47,57 Nonenzymatic

components include helospectins and helodermin, which are vasoactive peptides that activate adenylatecyclase, and exendin-3 and exendin-4, which stimulate glucose-dependent insulin secretion. Discovery ofexendins in Heloderma venom lead to development of exenatide (Byetta), a glucagonlike peptide-1 (GLP-1)

receptor agonist used in the management of diabetes.25,57 Another important component of Helodermavenom is gilatoxin. Gilatoxin is a serine protease with kallikreinlike activity, thought to be responsible for the

hypotension and angioedema that occur in some human envenomations.57

PHARMACOKINETICS AND TOXICOKINETICS

Snakes

Very few pharmacokinetic studies of snake venom exist, and much remains unknown regarding absorption,distribution, and elimination of venom following a bite. When a snake bites, venom is usually depositedsubcutaneously. In some cases fangs reach muscle or even directly access vasculature. Systemic absorptionof venom usually occurs via the lymphatic system. Available human and animal data suggest that venomantigens are absorbed into blood within minutes of envenomation, with peak concentrations detected

within 4 hours.10,31,50 Venom antigen concentrations measured in the first 4 hours following a bite correlate

roughly with grade of envenomation.3,9,31 Venom antigens are also detected in urine as early as 30 minutes

a�er envenomation.31 A�er administration of adequate doses of antivenom, venom antigens are no longer

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detected in blood; however, antigenemia may recur, and such recurrence is associated with reemergence of

clinical e�ects.31,50

The elimination half-life of snake venom appears to be long. Following subcutaneous injection of C. atrox

venom in a rabbit model, mean half-life was 20 hours, and venom was still detectable in blood at 96 hours.10

Lizards

Pharmacokinetic studies of helodermatid venom are not available. Clinical reports suggest that venom isabsorbed systemically within minutes of a bite.

PATHOPHYSIOLOGY

Snakes

Pit Vipers

Crotaline venom has the potential to simultaneously damage tissue, a�ect blood vessels and blood, and altertransmission at the neuromuscular junction. It is di�icult to attribute specific pathology or pathophysiologyto any particular component of snake venom. In fact, clinical e�ects o�en occur as the result of severalvenom components (Table 119–2). For instance, local tissue damage results from venom metalloproteinasesand hyaluronidase, which both contribute to swelling through disruption of the extracellular matrix and

basement membrane surrounding microvascular endothelial cells.29 As a result of reduced blood flowthrough damaged capillaries, they also contribute to myonecrosis, which results primarily from the action of

phospholipase A2 enzymes (PLA2) on muscle.29 Additionally, venom metalloproteinases contribute to

dermatonecrosis, both directly and through activation of endogenous inflammatory mediators.29,55

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aVenom contains both pro- and anticoagulants, with anticoagulant e�ects predominating in North American crotaline

envenomation.

bInclude thrombinlike enzymes as well as fibrinogenolytic enzymes.

Venom may contain factors that inhibit, activate, or a�ect aggregation of platelets.

TABLE 119–2

Major Venom Components of Crotalinae Snakes

General Clinical E�ect Responsible Venom Components

Local tissue damage Metalloproteinases

Phospholipases A2

Hyaluronidase

Coagulation e�ectsa C-type lectinlike proteins

Metalloproteinasesb

Serine proteasesb

Phospholipases A2

Platelet e�ectsc Disintegrins

C-type lectinlike proteins

Metalloproteinases

Phospholipases A2

Neurotoxic e�ects Phospholipases A2

Venom e�ects on the hematologic system are especially complex. Numerous components act asanticoagulants, and many others act as procoagulants. Similarly, platelets are inhibited, activated,agglutinated, aggregated, or inhibited from aggregating by various venom components. Venom componentscan be grouped according to certain characteristics, such as structure and enzymatic activity, but as noted

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above with local tissue damage, components within several groups may contribute to similar e�ects. Forinstance, anticoagulants in snake venoms are found among the C-type lectinlike proteins (CLPs), PLA2

enzymes, serine proteases, and metalloproteinases. Conversely, components within a single group may havemany di�erent actions. Various CLPs in venom act as anticoagulants, procoagulants, or platelet modulators.PLA2 enzymes are especially diverse, acting as anticoagulants and platelet modulators in addition to

producing myotoxic and neurotoxic e�ects. Platelet e�ects result mainly from the action of disintegrins,

although CLPs, PLA2 enzymes, and other proteinases also have platelet-modulating e�ects.40,65

Specific hematologic e�ects are species dependent, with no single venom containing all of the identifiedhemostatically active components. Of particular importance to North American rattlesnake envenomationare the thrombinlike enzymes and fibrinogenolytic enzymes. Thrombinlike enzymes are metalloproteinasesand serine proteases that preferentially cleave fibrinopeptide A or fibrinopeptide B from fibrinogen. Unlikethrombin, they do not activate factor XIII. The end result is production of a poorly cross-linked fibrin clot thateasily degrades. Multiple other venom components exist, some of which a�ect the vascular system andcontribute to the hypotension that sometimes occurs clinically. Examples include bradykinin-potentiating

peptides and vascular endothelial growth factors (Chaps. 20 and 58).53,65

Snake neurotoxins act at the neuromuscular junction and do not cross the blood–brain barrier. They areclassified as α-neurotoxins, which act postsynaptically, and β-neurotoxins, which act presynaptically. Certainpopulations of the Mojave rattlesnake, C. scutulatus, possess a neurotoxin, Mojave toxin, which is a PLA2 that

acts at the presynaptic terminal of the neuromuscular junction to inhibit acetylcholine release. The presenceof Mojave toxin in venom appears to be geographically distributed, with Mojave rattlesnake populations inCalifornia and southeast Arizona possessing functional Mojave toxin, and central Arizona populations lacking

the neurotoxin.28,64 Mojave toxin is also identified in the venom of some Southern Pacific rattlesnakes (C.oreganus helleri) found in southern California, and envenomations by this species are reported to produce

neurologic symptoms in some victims.14,24

Coral Snakes

Coral snake venom contains neurotoxins that produce systemic neurotoxicity. Unlike crotaline venom, coralsnake venom does not cause local tissue injury. Similar to neurotoxins present in other elapid species, α-neurotoxins bind and competitively block postsynaptic acetylcholine receptors at the neuromuscularjunction, leading to weakness and paralysis. Phospholipase A2 can also cause myotoxicity, although this

appears to be of less clinical importance. The LD50 of M. fulvius venom (0.279 mg/kg) is lower than that of M.

tener venom (0.779 mg/kg), which corresponds to the more severe e�ects noted in humans following Eastern

coral snake envenomations.48

Lizards

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The pathophysiology of helodermatid venom is poorly understood. It is suggested that hyaluronidase

contributes to spreading of venom throughout tissue.52 Gilatoxin is believed to produce hypotension and

other findings such as angioedema by increasing bradykinin levels.57

CLINICAL MANIFESTATIONS

Snakes

The clinical presentation of North American snake envenomation is highly variable and depends upon manyfactors, including the species of snake, the amount and potency of venom deposited, the location of the bite,and patient factors, such as comorbidities. It is important for the clinician to be familiar with endemicvenomous snake species in order to anticipate clinical e�ects when presented with an envenomed patient.For bites by nonnative species, it is important to identify the species so that specific antivenom can besought.

Pit Vipers

Envenomation by North American pit vipers is characterized by local swelling and cytotoxic e�ects.Hematologic e�ects are common, and there is the potential for development of systemic illness andneurotoxicity. Most patients exhibit only a subset of possible e�ects of envenomation. In addition, some ofthe signs and symptoms in a given individual, such as nausea or tachycardia, may be related to fear ratherthan to envenomation.

The clinical presentation following a pit viper bite can range from benign to life threatening (Table 119–3).One finding common to nearly all victims is the presence of an identifiable disruption of skin integrity. Mostcommonly, one or 2 distinct punctures are present, though occasionally, patients exhibit multiple punctures,small lacerations, or scratches.

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TABLE 119–3

Evaluation and Treatment of Crotaline Envenomation

Extent of

EnvenomationClinical Observations

Antivenom

Recommendeda

Other

TreatmentDisposition

None (“dry

bite”)

Fang marks are present, but no local

or systemic e�ects a�er 8–12 hours

No Local wound

care Tetanus

prophylaxis

Discharge

a�er 8–12

hours of

observation

Minimal Minor, nonprogressing, local swelling

and discomfort without systemic

e�ects or hematologic abnormalities

No Local wound

care Tetanus

prophylaxis

Admit to

monitored

unit for 24-

hour

observation

Moderate Progression of swelling beyond area of

bite with or without local tissue

destruction, hematologic

abnormalities, or non–life-threatening

systemic e�ects

Yes Intravenous

fluids

Cardiac

monitoring

Analgesics

Follow

laboratory

parameters

Tetanus

prophylaxis

Admit to

intensive

care unit

Severe Marked progressive swelling, pain with

or without local tissue destruction

Yes Intravenous

fluids

Cardiac

monitoring

Analgesics

Admit to

intensive

care unit

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aSee Antidotes in Depth: A39 for dosing recommendations.

Extent of

EnvenomationClinical Observations

Antivenom

Recommendeda

Other

TreatmentDisposition

  Systemic e�ects such as diarrhea,

weakness, shock, or angioedema,

and/or pronounced thrombocytopenia

or coagulopathy

  Follow

laboratory

parameters

Oxygen

Vasopressors

Tetanus

prophylaxis

 

Because pit viper bites result in injection of venom only about 75% of the time, approximately 25% of bitesdo not result in envenomation and are considered “dry bites.” Unfortunately, it is impossible to diagnose adry bite without an extended period of observation, because some patients have delayed onset of findingsfor as much as 8 to 10 hours following the bite and some subsequently develop serious illness. Even patientswho do present with symptoms require a number of hours for the full extent of clinical illness to becomeevident. As a general rule, however, it is assumed that envenomation from a pit viper has not occurred if nofindings develop within 8 to 10 hours from the time of the bite.

Of the North American pit vipers, rattlesnakes are responsible for the most severe clinical presentations.Agkistrodon (cottonmouth and copperhead) bites generally tend to produce less severe local and systemicpathology than rattlesnake bites. Copperhead bites in particular rarely cause systemic e�ects, and pathology

is usually limited to so� tissue swelling without necrosis.60 However, serious copperhead envenomations

occasionally occur, and at least one death is associated with a bite from this species.49

Local reactions. Generally, within minutes a�er pit viper envenomation, the area around the puncture sitebecomes swollen and painful, and oozing of blood from the wound may occur. Edema stabilizes quickly inmild envenomations, but more commonly, edema will gradually worsen over hours. In severe cases, edemaprogresses to involve an entire extremity within just a few hours. Swelling can worsen for days whenuntreated, extending proximally to involve the torso following bites to a distal extremity. Rarely, onset ofappreciable swelling is delayed for as long as 10 hours. This is most o�en noted in lower extremityenvenomations.

Ecchymosis may develop early at the wound site. Bites to the feet o�en exhibit a characteristic bluish tingeover the entire dorsal surface of the foot. Toes remain pink and well perfused, allowing distinction of thisecchymosis from cyanosis (Fig. 119–5). In the days to weeks following the envenomation, ecchymosis willo�en extend or new ecchymosis develops proximally, even in the absence of significant venom-inducedhemotoxicity.

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FIGURE 119–5.

Rattlesnake bite to the lower leg, with characteristic edema and bluish discoloration of the foot due toecchymosis. (Used with the permission from Michelle Ruha, MD.)

Erythema o�en develops at the envenomation site and sometimes spreads proximally from the wound alonglymphatic pathways. Lymphangitic streaks are rare but may occur early a�er the envenomation in theabsence of infection.

Hemorrhagic blisters (blebs or bullae) o�en form at the site of a rattlesnake bite. This most commonly occursa�er bites to digits but in rare instances occurs at other bite locations or dependent areas distant from thebite (Fig. 119–6). Blebs usually do not appear for several hours a�er the envenomation but when they dodevelop they o�en progress for several days. The tissue underlying blebs is o�en healthy, but extensive blebdevelopment may signify underlying tissue necrosis (Fig. 119–7).

FIGURE 119–6.

(A) Hemorrhagic bullae involving the entire digit a�er rattlesnake bite to the second digit. (Used with thepermission from Michelle Ruha, MD.) (B) Hemorrhagic bullae involving the antecubital fossa a�er rattlesnakebite to the hand. (Used with the permission from Michelle Ruha, MD.)

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FIGURE 119–7.

Debridement of hemorrhagic bullae revealed the underlying tissue to be dark and necrotic in this patient.(Used with the permission from Michelle Ruha, MD.)

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Myonecrosis is not a feature of most native pit viper envenomations but does sometimes occur. In rare cases,fangs directly penetrate muscle leading to localized necrosis. With subfascial envenomation, there is a riskfor compartment syndrome, which could lead to deep tissue necrosis. Compartment syndrome is very rarefollowing North American snakebite and cannot be reliably diagnosed in envenomed extremities withoutdirectly measuring compartment pressures. More o�en than not, envenomation simply mimics acompartment syndrome by producing distal paresthesias, tense superficial so� tissue swelling, pain onpassive stretch of muscles within a compartment, and muscular weakness. One study using noninvasivevascular arterial studies and skin temperature determinations in patients with rattlesnake envenomation,demonstrated that pulsatile arterial blood flow to an envenomed extremity actually increased a�er

envenomation, even distal to the site of envenomation.19

In addition to local myonecrosis, generalized severe rhabdomyolysis occurs in the absence of impressivemuscular swelling following some pit viper envenomations. This finding is considered characteristic a�erenvenomation by the Canebrake rattlesnake (Crotalus horridus atricaudatus), which was previouslyclassified as a subspecies of the Timber rattlesnake (C. horridus). Current prevailing opinion is that they are

the same species.16,56

Hematologic toxicity. Venom-induced e�ects on the hematologic system are common following bites byNorth American pit vipers, in particular rattlesnakes. In rare cases, coagulopathy, thrombocytopenia, or acombination of the 2, are present despite a paucity of other local or systemic e�ects. The onset, progression,and severity of thrombocytopenia and coagulopathy in patients who exhibit this e�ect is quite variable.Drops in platelets and fibrinogen are sometimes mild initially, yet continue to worsen for several days

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following the envenomation. Alternatively, severe decreases in platelet counts (in the 5,000–50,000/mm3

range) and fibrinogen concentrations (to near zero) with immeasurably high prothrombin times (PTs) canoccur within minutes to hours of crotaline envenomation. A rise in PT generally follows a drop in fibrinogen,as concentrations of clotting factors remain normal in victims of North American crotaline envenomation

with coagulopathy.15 The likelihood of thrombocytopenia or coagulopathy occurring a�er a given snakebitedepends on the particular species and venom populations present in the geographic area. In the desertsouthwest, coagulopathy occurs in approximately half and thrombocytopenia in one-third of patients

presenting with envenomation.46 Thrombocytopenia appears to be especially common and o�en severe

a�er the bite of the Timber rattlesnake (Crotalus horridus).4 The protein crotalocytin that is found in Timberrattlesnake venom causes platelet aggregation and is thought to be at least partially responsible for thethrombocytopenia.

Despite the high rate of hematologic e�ects following rattlesnake envenomations, the vast majority ofpatients have no clinical bleeding, even when severe laboratory abnormalities are present. Bleeding appearsto be more common when platelets are very low or when both coagulopathy and thrombocytopenia arepresent and severe.

Systemic toxicity. Clinical findings following most pit viper bites are limited to local tissue damage orhematologic pathology, but systemic symptoms occur. When present, systemic signs and symptoms areo�en mild and include nausea, metallic taste, restlessness, and nonspecific weakness. More concerning aretachycardia, vomiting, diarrhea, or confusion, which sometimes precede severe systemic toxicity. In the mostsevere cases, patients quickly develop circulatory shock or airway edema with obstruction, which is thoughtto be caused by anaphylactoid responses to venom components.

Rarely, patients bitten by crotalids experience classic anaphylaxis from the venom itself, which complicatesevaluation or mimics a severe systemic reaction to venom. Previous sensitization to venom results indevelopment of IgE antibodies to venom in these patients. This is thought to occur more frequently inpatients who have previously experienced a snakebite, but is also observed in snake handlers who arethought to be sensitized to snake proteins through inhalation or skin contact. The presence of pruritus andurticaria or wheezing, uncommon with envenomation, should suggest anaphylaxis.

There are rare reports of true disseminated intravascular coagulation (DIC) with spontaneous bleeding alongwith significant hypotension and multiorgan system failure following rattlesnake bite. In such cases of trueDIC, the patient has evidence of organ infarction and hemolysis. This is reported a�er intravascular

envenomation.20

Neurotoxicity. Although local tissue destruction dominates the picture of Crotalinae envenomations,neurotoxic e�ects sometimes occur. The Mojave rattlesnake (C. scutulatus) is best known for its neurotoxicvenom. Some populations of the Mojave rattlesnake possess a neurotoxin, Mojave toxin, which can result in

weakness, cranial nerve dysfunction, and respiratory paralysis in victims.33 The Timber rattlesnake (C.horridus) is noted to commonly cause rippling fasciculations of the skin (myokymia), particularly of the facial

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muscles.6 Fasciculations are reported following envenomation by several other species of rattlesnake,including the Western diamondback (C. atrox), Mojave (C. scutulatus), and the Southern Pacific (C. o.

helleri).17 Fasciculations involving the shoulders, chest wall, and torso are associated with development of

respiratory failure.58

Coral Snakes

Coral snake fangs are small and nonmobile, and as a result, bites are less likely than pit viper bites to lead toenvenomation. An estimated 40% of patients bitten by a coral snake are subsequently determined to be

envenomed, with rates for the Eastern coral snake species possibly higher.35 The venom of the Eastern coralsnake (Micrurus fulvius) and Texas coral snake (M. tener) are more potent than that of the Sonoran coralsnake (Micruroides euryoxanthus). In fact, there are no reported cases of serious toxicity a�er the bite of theSonoran coral snake, which is found primarily in Arizona and western New Mexico.

Coral snake fangs do not always produce easily identifiable puncture wounds. In addition to the absence of adiscernable wound in some victims, coral snake envenomations are characterized by potentially seriousneurotoxicity without impressive local symptoms. The e�ects of envenomation are characteristically delayedfor a number of hours. One report described a patient who had an asymptomatic period of 13 hours followed

by rapid development of paralysis severe enough to require ventilatory support.35 Neurologic abnormalitiesreported with coral snake envenomation include paresthesias, slurred speech, ptosis, diplopia, dysphagia,stridor, muscle weakness, fasciculations, and paralysis. The major cause of death is respiratory failuresecondary to neuromuscular weakness. Muscle weakness takes weeks to months to resolve completely. Withrespiratory support, however, paralysis is completely reversible. Pulmonary aspiration is a common sequelain the subacute phase.

Lizards

The rate of envenomation following Gila monster bites is not known, but one case series reported 40% dry

bites.47 Heloderma species are known for hanging on to their victims when they bite. Multiple reports aredocumented where Gila monsters were attached to the victim for up to 15 minutes, and in some cases teethhave broken o� in the wound.

Pain is immediate following a bite, and local so� tissue edema o�en develops within minutes. Swellingextends from the puncture site, though not as commonly or dramatically as occurs following pit viperenvenomation. Helodermatid venom does not produce local tissue necrosis, but erythema at the wound siteand extension of erythema to an entire extremity is well described. Lymphangitic streaking is also

reported.23,32,52

Nausea, vomiting, and diaphoresis are reported following helodermatid envenomation. Patients are o�entachycardic and hypotension is common. There are numerous reports of upper airway angioedemadeveloping a�er bites by both Gila monsters and beaded lizards. There is a single report of a young man

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developing a myocardial infarction a�er a Gila monster envenomation.44 This patient also exhibited acoagulopathy although Gila monster venom does not typically produce abnormalities in platelet counts orclotting factors. It is suggested that the coagulopathy occurred as a result of endothelial damage rather than

direct e�ect of venom on the hematologic system.52 Leukocytosis is common following Gila monster

envenomation, with reported white blood cell counts as high as 48,000/mm3.44

DIAGNOSTIC TESTING

Snakes

Diagnosis of North American snake envenomation is based on a history of a snakebite and presence ofclinical signs of envenomation. There are no available laboratory assays for detection of venom in a wound.Although it is possible to measure blood and urine venom antigen concentrations using enzyme-linkedimmunosorbent assay (ELISA), this is only available in research settings and is not useful for early diagnosisor clinical management of envenomation.

Platelet counts, fibrinogen concentrations, and PTs are useful in the diagnosis of pit viper envenomation ifthey are abnormal. However, normal results do not exclude envenomation because thrombocytopenia andcoagulopathy do not develop in all patients with pit viper envenomation.

A validated severity score for the objective assessment of crotaline envenomation has been developed and

can be useful in a research setting.21 Its purpose is to assess the clinical condition of patients with snakebite,but it is not intended as a diagnostic tool. Caution should be used when applying this scale becauseenvenomation is a dynamic process and severity can worsen or improve with time, limiting the utility of thescore obtained at any given point in time.

Lizards

The diagnosis of helodermatid envenomation is based on the history of a bite and presence of physicalexamination findings consistent with envenomation. There are no laboratory studies that are available toconfirm or exclude the diagnosis, but a complete blood count may reveal leukocytosis.

MANAGEMENT

Snakes

When a patient with a snake bite presents for care, the initial objectives are to determine the presence orabsence of envenomation, provide basic supportive therapy, treat the local and systemic e�ects ofenvenomation, and limit tissue loss or functional disability (Table 119–3). A combination of medical therapy(mainly supportive care and, o�en, antivenom) and in some cases conservative surgical treatment (mainly

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debridement of devitalized tissue), individualized for each patient, will provide the best results. In general,the more rapidly treatment is instituted, the shorter the period of disability.

Pit Vipers

Prehospital care. No first aid measure or specific field treatment has been proven to positively a�ectoutcome following a crotaline envenomation. Prehospital care should generally be limited to immobilizationof the a�ected limb, placement of an intravenous catheter, treatment of life-threatening clinical findings, andrapid transport to a medical facility. If transport time is long and pain is severe, administration of analgesicsis recommended. Patients who are volume depleted, vomiting, or experiencing systemic e�ects such asdiarrhea should be given an intravenous fluid bolus. Hypotension that does not quickly respond to a fluidbolus should be treated with epinephrine, since early hypotension is most likely due to anaphylaxis,anaphylactoid reaction to venom, or venom-induced vasodilation. Epinephrine counteracts these e�ectsthrough stimulation of α-adrenergic receptors on vasculature as well as through inhibition of release ofinflammatory mediators.

In the past, various methods were advocated to prevent systemic absorption of venom a�er snakebites. All ofthese methods are either ine�ective, delay time to definitive care, or are potentially harmful. Such uselessand potentially dangerous therapies include tourniquets, incision and suction, venom extractors,

electrotherapy, and cryotherapy.1,12

Pressure immobilization bandages (PIBs), which are lymphatic-restricting bandages that are applied to thebitten extremity prior to immobilization with a splint, should not be used in patients with North AmericanCrotalinae bites. A randomized, controlled study of pressure immobilization versus observation in a porcinemodel with intramuscular injection of Crotalus atrox venom showed markedly increased compartmentpressures in the pressure immobilization group. All animals died in this study, but the pressureimmobilization group showed a prolonged time to death as compared to the control group. With local tissuenecrosis being the major morbidity associated with pit viper envenomations in humans, not death, the

authors concluded that PIB application cannot be recommended as a routine field procedure.11 TheAmerican College of Medical Toxicology, along with 5 other international organizations, released a position

statement recommending against use of PIB for North American Crotalinae bites.2

Hospital care. When a patient presents to the hospital with history of crotaline snakebite, it is important tofirst determine whether an envenomation has occurred. Although most patients do show early evidence ofenvenomation, absence of symptoms at presentation is not uncommon, and not all asymptomatic patientsultimately have “dry” bites. Patients who present with puncture wounds but without swelling or otherevidence of envenomation must be observed for delayed onset of symptoms. An observation period of 8

hours for Agkistrodon bites and 12 hours for rattlesnake bites is recommended.38 If no swelling develops,and laboratory study samples drawn at least 8 hours from the time of the bite remain normal andunchanged, the bite is likely “dry” and the patient is safe for discharge from medical care with instructions toreturn if new pain or swelling develops.

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Supportive. The initial in-hospital assessment of North American crotaline envenomation should focus onairway, breathing, and circulation. Patients with evidence of angioedema or with bites to the face or tongueneed to be observed closely for signs of airway compromise and intubated early, before swelling progressesto the point of airway obstruction. All patients, regardless of presenting symptoms, should have anintravenous catheter placed in an una�ected extremity and an IV fluid bolus is recommended. Patientspresenting with cardiovascular collapse should receive large volumes of fluid. An epinephrine continuousinfusion, starting at 0.1 mcg/kg/min and titrating as needed, is the authors’ vasopressor of choice for signs ofshock following envenomation.

Immobilization of the a�ected extremity in a padded splint in near-full extension and elevation above thelevel of the heart to avoid dependent edema is recommended. Although there are no studies to determinethe e�ect of limb elevation on outcome the authors find this helpful because it appears to decreasedependent edema, which contributes to increased pain and physical examination findings concerning forcompartment syndrome. The authors maximally elevate a�ected upper extremities by applying stocking netaround the limb and attaching the distal end to a raised IV pole.

Marking the leading edge of swelling with a pen or sequentially measuring extremity circumference will helpto identify progression of edema. A baseline complete blood count, PT, and fibrinogen concentration shouldbe obtained initially and repeated in 4 to 6 hours. Patients who are systemically ill should also haveelectrolytes, creatinine phosphokinase, creatinine, glucose, and urinalysis checked.

A comprehensive physical examination should be done, with emphasis on vital signs, cardiorespiratory andneurologic status, neurovascular status of the a�ected extremity, and evaluation for evidence of bleeding.Pain should be treated with opioid analgesics as needed, and tetanus prophylaxis should be addressed. Thepatient should be reassessed frequently with repeat physical examinations, specifically noting anyprogression of swelling. This is best accomplished by taking serial circumferential measurements of theinvolved extremity at multiple points proximal to the wound.

Prophylactic antibiotics should not be given, as studies show extremely low (0%–3%) rates of wound

infections.39 There is no indication for corticosteroids or antihistamines in the routine treatment of patientswith snakebites, except for treatment of anaphylaxis.

Antivenom. Patients with dry bites or mild envenomations, such as those who present with only localized

swelling that fails to progress, do not meet criteria for antivenom38 (Table 119–3). Patients who present withprogressive swelling, thrombocytopenia, coagulopathy, neurotoxicity, or significant systemic toxicity arecandidates for antivenom therapy. Antivenom given in a timely manner can reverse coagulopathy andthrombocytopenia and halt progression of local swelling. Antivenom has also been shown to reducescompartment pressure and limits venom-induced decreases in perfusion pressure, potentially preventing

the need for fasciotomy.26,54 There is no evidence, however, that antivenom can prevent or reverse thedevelopment of tissue necrosis, so patients should be informed of the risk of tissue loss. This is mostcommonly noted with rattlesnake bites to the fingers, which occasionally lead to amputation of the digitdespite appropriate treatment with antivenom.

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Until fall of 2018, the only available FDA-approved antivenom for North American pit viper envenomation isCrotalidae polyvalent immune Fab (CroFab, BTG). Crotalidae polyvalent immune Fab is an ovine-derived Fabfragment antivenom developed from commonly encountered North American pit vipers (C. atrox, C.adamanteus, C. scutulatus, A. piscivorus). Crotalidae polyvalent immune Fab is administered IV in an initialdose of 4 to 6 vials reconstituted in 0.9% sodium chloride solution. The recommended starting dose for

patients who present with cardiovascular collapse or serious active bleeding is 8 to 12 vials.38 The infusion isinitiated at a slow rate for several minutes, and if no signs of an anaphylactoid reaction develop, increased tocomplete the infusion over one hour. The patient should be reassessed a�er completion of the infusion forevidence of continued swelling or worsening thrombocytopenia, and, if present, an additional 4- to 6-vialdose is infused. This process is repeated until control of symptoms is achieved. Fibrinogen and PT aresometimes slower to recover in response to antivenom. If these are the only findings that continue to beabnormal a�er antivenom, it is reasonable to repeat these studies in 4 hours to determine if redosing ofantivenom is necessary. Control is generally considered cessation of progression of swelling and systemicsymptoms in addition to improvement in coagulopathy and thrombocytopenia. A�er control is achieved,maintenance doses of antivenom are given as 2 vials every 6 hours for 3 doses (6 total additional vials a�ercontrol). Although recommended in the package insert for Crotalidae polyvalent immune Fab, maintenance

therapy is not routinely administered by all practitioners.7 The authors recommend use of maintenancedoses unless the patient can be observed closely in the hospital for 18 hours a�er control of theenvenomation is achieved. During this observation period, additional antivenom is given as needed for localor hematologic recurrence.

An alternative antivenom for the treatment of North American rattlesnake envenomation was approved bythe FDA in 2015 but is not expected to be available until the fall of 2018. This antivenom, Crotalidae equineimmune F(ab′)2 (Anavip), is made using venoms of Bothrops asper and Crotalus simus. A randomized

controlled trial comparing Crotalidae polyvalent immune Fab to Crotalidae equine immune F(ab′)2 found less

late hematologic toxicity in patients who received Crotalidae equine immune F(ab′)2.13 This is likely due to

the longer half-life of Fab2 fragments as compared to Fab fragments. The initial dose of Crotalidae equine

immune F(ab′)2 is 10 vials. A�er infusion, the patient should be reassessed for further progression of

swelling, worsening hematologic toxicity, or continuation of other systemic venom e�ects, such asneurotoxicity. Additional 10 vial doses are administered until control of the envenomation is achieved.Following control, the patient should be observed for another 18 hours for signs of recurrent venom toxicity.

If these occur, additional 4 vial doses of Anavip are given (Antidotes in Depth: A39).22

Antivenom administration in children follows the same guidelines as adults, with doses based on clinicalpresentation and laboratory findings rather than weight. Attention should be paid to total amount of fluidreceived, and if necessary, antivenom can be reconstituted in a smaller total volume of fluid. Generally,patients with severe snake envenomation have large fluid requirements, and pulmonary edema as a result ofantivenom administration has not been reported.

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Pregnant patients who meet criteria for treatment should also receive antivenom. Crotalidae polyvalentimmune Fab (ovine) and Crotalidae equine immune F(ab′)2 are currently listed as pregnancy category C, but

the former has been used safely during pregnancy.36 Given the relative safety of these antivenoms and thepotential for fetal demise a�er envenomation, a low threshold for treatment should be considered. Fetal and

maternal monitoring should be carried out throughout the patient’s care.37

Surgery. Surgery is not routinely indicated following snakebites. An extensive review of the literature failed to

identify any evidence to support the use of fasciotomy in the treatment of snakebites.18 There are reportedcases of elevated compartment pressure a�er pit viper envenomation successfully managed withoutfasciotomy. When compartment syndrome is suspected, intracompartmental pressures should be measured.It is reasonable to attempt to treat moderately elevated compartment pressures with antivenom initially, butclinical examination and compartment pressures should be followed closely. If compartment pressures arerising despite administration of antivenom or if the patient develops evidence of limb ischemia, fasciotomy isrecommended.

Patients with bites to the digit sometimes present with evidence of ischemia. The compromised fingerappears cyanotic or pale, tense, and lacks sensation. The small diameter of the digit and limited ability of theskin to expand essentially creates a small compartment. In such cases it is recommended to perform a digitaldermotomy, where a longitudinal incision is made through the skin on the medial or lateral aspect of thedigit in order to decompress the neurovascular structures. Dermotomy should not be performedprophylactically in cases of digital envenomation, as most patients have good outcome without any surgical

intervention.30

Debridement of hemorrhagic blebs and blisters is o�en performed to evaluate underlying tissue and relievediscomfort. Some patients require surgical debridement of necrotic tissue or even amputation of a digit 1 to2 weeks a�er the bite. Referral to a hand surgeon is appropriate for patients with evidence of extensive tissuenecrosis.

Blood Products. Immeasurably low fibrinogen concentrations, PTs greater than 100 seconds, and platelet

counts lower than 20,000/mm3 are routinely encountered a�er rattlesnake envenomation. Such abnormallaboratory results alone should not prompt the clinician to treat with blood products in the absence ofclinically significant bleeding. The circulating crotaline venom responsible for the thrombocytopenia andcoagulopathy is still present and will likely inactivate any transfused components. For this reason, themainstay of treatment for crotaline envenomation–induced hematopathology is antivenom, not bloodproducts. Correction of coagulopathy, thrombocytopenia, and bleeding is usually achieved with antivenomalone. Rarely, a patient will have clinically significant bleeding, and antivenom alone will not correct theplatelets and fibrinogen. In such cases, fresh-frozen plasma, cryoprecipitate, packed red blood cells, orplatelet transfusions are recommended to replace losses.

In some cases, thrombocytopenia is di�icult, or impossible, to correct with even large amounts ofantivenom. The Timber rattlesnake, for example, is known for producing thrombocytopenia resistant to

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antivenom. The initial correction of platelet counts a�er treatment is typically transient (lasting only 12–24hours), with thrombocytopenia sometimes persisting for days to weeks a�er normalization of othercoagulation parameters. In the absence of bleeding, thrombocytopenia is a benign, self-limiting disorder,resolving within 2 to 3 weeks of envenomation. It is best to closely follow patients with resistantthrombocytopenia who are not bleeding, rather than attempt further platelet transfusions or antivenom

administration.42

Follow-up care. Hospital stays for patients with uncomplicated pit viper envenomations are typically short,

lasting approximately 1 to 2 days.46 Upon discharge from the hospital, patients o�en have residual swellingand functional disability. Some will have continued progression of hemorrhagic bullae with underlyingnecrosis. Patients should have an out-patient follow-up evaluation to ensure wounds are healingappropriately and extremity function is returning. If joint mobility does not return to baseline as swellingresolves, the patient should be referred for physical and occupational therapy.

In a significant proportion of rattlesnake bite patients treated with Crotalidae polyvalent immune Fabantivenom, a return of swelling, coagulopathy, or thrombocytopenia is noted days to weeks a�er initialresolution with e�ective antivenom treatment. This is termed “recurrence” of venom e�ect and is attributed

to the interrelated kinetics and dynamics of venom and antivenom.5,46 Simply stated, Fab antivenom has aclinical half-life shorter than that of venom. Administration of maintenance doses of antivenom is used in anattempt to prevent development of recurrent e�ects. Maintenance doses appear to be e�ective in preventingrecurrence of local swelling in most cases, but many patients develop hematologic recurrence within 3 to 7days of antivenom treatment despite administration of maintenance doses. Additionally, some patients whonever manifested thrombocytopenia or coagulopathy during their hospital presentation later develop thee�ect, presumably because of initial “masking” of the e�ect by early antivenom administration. These

recurrent or late hematologic e�ects have been associated with life-threatening bleeding.34 No risk factorshave been identified to predict which patients will develop late thrombocytopenia or coagulopathy.

The most reasonable way to address possible late hematologic e�ects of crotaline envenomation is carefuloutpatient follow-up a�er hospital discharge. Provide careful discharge instructions and consider all patientswho have been treated with Crotalidae polyvalent immune Fab antivenom to be at risk for late hematologictoxicity. Patients who use antiplatelet or anticoagulant medications should be continued on thesemedications only a�er a careful risk–benefit analysis. Whenever possible the medications should bediscontinued until the risk of recurrent or late hematologic toxicity passes. Patients must be warned not toundergo dental or surgical procedures for up to 3 weeks unless platelet and coagulation studies aredocumented to be normal immediately prior to the procedure. High-risk activities, such as contact sports,should be avoided. All patients with rattlesnake bites should have platelets and coagulation studiesmeasured 2 to 3 days, and again 5 to 7 days, a�er the last antivenom treatment. If values are abnormal ortrending in the wrong direction, the studies should be repeated every few days until normal and stable.Because copperhead envenomation is much less likely to produce severe hemotoxicity, one set of follow-uplaboratory studies to screen for late thrombocytopenia or coagulopathy is reasonable in this population.Patients should be advised to avoid surgical procedures and activities that place them at risk for injury.

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Opinions on when to retreat patients exhibiting late hematologic toxicity with antivenom vary. The generalapproach of the authors is to retreat any patient with evidence of bleeding, as well as patients with severe

isolated thrombocytopenia (platelets <25,000/mm3) or moderate thrombocytopenia (platelets 25,000–

50,000/mm3) in combination with severe coagulopathy (fibrinogen <80 mg/dL).46 Many clinicians choose toobserve patients with isolated coagulopathy cautiously as outpatients rather than to retreat them withantivenom. However, if patients with isolated severe coagulopathy have other risk factors for bleeding, suchas use of antiplatelet medications, high risk of injury, recent venom-induced shock, or pregnancy,retreatment with antivenom is recommended.

When the decision is made to retreat a patient with late hemotoxicity with antivenom, an initial starting doseof 2 vials is recommended. Late thrombocytopenia appears to be more resistant to antivenom than earlyvenom-induced thrombocytopenia, and it is unclear whether a di�erent mechanism is responsible for thelate e�ect. It is unknown how much antivenom is needed to reverse late thrombocytopenia or at what dose apatient is considered “resistant” to antivenom. Based on anecdotal experience, if platelet counts do notincrease a�er 2 to 3 doses of antivenom, additional antivenom is unlikely to be e�ective. Response toplatelet transfusions is also o�en poor. Some clinicians give steroids to patients who have not responded toantivenom and platelet transfusions, but there is no evidence to support this treatment, which has not beenstudied.

Coral Snakes

As with North American pit viper bites, patients who are bitten by North American coral snakes should betaken to a hospital for definitive medical care as soon as possible. There are no field treatments that havebeen shown to a�ect outcome in these patients, although use of PIBs is reasonable if transport to a hospitalwill be prolonged or delayed. Unlike with crotalid bites, worsening of local tissue injury as a result of PIBs isnot a concern with coral snakebite. Pressure immobilization bandages delay the systemic absorption ofvenom from Australian elapid snakes, and a swine model of coral snake envenomation supports a similar

e�ect.27 Patients who present for care a�er a PIB has been placed should have the dressing le� in place untilresuscitative equipment and personnel are present and, ideally, antivenom is available. The PIB should bechecked to ensure it is not functioning as a tourniquet.

Patients with a history concerning for possible Eastern or Texas coral snakebite should be observed for 24hours in a monitored unit where resuscitative measures, including endotracheal intubation, can beperformed. Because neuromuscular weakness and respiratory paralysis can develop quickly, endotrachealintubation is reasonable at the first sign of bulbar paralysis. In the past, treatment with Wyeth Antivenin(Micrurus fulvius) (equine origin) North American Coral Snake Antivenin was recommended for all patients inwhom there is strong suspicion of coral snakebite, even in the absence of signs of envenomation. This ismainly because paralysis can develop quickly and symptoms may not reverse following antivenomtreatment. However, a study comparing patients who received empiric treatment with antivenom to patientswho were treated when symptoms developed suggests that a conservative approach (waiting for symptoms

to develop before administering antivenom) does not result in worse outcomes for patients.63 North

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American Coral Snake Antivenom (Equine) is now available from Pfizer, and administration to asymptomatic

patients is listed as a contraindication in the package insert.43

If a patient is symptomatic following a coral snake envenomation, antivenom, if available, is indicated. Ifantivenom is unavailable, supportive care including mechanical ventilation may be necessary for manyweeks. Acetylcholinesterase inhibitors have been inconsistently successful in treating patients with South

American coral snakebites.8 If availability of coral snake antivenom is delayed, a trial of neostigmine toreverse the neurotoxic e�ects of venom is reasonable.

Sonoran coral snakes, indigenous to Arizona and California, have never been reported to cause significanttoxicity, and bite victims do not require observation in the hospital or antivenom administration.

Lizards

Management of helodermatid envenomation consists of supportive care. There is no antivenom availableagainst lizard venom. Routine wound care should be performed, and the clinician should look for thepresence of teeth in the wound. There is no evidence to guide clinicians when deciding whether toadminister antibiotics to patients with erythema surrounding and extending from the bite site. Most casereports describing patients with erythema also report empiric use of antibiotics. There are no reports ofconfirmed infections following these bites.

Patients who are symptomatic following a bite should be attached to a cardiac monitor and have anintravenous catheter placed. Although serious morbidity from lizard bites is unusual, life-threateningmanifestations of envenomation are reported. Angioedema, other evidence of respiratory compromise, orairway obstruction should prompt endotracheal intubation. Hypotension should be treated with intravenousfluid boluses as well as vasopressors such as epinephrine. Epinephrine, corticosteroids, and antihistaminesare recommended for the treatment of anaphylactoid reactions.

SUMMARY

Most native snake envenomations result from bites by Crotalinae species of snakes, also known as pit vipers,and commonly produce local tissue swelling and hematologic toxicity.

A small percentage of envenomations are due to bites by coral snakes, which are known for producingneurotoxicity without local tissue e�ects.

Management of patients with pit viper and coral snake envenomation should focus on aggressive supportivecare and specific antivenom when indicated.

Envenomations by Helodermatid lizards are o�en associated with local pain, erythema, hypotension, andangioedema.

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1. 

2. 

3. 

4. 

5. 

6. 

7. 

8. 

9. 

10. 

11. 

Clinicians are encouraged to contact a regional poison control center when a patient presents a�er a snakeor lizard envenomation.

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