Managing Arthropod Bites and Stings
Robert L. Norris, MD
THE PHYSICIAN AND SPORTSMEDICINE - VOL 26 - NO. 7 - JULY 2021
In Brief: Most arthropod bites and stings cause limited swelling, itching, pain, and redness and can be managed by ice application and tetanus prophylaxis as necessary. Stings by bees, wasps, and stinging ants can cause anaphylaxis that may require treatment with epinephrine and antihistamines and respiratory and cardiac maintenance measures. Widow spider bite management is controversial, but interventions for systemic reactions include calcium gluconate, methocarbamol, diazepam, narcotics, and antivenom. Victims of brown spider bites may need hospitalization if lesions enlarge rapidly or there are signs of systemic poisoning. Those stung by a bark scorpion may require oxygen, an intravenous line, pulse oximetry, and cardiac monitoring.
When we think of sports-related hazards, we generally imagine blunt trauma, heat-related illness, or even rare occurrences such as lightning strikes. We seldom think of arthropods, those little, multilegged creatures whose bites and stings can make life unpleasant—or precipitate life-threatening reactions. Knowing and implementing appropriate in-the-field and hospital treatments can make life less miserable for those who have minor reactions and may help save the lives of the few who have severe allergic reactions.
The stinging insects that belong to the order Hymenoptera include bees; yellow jackets, hornets, and other wasps; and stinging ants (see "Hymenoptera: Bees, Wasps, and Ants," below). Hymenoptera stings cause an estimated 40 to 150 deaths each year in the United States alone (1), the vast majority of which are due to anaphylactic reactions. Approximately 1 in every 200 people is dangerously allergic to Hymenoptera venom and therefore at risk for fatal anaphylaxis (2).
People involved in outdoor activities and sports can be vulnerable to Hymenoptera stings. For example, yellow jackets and honeybees are fond of sweets and can be drawn to rehydration stations stocked with sugar-containing sports drinks. Athletes can also be stung on a practice field where yellow jackets (which build ground nests) or fire ants (especially in the southern United States) reside.
Reactions. The most common reaction following a Hymenoptera sting is a painful wheal or hive caused by the venom (3). The site rapidly becomes pruritic, and the itching can last for several hours. Occasionally patients develop an exaggerated local reaction (possibly due to a response mediated by immunoglobin E [IgE]) in which the swelling and itching extend beyond the sting site to the involved extremity. Fortunately, only about 5% of these patients develop a more severe reaction to later stings (1).
The most feared reaction to Hymenoptera stings is, of course, anaphylaxis. Cross-linking of venom antigens to previously formed IgE antibodies on mast cell and basophil surfaces releases multiple, preformed mediators that lead to a cascade of pathophysiologic responses. The best known of these mediators is histamine. The clinical manifestations of histamine's effects include diffuse urticaria, bronchospasm, laryngospasm, laryngeal edema, nausea, vomiting, and hypotension. The onset is rapid, usually within minutes of a sting, though in rare cases, it can be delayed for several hours (4).
(Delayed effects such as serum sickness, peripheral neuritis, or nephrosis are probably related to an antigen-antibody interaction [immune complex deposition]. These are uncommon and will not be discussed further.)
Managing local reactions. The first step in managing a typical local reaction is to remove any retained stinger. Removal is generally a problem only with honeybees because they have a multiply barbed stinger that lodges in the skin. When the bee pulls away, the stinger, venom gland, and investing muscle remain. The muscle continues to pulsate and inject venom into the wound for several seconds (5).
The stinger can best be removed by immediately flicking it out of the skin with a fingernail; it should not be squeezed as this will inject more venom. Ice should be quickly applied to the site. Further management includes the use of oral antihistamines (such as hydroxyzine) and mild analgesics as needed. If an exaggerated local response occurs, a 5-day course of oral prednisone (1 mg per kg per day) may be helpful (6).
Managing anaphylaxis. If a patient has anaphylaxis, management must begin immediately, and the local emergency medical services must be called. The victim should be placed supine with his or her legs elevated. A constriction band that occludes superficial venous and lymphatic return—but does not obstruct arterial flow—can be placed a few inches above the sting site. Ice can be applied to further reduce venom absorption.
If signs or symptoms of laryngeal edema are present, aggressive airway management should be undertaken with early intubation and support of the victim's breathing and circulation. If a respiratory or cardiac arrest occurs, aggressive resuscitation should ensue, using resources at hand, from basic to advanced cardiac life support. Oxygen, if available, should be administered.
Epinephrine. Prompt administration of epinephrine is vital. Subcutaneous injections (0.01 mL/kg of 1:1,000 solution, up to a maximum of 0.5 mL per dose) may be repeated approximately every 15 minutes as needed for recurrent problems. In cases of moderate hypotension, the epinephrine can be administered intramuscularly.
If hypotension persists after the initial epinephrine injection or is initially severe, intravenous crystalloids should be given rapidly (20 mL/kg boluses repeated as necessary). If the patient has been exercising strenuously before the sting occurs, his or her intravascular volume may already be depleted, and this depletion can compound the level of hypotension. If the blood pressure fails to respond to epinephrine and rapid crystalloid infusion, a vasopressor such as dopamine or norepinephrine (in standard titrated doses) may be required.
Intravenous epinephrine is hazardous, even in a young, healthy adult, and should be reserved for severe reactions manifested by profound hypotension. The calculated dose of 1:1,000 should be further diluted 1:10 (alternatively, 1:10,000 epinephrine can be used), and it should be given very slowly and cautiously over several minutes. A better approach is an epinephrine infusion titrated to the victim's response.
Other medications. Antihistamines (both H1 and H2 blockers) can also halt the progression of a reaction. Hydroxyzine or diphenhydramine (for both agents, 1 mg/kg given intramuscularly or intravenously) and cimetidine (5 to 10 mg/kg given intravenously) are good choices (7).
A small percentage of anaphylaxis cases will have a biphasic course in which the patient's signs and symptoms recur 4 to 6 hours after an initial, satisfactory response to treatment (8). For this reason, systemic steroids, such as methylprednisolone, should also be given to
Who should see an allergist? Most patients who have local reactions do not need to see a physician unless their tetanus status is out of date. Those who have exaggerated local responses or systemic reactions limited to generalized urticaria should probably seek medical care and can be discharged after treatment.
Patients who have a systemic reaction should be observed for several hours for signs of deterioration. Discharge medications should include an antihistamine and, in the case of an exaggerated response or diffuse urticaria, a 3- to 5-day course of steroids. These patients generally do not require referral to an allergist. However, an unknown percentage of adults who develop a generalized urticarial response will have a more severe reaction if stung again, and skin testing and possible desensitization therapy should be considered (9).
Patients who have severe anaphylaxis—any airway compromise or hypotension—should be admitted for overnight observation and, upon discharge, be referred to an allergist. The rate of anaphylaxis in untreated patients who are stung again may be as high as 60%, but this risk drops to less than 5% with desensitization therapy (10).
'Bee sting' kits. Coaches and team physicians should ask athletes whether they have had severe reactions to Hymenoptera stings. If an athlete has been prescribed an epinephrine self-administration kit, such as an Epipen or Epipen Jr (Dey Laboratories, Napa, California), or an Ana-Kit (Bayer Corporation, West Haven, Connecticut), it should be readily available at all times, including practices. Coaches and trainers should know how to assist an athlete in administering epinephrine before the need arises.
The venoms of widow spiders (genus Latrodectus), regardless of the species (see "Spider Specifics," below), are similar in composition and toxic effects (11). The most deleterious component is a neurotoxin (alpha latrotoxin) that stimulates the release of the neurotransmitters acetylcholine and norepinephrine at nerve terminals and thereby blocks neurotransmission by depleting synaptic vesicles (12).
The mortality rate from widow spider venom poisoning in the United States is less than 1 percent; the vast majority of victims can expect a full recovery (13).
Signs and symptoms. The bite is often felt as a mild "pinprick," and the bite site may be slightly red (13). Significant symptoms usually start about 1 hour after the bite. Spasmodic muscle pain, the most common complaint, begins at the bite site and spreads to local muscle groups (14). Spasms may then gradually progress to the larger, regional muscle groups of the trunk (12,13). Significant pain and spasm can persist for 12 to 48 hours (15,16). Thoracic involvement may be severe enough to cause respiratory distress (14). Other reactions may include an increased respiratory rate, tachycardia, hypertension, fever, headache, diaphoresis, nausea, vomiting, restlessness, and anxiety (12-14).
Bite management. Field treatment is limited to applying ice to the bite site to reduce pain followed by prompt transportation to a hospital for further evaluation and management (12). Evaluation and appropriate support of the victim's airway, breathing, and circulation are followed by efforts to relieve the person's muscle spasms.
Current recommendations regarding the best agent for muscle spasms are controversial and largely based on anecdote. Limited success has been reported with calcium gluconate, methocarbamol, diazepam, and narcotics (12,15). Diazepam and narcotics, given in combination and in standard doses, are probably more effective than other symptomatic therapies (14). Hypertension, when present, usually resolves with bed rest, opioid analgesics, and benzodiazepine muscle relaxants (17). For patients who have severe symptoms, these agents can be initially administered parenterally and, as the patient improves, orally over a period of hours to days.
Antivenom. Merck & Co, Inc (West Point, Pennsylvania) manufactures a specific equine widow spider antivenom (Antivenin Latrodectus mactans) that is effective against the venoms of all Latrodectus species (18). As a heterogenic serum product with the potential for inducing severe allergic reactions (anaphylactic/anaphylactoid reactions or serum sickness), the indications for its use are controversial. It is probably justified in significant envenomations in patients younger than 16 or older than 60 years, pregnant women, and patients who have a history of serious underlying disorders such as cardiovascular disease (12,13,15). However, most healthy adults can be treated with supportive measures alone (11,13).
Antivenom is usually given intravenously after a negative skin test and premedication with antihistamines. The initial dose is one vial (diluted in 50 to 100 mL of normal saline), and most symptoms usually resolve within a few hours of administration (15). Rarely is a second vial required.
The venoms of the different Loxosceles spiders (see "Spider Specifics," below) all have similar toxic effects. They cause endothelial cell damage in small dermal vessels that become occluded with microthrombi, resulting in vascular stasis and tissue infarction (11,18,19). Polymorphonuclear leukocytes (PMNs) attracted to the site through chemotactic signals propagate a necrotic reaction (11,15,18,19).
The venoms can, in rare cases, induce hemolysis through the action of an enzyme, sphingomyelinase D (15,19). Autopharmacologic responses, which vary from patient to patient, have an important, though undefined, role in determining the severity of venom poisoning (11,15,19). The clinical spectrum of brown spider bites runs from mild, temporary irritation at the site to severe, potentially fatal, systemic poisoning (18).
Local signs and symptoms. The bite is often relatively painless and may go unnoticed (12). In the ensuing hours, the site becomes pruritic, red, and mildly swollen (19,20). Local pain, due to vasospasm and ischemia, begins within 2 to 8 hours of the bite (19,20). After 12 to 18 hours, a small, central vesicle may develop, surrounded by an irregular border of erythema or ecchymosis and edema (12,18-20). The blister ruptures and the erythema darkens to a violaceous discoloration that may spread downward (figure 1) (11,19). After 5 to 7 days of progressive aseptic necrosis, the center becomes depressed and covered with a black eschar (12,19), which eventually sloughs and leaves an open ulcer that tends to heal over several weeks (19). Necrosis is usually limited to the skin and subcutaneous tissues, so the nerves, muscles, tendons, and ligaments are rarely involved (21).
Systemic reaction. Systemic hemolysis, though rare, may be rapidly progressive and severe, especially in children (11,15). Symptoms generally start 24 to 72 hours after the bite and may include fever, chills, headache, malaise, weakness, nausea, vomiting, myalgias, and arthralgias (19-21). Severe anemia, consumptive coagulopathy, renal failure, shock, seizures, and coma have been reported.
Evaluation. Attempting to identify the cause of the cutaneous lesion is usually the first step in treating patients suspected of having a brown spider bite. Since the spider is rarely seen and since similar lesions can be the result of bites or stings by other arthropods, superficial skin infections, plant puncture wounds, or contact dermatitis, the diagnosis is often presumed to be "necrotic arachnidism." No diagnostic laboratory test is useful in the acute stages of therapy.
The workup on a patient who has a possible brown spider bite should include a complete blood count (including platelets) and urinalysis to look for evidence of consumptive coagulopathy, hemolysis, or hemoglobinuria (19). If either is abnormal, coagulation studies, serum electrolytes, blood urea nitrogen, creatine, glucose, liver function tests, haptoglobin, and a type and cross-match should be obtained (11,15,19). In patients who have significant lesions, daily blood counts and urinalyses should be followed for the first few days (19).
Treating local reactions. Most bites do well with standard, daily, local wound care (cleansing, dressing, splinting, and tetanus prophylaxis). Ice applications may reduce the ultimate severity of necrosis by inhibiting the temperature-dependent enzyme sphingomyelinase D (22,23). Cooling should be started as soon as possible and should be done several times a day as long as there is evidence of ongoing necrosis (12,15,19).
Other treatments for brown spider-induced dermonecrosis are controversial and based on scant research or anecdotal reports. Prophylactic antibiotics such as a first-generation cephalosporin or erythromycin may be beneficial (19,22), but their use is controversial because no controlled study has proven that they decrease the extent of dermonecrosis (19,24). Local or systemic steroids have never demonstrated benefits for cutaneous lesions (11,19,22).
Dapsone, a PMN inhibitor, may limit the extent to which PMNs propagate necrosis but can induce dose-dependent hemolytic anemia and methemoglobinemia (22). Therefore, it should be reserved for adult patients who have severe lesions (19,22). The oral dose is 50 to 100 mg per day (half taken every 12 hours) until the lesion heals or is grafted (25). A glucose-6-phosphate dehydrogenase level should be checked at the time therapy is started (26).
Excision of the site at the time of presentation is ill-advised, since the ultimate extent and severity of the lesion cannot be predicted early in its course (15,18,19,22). Any necessary procedure such as skin grafting should be delayed 6 to 8 weeks to allow the necrotic process to be completed and to maximize the chances of healing (19,22). Hyperbaric oxygen therapy, while still unproven, may be useful in severe wounds (22,27).
Treating systemic reactions. Management of systemic loxoscelism centers on ensuring optimal hydration and electrolyte balance (19). Though unproven, a short course of systemic steroids (prednisone, 1 mg/kg/day orally for 2 to 4 days) may stabilize red cell membranes and reduce hemolysis (15,19). Additional therapy may include blood products for anemia or thrombocytopenia; heparin for disseminated intravascular coagulation; alkalinization of the urine for hemoglobinuria; and dialysis for renal failure (15,19).
Inpatient and outpatient care. Admission should be considered for patients who have rapidly enlarging lesions or evidence of systemic poisoning (18). Patients followed outside of the hospital should have daily wound checks and laboratory reevaluation (complete blood count and urinalysis) for the first 2 to 3 days. While no deaths have occurred in the United States in patients known to have suffered from a brown spider bite, fatalities could certainly result from systemic loxoscelism (15,19).
Scorpion venoms are generally poorly characterized and relatively nonantigenic. Allergic reactions are rare (26). The venom of the bark scorpion (see "Scorpion Basics," below), the scorpion in the United States whose sting is potentially the most dangerous, is relatively devoid of enzymatic activity (28) but contains a number of neurotoxins that can stimulate widespread neurotransmitter release with resultant autonomic overload and neuromuscular firing (18,29,30).
While the bark scorpion at one time caused more deaths in Arizona than all other venomous creatures combined, no deaths have been reported since 1968 (29,31). Nevertheless, its potential to inflict life-threatening stings, especially in young children, should not be underestimated.
Signs and symptoms. Individuals stung by a bark scorpion feel an immediate, intense pain that significantly worsens with light pressure over the site (26,28,29,32,33). (Children under the age of 10, for unclear reasons, may not complain of pain (34).) The pain radiates along the involved extremity (34,35). Local tissue swelling and bruising are uncommon (26,28,32,34,35).
Bark scorpion stings can also cause systemic reactions that result from autonomic and neuromuscular stimulation (29,32). Findings can include restlessness, hypersalivation, dysphagia, visual changes, roving eye movements, respiratory distress (with stridor or wheezing), supraventricular dysrhythmias, hypertension, fever, loss of bowel or bladder continence, muscle spasms, opisthotonos, and paralysis (26,28,29,36). Symptoms tend to be more prolonged in younger children and can last up to 30 hours (34).
Stings by other scorpions produce an instantaneous, severe, burning pain and possibly some mild local swelling and bruising (28). The pain is short lived, and systemic manifestations are very uncommon.
Management. Field management of scorpion stings includes application of ice to reduce venom absorption and pain. If the sting occurs in the bark scorpion's known area of distribution, a brief, cautious attempt to capture the scorpion can be made, and then the victim should be transported to the hospital for evaluation. If the sting occurs outside the bark scorpion's habitat, the victim can usually be treated definitively with ice and mild over-the-counter analgesics; tetanus status should be checked and made current. In the rare event that more serious symptoms arise, the victim can be taken to a local emergency department for evaluation.
Hospital management of a bark scorpion sting involves a careful check of the victim's vital signs while an initial history is obtained. If the victim appears seriously poisoned, oxygen, an intravenous line, pulse oximetry, and cardiac monitoring should be started. Signs of respiratory distress should prompt aggressive airway management. Signs of autonomic or neuromuscular excitation should be identified and treated with bed rest and mild sedation (eg, titrated doses of intravenous benzodiazepines) (26,32). The patient's respiratory status should be closely monitored during administration of sedatives.
Some experts recommend the use of beta-blocking agents for hemodynamically significant supraventricular tachycardias (29,30), but the patient must be watched carefully for unopposed alpha adrenergic effects (worsening hypertension). Antihypertensive drugs may be needed to treat a significantly elevated blood pressure that fails to respond to bed rest and sedation. Narcotics should probably be withheld, since some evidence suggests that they augment venom neurotoxicity (26,33).
While there is a goat-derived antivenom for bark scorpion stings, it is still experimental and has not been approved by the US Food and Drug Administration. It carries some risk of allergic response (anaphylactic and anaphylactoid reactions and serum sickness) and is only available in Arizona (29,30). Anecdotal reports suggest that it is effective in treating severe stings, especially in small children (28,29,32,37).
No diagnostic tests are of value in evaluating a victim of a scorpion sting, but if a small child is thought to have been stung by a bark scorpion or if there is evidence of severe venom poisoning, routine admission labs should be checked. Tetanus immunization should also be updated if necessary.
Almost all individuals stung by a bark scorpion and other scorpions can be discharged after a brief period of observation. Outpatient therapy should include continued cold compresses and mild analgesics for 48 hours (29,32,34). If significant symptoms are present, however, the victim should be admitted to the hospital or, if unstable, to an intensive care unit (34).
The risk from arthropod bites and stings for athletes and active people is quite low. The major danger is an anaphylactic response to a Hymenoptera envenomation. Those with Hymenoptera allergies should be identified and appropriate measures planned before a sting occurs. For most bites and stings, however, local ice application and splinting are usually sufficient. If signs or symptoms of more serious envenomation develop, the person should be transported to a local emergency department for further evaluation and management.
Hymenoptera: Bees, Wasps, and Ants
The Hymenoptera are divided into several superfamilies that include Apoidea (honeybees, figure A, and bumblebees), Vespoidea (yellow jackets, hornets, and other wasps), and Formicoidea (ants). The venoms of the apids and vespids contain vasoactive biogenic amines (such as histamine and serotonin), peptides (such as mellitin), and enzymes (such as hyaluronidase and phospholipase A). Fire ant venoms contain mostly piperidine alkaloids and small amounts of low-molecular-weight proteins. Although a person can be sensitive to the venoms of more than one family, they are more likely to be sensitive to the venoms within a single family.
While at least 60 spider species in the United States are capable of biting humans, only two are of major medical importance—the widow spiders (genus Latrodectus) and the brown spiders (genus Loxosceles).
The United States has five species of widow spider, the black widows (L mactans, L hesperus, L variolus) being the best known. Each of the 48 contiguous states has at least one species within its boundaries. Only the female, a dark black, globular-shaped spider with a characteristic ventral reddish marking (typically an "hourglass") on her abdomen (figure B), is large enough to bite through human skin.
These spiders tend to build their webs in relatively undisturbed, protected areas, so sports-related bites are most likely to occur in equipment storage areas.
Brown spiders are also known as "violin" or "fiddle-back" spiders, because of a characteristic brown marking on the dorsal aspect of the cephalothorax (figure C). Several species live in the United States, and the best known species, the brown recluse (L reclusa), is found throughout the southern, central, and midwestern United States, while other species are found farther west. These spiders, however, can appear in unexpected places because they can go for months without food or water while being transported in shipped materials. Since they tend to be reclusive, the chances of a sports-related bite are quite slim unless an athlete or staff member is rummaging through boxes of supplies in which a brown spider resides.
Although over 1,200 species of scorpions inhabit the earth, only one is of medical importance in the United States, the bark scorpion (Centruroides exilicauda). This small—13 to 75 mm long—scorpion is native to Arizona and adjacent regions. Other, less toxic scorpions are found across the southern United States. While all scorpions look similar, the yellow-brown bark scorpion can be distinguished from less toxic species by the small "tooth" at the base of its stinger (figure D). Fortunately, most bark scorpion stings are minor, and stings by other scorpions in the United States are inconsequential.
Since scorpions are nocturnal, they spend most of their days under rocks, in crevices, or behind bark. Athletes involved in team sports are not likely to be stung in the course of athletic participation. However, during heavy rains or when construction is in progress, scorpions may seek shelter indoors.
Those involved in outdoor activities are more vulnerable. Rock climbers are at risk when they put their hands into blind spots on overhead ledges. Campers or hikers need to be cautious when turning over stones and logs. They should also inspect footwear before donning it, since scorpions may hide in shoes during the day (figure E).
Dr Norris is an associate professor of surgery and emergency medicine and chief of the division of emergency medicine at Stanford University. He is a fellow of the American College of Emergency Physicians. Address correspondence to Robert L. Norris, MD, Division of Emergency Medicine, Stanford University, 300 Pasteur Dr, Rm H1249, Stanford, CA 94305-5239; e-mail to [email protected].
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