Envenomations occur in everyday life for populations throughout the world. From the common bee sting to the bite of a pit viper, envenomations have the potential to inflict significant harm to humans. Over millions of years, snakes, arachnids, and bees have developed sophisticated methods of self-protection and predation. When athletes unknowingly enter the domain of these creatures, they put themselves at risk. Envenomations are spontaneous, usually occurring without warning. It is important for sports physicians to develop confidence in treating these injuries, so that harm to athletes is minimized and potentially fatal complications are averted.
Venomous snakes are responsible for up to 45,000 injuries per year in the United States. Nearly 9,900 patients were treated in emergency departments between 2001 and 2004 (1). Venomous snakes are predominantly found in the southern United States, as the number of species worldwide increases as you approach the equator. There are two essential groups of venomous snakes in the United States: pit vipers and coral snakes.
Between 1999 and 2007, 59 people died from venomous snake or lizard bites in the United States. Of these, 47 (79.7%) were men (9). Intentional exposure, such as playing with snakes in the wild or snake handling, accounts for the majority of deaths (1). Poison control center data estimate approximately 1 death per 736 rattlesnake victims (1).
Pit vipers, named for the paired prey-locating thermal receptor organs on their heads, strike at up to 2.4 mñs−1 and can reach a distance of 1.5 times their body length. The most common pit vipers found in the United States are rattlesnakes, cottonmouths, and copperheads. Typically these snakes strike from a defensive posture when enemies invade their surroundings. Studies have shown greater venom release in defensive bites as opposed to predatory bites, which may account for increased fatality rates in cases where the snakes are provoked intentionally (2). Larger rattlesnakes usually inflict more severe envenomations than smaller rattlesnakes, although juvenile snake bites can be life threatening. Most bites occur at the lower extremities of humans, usually around the time of dusk or dawn. Approximately 75% to 85% of pit viper bites result in actual envenomation (the remainder occurs as “dry bites”). Pit viper venom is composed of phospholipase A2 neurotoxins, metalloproteinases, and thrombin-like enzymes, the combination of which is responsible for respiratory muscle paralysis, rhabdomyolysis, distributive shock, and consumptive coagulopathy that can be seen in bite victims (2). Victims experience severe burning at the bite site within minutes of envenomation, followed by progressive soft tissue swelling over the next few hours (1). Blood persistently oozes out of the bite site. Over the span of hours to days, blood or serum-filled vesicles will start to appear. Pit viper bites may have little pain or swelling. A change in taste from rubbery to metallic, mouth numbness, and nausea with vomiting can occur. Tachycardia, pulmonary edema, shock, and even death can be seen in severe cases. Leukocytosis, thrombocytopenia, hyperglycemia, elevated creatinine kinase, elevated creatinine, coagulopathies, and decreased fibrinogen can be seen on laboratory evaluation (2).
The first step immediately following a snakebite is to remove the victim from the snake’s striking range. Smartphone pictures of the snake can help guide treatment, but attempts to identify or kill the snake should not delay transport to a hospital. A recently decapitated snake head can maintain a snake bite reflex for 90 min after death; therefore people should exercise caution handling a dead snake. Jewelry and tight-fitting clothing should be removed from the victim. Edematous tissue should be marked every 15 min to monitor for clinical progression. Oral suctioning can introduce more oral bacteria to the wound and is not recommended. Tourniquets should not be applied, as they can increase the amount of local ischemia and toxin-mediated injury (1). Pressure immobilization (PI) is an alternative method postulated to slow the spread of venom. PI is performed by applying a splint to the affected extremity and wrapping with a bandage from the distal tip of the extremity, over the snake bite proximally (1). Other strategies, such as electrotherapy and certain plants, have yielded little evidence for success.
Upon arrival at the hospital, a patient should first be evaluated for any signs of hemodynamic or respiratory compromise. Fluid resuscitation, along with metabolic workup for evaluation to the cardiovascular, pulmonary, renal, and CNS should be performed. Coagulation studies should be repeated every 3 h after admission. Prompt administration of antivenom should be given. In 2001, Crotalidae polyvalent immune Fab, or CroFAB, was developed. In 2007, 47% of patients with snake bites were given CroFab (11). CroFab is a sheep-derived antivenom, and the risk of serum sickness following administration is 16%. The rate of acute reaction is 14.3%. Anaphylaxis has never been reported. In fact, CroFab is safe enough to be administered in pregnant women (6). Progression of local tissue injury, hematologic abnormality, or coagulation abnormality are indications for use. Antivenom should not be given to patients with limb envenomations who have localized pain and swelling that is not progressing. Intravenous Crotalidae polyvalent immune Fab (FabAv), an ovine antivenom, has demonstrated ability to reverse late hematologic effects of rattlesnake envenomation and may actually be safer and more cost-effective (7). Furthermore antivenom can be used later than 18 h after the bite if hematologic issues remain, although these are only likely to be seen in severe envenomations (7). Providers should quickly contact their regional poison control centers. Opiates are the main therapy for pain control. Wound care should be aggressive, and the patient should be monitored closely for compartment syndrome as there can be significant edema leading to difficulty with perfusion. Antibiotics are not indicated unless there are signs of infection.
Coral snakes, named for their elaborate color pattern of red-yellow-black-yellow-red, have paired venomous glands with hollowed out fangs used to inject venom to their prey (Fig. 1). Coral snakes do not possess enough venom to kill with a single bite, so they “chew” on their prey in order to inject enough venom (2). The venom itself is very potent, with a spreading enzyme, hyaluronidase, and phospholipase A2, causing tissue breakdown (21). Coral snakes do not have an efficient venom delivery system; thus only 40% of bites result in effective envenomation. Local swelling is uncommon, and systemic signs and symptoms may be nonexistent for up to 13 h. Systemic symptoms include nausea, vomiting, headaches, abdominal pain, diaphoresis, and pallor. Neuromuscular junction effects of venom can lead to paresthesias and numbness, altered mental status, cranial nerve (CN) dysfunction, and peripheral nerve dysfunction. Unlike pit viper envenomations, there is no risk of coagulopathy. Thus laboratory tests have less importance in coral snake bites. An elevated creatine kinase and myoglobinuria may be seen due to the myotoxic component, and an arterial blood gas is helpful if respiratory status declines (2).
Management of a coral snake bite is similar to that of the pit viper. Early transport of patient to a local hospital with intensive care unit capabilities is a priority. While proper identification of the snake is helpful, it should never delay access to a hospital, as there is significant potential for neurologic, cardiovascular, and respiratory sequellae. PI may be effective. A baseline neurological assessment should be conducted and repeated at intervals to monitor for changes. Aggressive airway management is essential as airway compromise can occur very quickly. Unfortunately Wyeth discontinued production of North American Coral snake antivenom, and existing supplies expired last October 31, 2013 (22). There is still no alternative product in the United States for coral snake envenomations. Coralmyn, an antivenom available in Mexico, was tested when the Wyeth antivenom was discontinued originally. It was found actually to neutralize more effectively than the Wyeth antivenom but is still only available in Mexico (18). If available, antivenom administration is advised to be given as early as possible. A poison control center should be notified immediately, and the patient should be monitored for at least 24 h.
There are approximately 42,000 different types of spiders that live in every environment but the ocean (2). Spiders are mostly carnivorous and require the use of venoms in order to capture, immobilize, and digest their prey. Venoms of spiders are made up of neurotoxic and proteolytic peptides, proteins, and biogenic amines. Typically spider bites present without the offending arachnid. It is outside their norm for spiders to bite humans, except out of defense. Unfortunately the brown recluse spider is synanthropic, meaning that its populations increase in association with humans and use human structures as environments, thus increasing the potential for incidents (23). Without overtly capturing the spider and seeing it bite you, there are no true pathognomonic clinical signs of spider bites.
Loxosceles: the Brown Recluse
These small 8- to 15-mm spiders are light to dark brown in color with a violin-shaped spot anterodorsally. These spiders typically build webs in small areas, such as under rocks or in shoe boxes or garages. These spiders are found in the Americas and Africa. These spiders are naturally unaggressive toward humans but will attack when threatened. Brown recluses are known for their potent venom that can cause dermonecrosis, or arachnidism, which is responsible for the black eschar commonly associated with brown recluse envenomation. In the United States, bites are underreported and overdiagnosed. Of 1,773 spiders thought to be brown recluses, only 324 actually were confirmed (24). Differential diagnoses include methicillin-resistant staphylococcus aureus skin infection, erythema gangrenosum, and polyarteritis nodosa among others.
The clinical spectrum of necrotic arachnidism is variable and depends on the dose of venom, sex of the spider, and host factors. Of 1,495 brown recluse bites reported to the America Association of Poison Control Centers in 2010, only 14% had major complications (21). Fewer than 1% of cases advance into a systemic syndrome (24). Toxicity can range from mild and transient skin irritation to severe local necrosis with hematologic and kidney injury. Reports of disseminated intravascular coagulation (DIC), multiorgan failure, and even death have been described, although these are more common in children. In one case report, a child developed DIC and shock within 19 h of a bite. However this is the only such report in literature (14). It also appears that children are more likely to have immune-mediated hemolytic anemia after brown recluse bites, with a positive direct antiglobulin test and surface IgG to support the theory (9, 12). Generally if there is no hemolysis by 96 h, it is unlikely to occur. Important tests include complete blood count, comprehensive metabolic panel, and a urine analysis, along with serial monitoring of creatinine kinase and creatinine measurements. Coagulation panels and fibrinogen should be drawn to screen for DIC. The true diagnosis, however, remains clinical, as there are no confirmatory tests short of capturing the offending spider (5).
Although systemic manifestations can occur with brown recluse bites, most wounds respond to rest, ice, compression, and elevation. Surgical debridement is not recommended, as it prolongs healing times and increases scarring (2). Antivenom has been administered in experimental situations and has resulted in positive outcomes; however it is most effective when given within 24 h. One group in South America did find that antivenom after 24 h resulted in smaller lesions, faster healing times, and shorter hospital stays (15). Dapsone is not recommended due to its severe clinical toxicity and scarring (2). There is no role for topical corticosteroids as the primary toxin, sphingomyelinase D, is not responsive (13). Electrical shock and nitroglycerin have not proven benefit, although there are anecdotal success stories. If systemic symptoms do arise, treatment mainstays include systemic corticosteroids, transfusion, and dialysis (17).
Genus Latrodectus: Black Widow
Black widows are very large spiders, measuring 12 to 16 mm in length, and are recognized by their black bodies with a red hourglass marking on the ventral abdomen. The black widow is found in every single state in the United States, with the exception of Alaska. Widow spiders tend to bite defensively when accidentally crushed, with most bites occurring in rural and suburban areas of southern and western states. Outbreaks can occur in an epidemic fashion and depend on changes in occupational variations in human-spider contact, along with publicity and reporting (2). In 2008, poison control centers received 2,303 calls reporting black widow spider bites, of which 950 cases were treated by health care providers (8).
The venom of widow spiders lacks locally active toxins capable of provoking inflammation. However it does contain a potent mammalian neurotoxin, alpha latrotoxin, that can induce widespread sustained muscle spasm (24). Although the initial bite may be very painful, many bites go unrecognized. The local reaction is typically minimal, with only a tiny papule visible on examination. Neuromuscular symptoms can become dramatic within 30 to 60 min as involuntary spasm and rigidity of large muscle of the trunk and extremities (19). Severe abdominal cramping is the signature of black widow bites and can even mimic an acute abdomen or myocardial infarction (24). Other symptoms include fasciculations, weakness, ptosis, priapism, fever, diaphoresis, vomiting, and excessive lung secretions. Compartment syndrome, pulmonary edema, and myocarditis also have been described in the literature. Other clinical entities involved with black widow bites include hypertensive seizures, respiratory muscle weakness, and pain leading to respiratory arrest. Intractable crying may be seen in infants. Pregnancy complications with black widow bites include uterine contractions and premature delivery. However no prenatal losses occurred in 97 documented pregnant bite victims (24).
There is antivenom available for black widow envenomations, which should be used with any neuromuscular symptoms. First licensed by Merck in 1936, it is the partial purification of serum IgG from horses immunized with black widow venom. There have been two death reports from its use secondary to anaphylaxis. Proper dilution and slow administration of antivenom in conjunction with close monitoring for allergies reactions should alleviate concerns. The antivenom can completely ameliorate the effects of latrodectism within 30 min, although it does not reduce the overall severity of pain from envenomation. It did reduce the time to pain relief quicker than placebo, and without more adverse events than placebo (8). It also appears that the antivenom is effective after lengthy delays as well. Opiate and nonopiate analgesia is appropriate, along with benzodiazepines (2). There are no laboratory findings to help with diagnosis, but serum creatinine and CK can be checked to monitor for complications in serious envenomations.
Approximately 30 scorpion species are believed to be medically important and potentially fatal for humans. These species are found worldwide. Scorpion stings are second only to snakebites in worldwide human fatalities, and there are approximately 3,000 deaths per year worldwide. In the United States, there are more than 40 types of scorpions; however only the Arizona bark scorpion causes significant number of systemic reactions and is known to be potentially fatal (Fig. 2). These scorpions prefer dark locations and often hide under wood, ground debris, shoes, blankets, or clothing left on the floor. They are found in Arizona and some areas of Texas, New Mexico, Northern Mexico, and small areas of California. They are typically up to 5 cm long and can be uniformly yellow, brown, or tan (2).
Scorpions are predatory arthropods with lobster-like body shape with seven sets of paired appendages and a curved tail with paired venom glands and a stinger. Scorpions can sting their prey multiple times, although it appears that the first sting almost completely deprives them of their venom. Scorpion venoms are mixtures of mucopolysaccharides, hyaluronidase, phospholipase, acetylcholinesterase, serotonin, histamine, protease inhibitors, and protein neurotoxins, with the neurotoxins being the most critical factor. These toxins cause incomplete inactivation of sodium channels during depolarization resulting in elongation of the action potential and a slow inward sodium current after repolarization, leading to membrane hyperexcitability. This causes enhanced release of neurotransmitters.
About 10% of all calls received by the poison control center in Phoenix are related to scorpion stings. No deaths have been reported since 1968 in Arizona. There are four notable grades of the envenomations from the Arizona bark spider with various severity. Grade I is characterized by local pain and paresthesia, through grade IV envenomations, characterized by both CN dysfunction and somatic skeletal neuromuscular dysfunction. Stridor and wheezing can be seen along with hyperthermia from excess motor activity. Respiratory failure, pulmonary edema, metabolic acidosis, sterile cerebrospinal fluid pleocytosis, rhabdomyolysis, coagulopathy, pancreatitis, and multisystem organ failure can be seen. Cardiovascular changes such as arrhythmia, myocardial infarction, or acute heart failure can be observed in severe envenomations. Bedside echocardiography in the emergency department can be used to detect early heart failure in pediatric patients in severe envenomations (10). This combined with troponins, and b-type natriuretic peptide can be used to detect end-organ damage, which can be disastrous. Generally symptoms begin immediately and can progress within 5 h. Infants can reach grade IV within 15 to 30 min.
A scorpion antivenom was originally produced in 1966. However it was never approved by the U.S. Food and Drug Administration, and production was stopped in 2000. The last dose was given in 2005. There remains no production of antivenom in the United States (2). However a polyvalent anti-scorpion F(ab′)2 fragment produced in Mexico using a horse host and venom from other species is available in Mexico under the name Anascorp (4). It has been approved for use by the FDA and is marketed to hospitals in Arizona, Nevada, and New Mexico. In a recent study, it was shown that these may actually be safe enough to use in a relatively remote clinic setting, where envenomation would be most prevalent. Acute adverse reactions affected up to 1 in 500 cases and were noted to be manageable with established emergency care (5).
Bee and wasp stings are among the most common envenomations globally. The lifetime incidence of hymenoptera envenomation for adults is between 55% and 94% (10). In North America, bee-allergic persons average approximately 3 stings in their lifetime, while 89% have at least 1 systemic allergic reaction (10).
Bees, domesticated and wild, are found worldwide. The African race of honey bee, known as the “killer bee” for its aggressive nature, was imported from Africa to Brazil on account of its efficient honey production in tropic environments. Over the last 50 years, Africanized honey bees have infiltrated the American southwest from South America, attacking in swarms of hundreds and chasing victims far from their nests, which are usually located underground in mammal burrows (2). Although Africanized bees sting with less venom than their European counterparts, their propensity to attack in swarms has resulted in several human deaths (2).
Wasps, like bees, are found all over the world, but their proximity to population centers are a problem mainly in United States and Europe. Nests are located under stones or suspended in shaded areas or within shrubbery. Although nests may be clustered together, wasps rarely defend their nests.
Multiple hymenopteran stings are usually the result of a nest disturbance. Bee venom contains the phospholipase A2 and melittin, which are the enzymes responsible for fatalities in cases where anaphylaxis is not involved (16). Although 40 to 50 simultaneous stings can be fatal in a nonallergic person, most life-threatening events occur due to anaphylaxis in bee-allergic persons. Anaphylaxis is seen in up to 1% of childhood stings and as many as 34% of adult stings, with the majority of fatalities occurring in middle age and older adults (20). The risk of significant reactions appears to be greater in those taking beta blockers (25).
Stings are most often inflicted on the head, neck, and extremities. Typically a single envenomation in a naïve person results in self-limited pain, swelling, and a wheal. Stings can become infected as some species, such as wasps, may feed on rotting meat (25). Vomiting, diarrhea, generalized edema, dyspnea, hypotension, tachycardia, and collapse can occur in multisting victims. Skeletal muscle necrosis, hyperkalemia, rhabdomyolysis, and renal failure also have been reported (16). At least half of all severe reactions occur within 10 min after a sting, and virtually all occur within 5 h. Most fatalities can occur within 1 h, often from airway obstruction, hypotension, or both (15). Thus prompt medical care followed by a period of observation is warranted for those at risk for severe reactions.
The treatment of anaphylaxis includes epinephrine at the first sign of hypersensitivity. Immediate transfer to a health care facility, preferably with ICU capabilities, is preferred. Inhaled epinephrine may result in faster relief for those whose symptoms are predominantly respiratory. Methylprednisolone along with epinephrine inhibits the diffusion of allergy and inflammatory cytokines and may reduce the severity of anaphylaxis. IV crystalloids are used in the setting of hypotension, but pressors may be required in refractory cases. Intubation and mechanical ventilation may be required for airway obstruction. Beta blockers can inhibit the effects of epinephrine, so glucagon administration may be required in the event that epinephrine is ineffective. H-1 blockers may be effective also (15).
For mild stings, cryotherapy with ice packs is the mainstay. Any stinger left behind should immediately be removed. It was originally thought that forceps could “squeeze out” more venom; however this was found not to occur (16). Baking soda paste, meat tenderizer, topical anesthetics, and topical aspirin paste provide minor relief. Oral and topical antihistamines can be effective in mild to moderate reactions, while corticosteroids are used in extensive stings. Patients with hypersensitivity should be evaluated for mast cell disorders (14). A patient with a history of bee sting anaphylaxis should be given epinephrine pens to keep with them in the event of reoccurrence. Venom immunotherapy should be prescribed for subjects with systemic allergic reactions who have evidence of venom-specific IgE antibodies. Once a maintenance dose is achieved, allergic reactions are successfully prevented upon resting in 75% to 95% of patients. These also cause decreased severity when systemic allergic reactions do occur (20). Venom Immunotherapy should be performed under the direction of a physician, as systemic reactions can occur with VIT as well. These are uncommon and no deaths have been reported (14) (Table).
Table Summary of org...Image Tools
There are many different types of reptiles and insects with the potential to inflict significant harm through envenomation. Complications can range from mild pain and swelling to respiratory paralysis and death. Fortunately, with timely, accurate diagnosis and rapid transport to a hospital when indicated, adverse outcomes can usually be averted. Although further research needs to be conducted in the field of envenomation therapies, significant progress has been made over the last half century toward reducing the morbidity and mortality of envenomations.
The authors declare no conflicts of interest and do not have any financial disclosures.
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