Background
The World Health Organization (WHO) has estimated that each year, as many as 2.7 million bites from venomous snakes occur worldwide, causing 81,000-138,000 deaths. [1] The vast majority of venomous snake species are viperids (eg, rattlesnakes and Gaboon vipers) or elapids (eg, cobras and taipans). Although most snakes in the Colubridae family are nonvenomous, some (eg, boomslangs) are venomous and responsible for significant morbidity and mortality.
In the United States, several thousand snakebites occur every year, resulting in fewer than 10 deaths. [2, 3, 4, 5, 6] There are four types of venomous snakes native to the United States, as follows:
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Copperheads
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Cottonmouths (water moccasins)
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Rattlesnakes
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Coral snakes
The first three are pit vipers in the family Viperidae, subfamily Crotalinae. There are approximately 25 species of rattlesnakes in the genera Crotalus and Sistrurus. The genus Agkistrodon includes both copperheads (Agkistrodon contortrix and Agkistrodon laticinctus) and cottonmouths (Agkistrodon piscivorus and Agkistrodon conanti). Collectively, these pit vipers account for more than 95% of all native snake envenomations. Coral snakes are the only elapids that are native to the Western hemisphere, and the three species of US coral snakes account for fewer than 5% of all native envenomations.
Pit vipers
Pit vipers are characterized by large, triangular heads, comparatively small eyes, large and retractable fangs, and a thermoreceptor “pit” located between the eye and the nostril. (See the images below.) Pit vipers also have a single row of subcaudal plates distal to the anus, and rattlesnakes have one or more keratin buttons that compose the “rattle” at the distal end.
Juvenile southern Pacific rattlesnake, Crotalus oreganus helleri. Image from Sean Bush, MD.
Although some references have suggested using the pupil shape as a way of distinguishing pit vipers from other snakes, it should be noted that all snakes can have round or elliptical pupils, depending on the amount of ambient light. Additionally, many nonvenomous snakes can flatten their heads into a triangle shape when they feel threatened. Experts generally recommend that people learn to recognize the venomous species in their vicinity rather than rely on mnemonics.
Coral snakes
There are three species of coral snakes in the United States. The Sonoran coral snake, Micruroides euryxanthus euryxanthus, is found in Arizona and western New Mexico. The Texas coral snake, Micrurus tener, is found in Texas, Louisiana, and Arkansas. (See the image below.) The eastern coral snake, Micrurus fulvius, is confined to the southeastern region of the United States as far north as North Carolina and as far west as Mississippi.
The rhyme "red on yellow, kill a fellow; red on black, venom lack" is commonly used to distinguish coral snakes from nonvenomous species (see the first image below), but there are many exceptions. Some native coral snakes have aberrant patterns that do not adhere to the rule (see the second image below), and nonnative coral snakes may have completely different coloration. Conversely, there are nonvenomous snakes (eg, shovel-nosed snakes, genus Chionactis) in which red touches yellow. In making a snake identification, it is best to look at a combination of features, including head shape, body habitus, and coloration. When one is in doubt, it is prudent to assume that a snake is venomous and leave it alone.
Comparison of harmless Mexican milksnake, Lampropeltis triangulum annulata (top), with Texas coral snake, Micrurus tener (bottom). Image from Charles Alfaro.
Venomous snakes not native to North America
Nonnative venomous snakes include members of the families Viperidae (eg, Gaboon vipers), Elapidae (eg, cobras and brown snakes), and Colubridae (eg, boomslangs). (See the images below.)
A large number of nonnative species are kept by both zoos and private collectors, making bites by nonindigenous species increasingly common. Among the most common nonnative species are the monocled (monocellated) cobra (Naja kaouthia), the African bush viper (Atheris squamigera), the eastern Gaboon viper (Bitis gabonica), and the white-lipped tree viper (Trimeresurus albolabris).
Pathophysiology
Pit viper envenomations
Pit viper venom is produced and stored in paired glands below the eyes. Pit vipers have hollow, mobile, relatively long fangs located in the front of the upper jaw and are capable of delivering venom quite efficiently. Fewer than 10% of pit viper bites are “dry” (meaning that no venom is deposited). A number of factors determine how much venom is delivered, including the species, age, size, and overall health of the snake, as well as its diet and the last time it had fed or released venom.
Snake venom has been described as a "soup of antigens" and comprises a variety of protein and nonprotein substances. Most pit viper venom contains a mixture of metalloproteinases, collagenase, phospholipase, and hyaluronidase that can cause myonecrosis and dermatonecrosis. [7] Multiple venom components, such as serine proteases, disintegrins, metalloproteinases, and C-type lectinlike proteins, produce a variety of hematologic effects, resulting in coagulopathy, platelet aggregation, platelet activation or inhibition, or increased coagulation, leading to thrombotic complications. [8]
Certain pit viper species have unique toxins. Crotalocytin, found in the timber rattlesnake (Crotalus horridus), causes platelet aggregation. [9] Mojave toxin, found in some populations of the Mojave rattlesnake (Crotalus scutulatus), inhibits the presynaptic release of acetylcholine, leading to weakness and paralysis. [10] Pit viper venom may also include bradykinin-related peptides that can lead to angioedema and hypotension. [11]
Coral snake envenomations
Coral snakes have shorter, fixed front fangs and a smaller mouth, which make them less efficient at delivering venom. In the wild, coral snakes often hang onto their prey until the venom takes effect. Despite the persistent myth, however, coral snakes do not need to "chew" in order to envenomate. It is estimated that 30% or more of coral snake bites are dry.
Coral snake venoms are complex mixtures that include phospholipase A2, multiple proteases, high-molecular-weight protein, and a variety of neurotoxins. Approximately 380 isoforms of phospholipase A2 have been identified in snake venoms, and their effects include neuromuscular paralysis, bleeding, myonecrosis, edema, widespread inflammation, and platelet aggregation. [12, 13] In coral snakes, the neuromuscular effects are most pronounced.
Several other neurotoxins are found in coral snake species. Most are alpha-toxins, which competitively antagonize postsynaptic acetylcholine receptors on the neuromuscular junction. Weakness and paralysis result, though these can be overcome by increasing local acetylcholine concentrations. Myotoxic and edematogenic effects have also been detected in several coral snake venoms, with particularly strong activity in the eastern coral snake (Mfulvius). [14] Coral snake venom components can also activate the classic complement pathway and subsequently generate anaphylatoxins, which contribute to vasodilation and allow greater distribution of other venom components. [15]
Nonnative snake envenomations
Because of the substantial heterogeneity of nonnative venomous snakes, a comprehensive review of their venom components is not possible in this article. In general, however, the venom of these snakes may have cytotoxic, neurotoxic, hematologic, myotoxic, or cardiotoxic effects, often attributable to venom components similar to those described above.
Etiology
A previous study suggested that most people become envenomated because they are intentionally interacting with the snake. [16] However, data from the North American Snakebite Registry (NASBR), a subregistry of the American College of Medical Toxicology's Toxicology Investigator’s Consortium (ToxIC), demonstrated that only 19% of the bites reported between 2013 and 2015 were the result of intentional interaction. [17] Males accounted for 91% of the bite victims, and 100% of bites that resulted from intentional interaction involved the upper extremity. Among US snakes, coral snakes are unique in that most bites do follow intentional interaction with the snake. [18]
It is a common misconception that most snakebite victims are under the influence of intoxicating substances when they are envenomated. In a study of snakebite reports to the American Association of Poison Control Centers (AAPCC; now America's Poison Centers), only 608 (0.7%) of 92,751 snakebites were associated with concomitant drug or alcohol use. [19] However, those who used alcohol were 27 times as likely to receive antivenom and 31 times as likely to die from the envenomation compared to those who had not consumed ethanol.
Epidemiology
US and international statistics
Snakebites, especially from nonvenomous snakes, frequently go unreported in the United States. Approximately 10,000 bites are reported annually, particularly in Texas, Florida, California, Arizona, North Carolina, and Georgia. Mortality from snakebites is rare in the United States, with no more than 10 deadly snakebites occurring annually.
Snakebites also frequently go unreported in the developing world. According to WHO estimates, as many as 2.7 million venomous snakebites occur worldwide each year, resulting in 81,000-138,000 annual deaths. [1] Worldwide, snakebites disproportionately affect low socioeconomic populations in more rural locations. They often occur as bites to the lower extremities sustained by farmers or workers who step on or disturb a snake in the field or rice paddies, or they can present as a bite to the head or trunk in individuals who sleep outside on the ground.
Although snakebites can occur throughout the year, they are most common in the summer months (from June to September in the Northern Hemisphere). [17]
Age-, sex-, and race-related demographics
Children younger than 13 years old accounted for 2044 (10.9%) of the 18,678 snakebites reported to the AAPCC (now America's Poison Centers) between 2020 and 2023. [2, 3, 4, 5] Children age 12 and younger accounted for 28.2% of snakebite patients recorded in the NASBR between 2013 and 2015. [17] Most bites in children (69.5%) involved the lower extremity.
During the period 2013-2015, according to NASBR data, 69.3% of victims were male and 30.7% were female. [17] In males, 45.2% of bites affected the lower extremity, and 54.8% involved the upper extremity; in females, 77.5% of bites were to the lower extremity, and only 22.5% affected the upper extremity.
During the sane period, 84.5% of US victims of snakebites were White. [17]
Prognosis
Death from snake envenomation is rare. In a study of US snakebites from 1989 through 2018, the average number of deaths annually was 3.4. [6] The states with the most deaths were Georgia (7), Kentucky (7), Texas (6), Arizona (6), Alabama (6), and Florida (6). When death occurs, it may result from intravenous deposition of venom, anaphylaxis, or nonimmune anaphylactoid reactions or may occur after systemic toxicity (eg, cardiovascular collapse or respiratory failure).
Most snakebite patients recover fully, though many victims, particularly those who are not treated or are undertreated, may have prolonged or even permanent disability. Timely administration of antivenom can accelerate recovery and reduce the likelihood of long-term deficits.
Patient Education
Prevention is key in limiting morbidity and mortality from snakebites. People who live in snake-endemic areas and those who engage in high-risk activities should be advised to wear proper attire and footwear and to avoid placing a hand or foot in a bush or other unseen area.
Anyone who is bitten should seek medical attention immediately. Victims should call emergency services (911) rather than attempt to drive themselves to the hospital. Many first-aid techniques that were once recommended for snakebites have since proved to be ineffective at best and dangerous at worst. Tourniquets, constriction bandages, pressure immobilization, electric "stun guns," and venom extractors may cause significant harm and should not be used.
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Eastern copperhead, Agkistrodon contortrix. Image from Spencer Greene, MD.
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Broad-banded copperhead, Agkistrodon laticinctus. Image from Kimberly Wyatt.
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Northern cottonmouth, Agkistrodon piscivorus. Image from Kimberly Wyatt.
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Western diamondback rattlesnake, Crotalus atrox.
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Texas coral snake, Micrurus tener. Image from Chip St John.
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Comparison of harmless Mexican milksnake, Lampropeltis triangulum annulata (top), with Texas coral snake, Micrurus tener (bottom). Image from Charles Alfaro.
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Aberrant Texas coral snake, Micrurus tener. Image from Reece Hammock.
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Juvenile southern Pacific rattlesnake, Crotalus oreganus helleri. Image from Sean Bush, MD.
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Copperhead bite. day 3. Initial wounds were to finger.
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Moderate rattlesnake envenomation in toddler after treatment with antivenom. Image from Sean Bush, MD.
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Hemorrhagic bleb following eastern copperhead (Agkistrodon contortrix) envenomation. Image from Spencer Greene, MD.
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Proper elevation of limb after upper-extremity bite. Image from Spencer Greene, MD.
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Swelling and bruising after pit viper envenomation. Image from Spencer Greene, MD.
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Copperhead bite, day 3. Initial wounds were to finger.
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Copperhead bite, day 3. Initial wounds were to finger.
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Superficial necrosis following copperhead envenomation. Patient improved completely within 1 week. Image from Spencer Greene, MD.
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Petechiae 1 week after treatment for black-tailed rattlesnake (Crotalus molossus) envenomation. Platelet count = 2,000 (reference range, 150,000-450,000). Image from Daniel Jarvis.
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Pseudonaja nuchalis (western brown snake).
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Typical appearance of southern California Mojave rattlesnake bite site. Image from Sean Bush, MD.
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Naja naja (Indian cobra). Image from Robert Norris, MD.
