Envenomations in Children
Authors: Sean P. Bush, MD, Clinical Instructor of Emergency Medicine, Loma Linda University School of Medicine, Loma Linda, CA.
Tamara L. Thomas, MD, FACEP, Assistant Professor of Emergency Medicine, Loma Linda University School of Medicine, Loma Linda, CA.
Eric S. Chin, MD, Resident Physician, Loma Linda University Medical Center, Loma Linda, CA.
Peer Reviewer: Robert L. Norris, MD, FACEP, Assistant Professor of Surgery/Emergency Medicine, Stanford University, Stanford, CA.
The bites of venomous snakes, spiders and scorpionsthree of the least appreciated and most avoided creatures on earthare discussed in this issue. Though few species can cause significant morbidity or mortality to humans, the threat of envenomation by any these can interfere with the outdoors enthusiast's peace of mind. While snakes have taken a bum rap throughout history beginning with the Garden of Eden, the snake has also been begrudgingly respected, as demonstrated by the caduceus with its intertwined serpents. For some, including the primary author of this issue, ophiology, the branch of herpetology dealing with snakes, is a lifelong fascination.
Venomous reptiles encountered in the United States include the pit vipers (rattlesnakes, copperheads, and cottonmouths), coral snakes, venomous lizards, colubrids, and exotic imports. (See Table 1.) Arachnids considered dangerous to humans include widow spiders, brown spiders, and bark scorpions.
The science surrounding treatment recommendations for animal envenomations is not yet clear and is often based on speculation and anecdote, and much of the literature is contradictory. Research in humans often involves chart reviews, which may contain region-specific bias. In addition, envenomation is an uncommon occurrence with an extremely variable presentation, ranging from no ill effects to multisystem failure and death. Furthermore, certain envenomations can have very subtle presentations and no visible wound site; a child presenting with unexplained crying, for example, may be the victim of a spider or scorpion envenomation. The clinician must make a quick diagnosis and accurately identify the source of the envenomation in order to determine the best therapeutic option. Although antivenoms exist for serious envenomations by many species, their use carries considerable risk of serious allergic complications. Although controversy exists, the recommendations in this article represent the majority of current standards of care.
The Editor
The pediatric population accounts for about 50% of the over 7000 reptile bites reported to the American Association of Poison Control Centers (AAPCC) in 1995.1 There have been no pediatric deaths from snakebite reported to the AAPCC since its first annual report in 1983. Although these figures are conservative due to under reporting, they illustrate the relatively low mortality associated with snakebite. While venomous snakes are prevalent, inhabiting every state in the United States except Alaska, Maine, and Hawaii,2 the highest incidence of envenomations occurs in the southeast and southwest regions of the country during the months of April to October, when snakes are most active.3
Pediatric Considerations. Although there are few comparative studies, most authorities agree that children may be affected differently than adults by snakebite.4-10 Many suggest that children may suffer more morbidity from snakebites than adults because the venom load is distributed over a smaller body volume.4,5,8,11 Toxic effects may be dose-related,4 and children receive a higher dose of venom per kilogram body weight.8 As a result, children may require more antivenom to neutralize more severe systemic effects.5,7 Snakebitten children may be at higher risk for certain complications and less prone to others.4 Finally, assessing envenomation severity in children may be difficult using grading scales designed for adults.12-14
Description. The majority of snakebites are caused by pit vipers, with rattlesnakes (Crotalus and Sistrurus) accounting for two-thirds of all venomous snakebites in the United States. Features that distinguish the pit vipers from other U.S. snakes include moveable fangs, venom glands, a triangular-shaped head with an elliptical pupil and "pits," and a tail with a row of single, undivided scales on the ventral surface (subcaudal) distal to the large anal plate scale.3 (See Table 2.) Rattlesnakes are distinguished in all but one species by a characteristic rattle at the end of the tail.
The "pit," located between each eye and nostril, is a special sensory organ used for the detection of minute quantities of heat. Using this organ, pit vipers have the ability to detect temperature gradients of 0.003°C from about 14 inches away.3,15,16 The pit is used in conjunction with the snake’s keen sense of smell to track warm-blooded prey (such as rodents) before and after envenomation. Snakes lack clarity of vision and are deaf to airborne sounds. In addition, pit vipers estimate how much venom to deliver to subdue prey or deter predators based on an assessment of size using the pit.2,17 "Dry bites," resulting in no evidence of envenomation, may occur in as many as 25-50% of pit viper bites to humans.18,19
Pathophysiology. Venom and Venom Apparatus. Pit viper fangs are located in the anterior mouth and fold back when the mouth is closed. When the snake strikes, fangs extend, and venom is injected through the hollow fangs with muscular contraction of the head. Venom is composed of substances adapted to quickly kill and efficiently digest prey as well as deter predators. Venom generally moves through tissue via lymphatics and via direct extension into adjacent tissues; it consists of water, enzymes, nonenzymatic proteins, peptides, and several unidentified substances.18
Most U.S. pit viper envenomations cause a predominance of local and hemotoxic effects. Others may lead to more neurologic changes. However, venom cannot be classified as purely "hemotoxic" or "neurotoxic" because of the complexity of its composition, the interactions of its various components, and the physiologic response to venom.2 Furthermore, the composition of each venom is species-specific and may even vary with geographic range within the same species.20
The majority of clinical features seen after envenomation by rattlesnakes are caused by alteration of the vascular endothelium and clotting system. The local reaction is due to altered blood vessel permeability and direct necrosis of the tissue. Altered blood vessel permeability due to injury of vascular endothelial cells causes third spacing, leading to hypovolemic shock, hemoconcentration, and lactic acidosis.
Digestive enzymes cause both local and systemic damage to tissue. Some of the major enzymes include phospholipase A (common to all snake venoms), which damages cell membranes and causes myonecrosis and hemolysis. Hyaluronidase facilitates the spread of venom. Amino acid esterase and thrombin-like enzymes are thought to contribute to defibrination and bleeding. Proteolytic enzymes RNAse, DNAse, and 5’ nucleotidase cause myonecrosis and local necrosis.3,18 Venom A, found in certain populations of Mojave rattlesnakes (Crotalus scutulatus), contains neurotoxins that can cause flaccid paralysis and respiratory impairment.
Clinical Presentation. Local Effects. Among the initial findings of pit viper envenomation are immediate pain, advancing edema, and ecchymosis of the tissues surrounding the bite site. Edema of the entire extremity can occur as rapidly as one hour or as long as 36 hours post bite.21 Rapid advancement of edema usually indicates a more severe envenomation. Hemorrhagic blebs and bullae may develop over a six- to 36-hour period.3
Compartment syndrome, characterized by pain on passive stretch of muscle, a "rock hard" feel to the muscle, diminished capillary refill, or absence of distal pulses (a late finding), may develop from severe local tissue reaction. True compartment syndrome is rare, even in patients with severe swelling, as most snakebites are subcutaneous.3,18 Children may be more at risk for compartment syndrome because they have less subcutaneous fat, making compartments more easily accessible to snake fangs.22,23 In addition, local myonecrosis may develop even in the absence of elevated compartment pressures because of a direct myotoxic effect of venom.18 Measurement of intracompartmental pressure is the only way to reliably diagnose compartment syndrome. Venom A (from the Mojave rattlesnake) may cause minimal local swelling, leading to underestimation of a severe systemic envenomation.7,21
Systemic Effects. In general, systemic response to envenomation is a combination of complex interactions between the varied venom components and human physiology. General systemic effects such as taste changes and fasciculations may occur.2 Hypotension and shock may be associated with severe envenomation.3 In children, shock is most often due to third spacing of circulating volume into an extremity.24 Severe bleeding, which may result from the snakebite, may also cause hypotension. Pit viper envenomation commonly results in coagulopathies associated with defibrination with or without thrombocytopenia, although full-blown disseminated intravascular coagulation (DIC) is rare.3,25 Hypotension may also be caused by a vasovagal response. Very rarely, venom may cause direct myocardial depression, leading to hypotension. Also rare, venom-induced anaphylaxis with hypotension has been reported.26
Severe systemic envenomation may cause hemorrhagic, myotoxic, and/or neurologic effects. In addition, nephrotoxicity and pulmonary injury can result. Rarely, direct cardiotoxicity or allergy to venom may occur. Any organ system(s) may be involved.3 Autonomic reactions, usually associated with fear and anxiety, may mimic or compound systemic envenomation.13 Symptoms such as vomiting, tachycardia, or near syncope may be associated with panic or with the envenomation itself. Neurologic symptoms may occur in individuals who are bitten by certain populations of Mojave rattlesnakes (C. scutulatus), resulting in cranial nerve dysfunction, lethargy, and progressive generalized muscle weakness that may lead to respiratory failure.27 Rhabdomyolysis may occur secondary to direct local or diffuse myotoxicity.28 Acute renal failure may result from hypotension, hemoglobin or myoglobin deposits in renal tubules, and/or direct nephrotoxicity of venom.2 Non-cardiogenic pulmonary edema has been reported.21,24 Infection may occur as a late complication of snakebite, but the incidence is low.29,30
Emergency Department Treatment and Disposition. Prehospital Care. Individuals who are bitten by venomous snakes should be transported immediately to the nearest facility where antivenom can be given. Airway, breathing, and circulation should be supported as needed. The patient’s movements should be restricted as much as possible, as movement may hasten the spread of venom. In cases where an individual is bitten in the wilderness, the risks vs. benefits of hiking out to medical care or waiting until appropriate transportation can be arranged must be weighed considering the conditions of the patient and environment.2 Jewelry, rings, or constricting items should be removed from the patient in anticipation of swelling, and caffeine, aspirin, and alcohol should be avoided.
A large-bore IV line should be placed in an area unaffected by the snakebite. Mark with ink and time the advancing edge of edema every 15 minutes. As a control, the circumferences of the unaffected extremity may also be measured at corresponding levels. These measurements will provide an indication of venom spread and severity. Rapid progression of edema is an indication of severe envenomation.
The utility of most first aid is limited, and definitive therapy depends on getting to a hospital.31 Obsolete because of unproven benefit or increased morbidity is field treatment such as cryotherapy, local application of ice, incision across the fang mark with drainage, electric shock, tourniquets (lymphatic constriction bands may benefit, however), elevation of the extremity, mouth suction, alcohol, stimulants, folk therapy, and spending time to capture or kill the snake. An extractor device ("Sawyer’s Extractor"), which uses suction without incision, can remove up to 30% of pit viper venom if used within three minutes after bite.32 Antivenom should not be given in the prehospital setting because of life-threatening complications associated with its use.
History and Exam. Initial ED treatment includes continued support of the patient’s airway, breathing, and circulation. A second IV should be started and the patient hydrated with boluses of normal saline. Again, pay close attention to vital signs, including pulse oximetry. Document the time of bite, and continue to mark and time the border of advancing edema and circumference every 15 minutes. Cleanse the bite area and administer pain control as needed. Ask about the size, description, and species of snake, and identify the snake, if possible. If a live or partially killed snake is brought to the ED, make sure the snake is adequately contained. Obtain a history of field therapy and discontinue any potentially harmful first aid. Find out about previous exposure to venom, antivenom, horse serum, allergies, medications, and past history. Perform a complete physical exam, including a neurological exam. Note the location and number of bites, and check for bleeding from the wounds or elsewhere on the body. Check for signs of compartment syndrome, and obtain compartment pressures if indicated. Call Poison Control.
Laboratory. Suggested laboratory studies includes complete blood count with platelets, coagulation profile (including prothrombin time, partial thromboplastin time, fibrin split products, and fibrinogen), monitor for hematologic abnormality, and type and cross match. Electrolytes, blood urea nitrogen, creatinine, and urinalysis may be obtained. If rhabdomyolysis is suspected, creatine phosphokinase, urine myoglobin, calcium, and phosphorus should also be obtained. For respiratory difficulty or neurologic abnormality, an arterial blood gas may be helpful (See Table 3).
Grading and Antivenom Administration. The severity of envenomation depends on the size of the snake, the quantity of venom injected, the toxicity of the venom, the size and general health of the victim, the location and depth of the bite, and length of time before definitive therapy begins. Criteria have been developed to estimate the severity of an envenomation and the amount of antivenom to administer.
Grading envenomations in children presents several problems. Various adult guidelines have correlated envenomation severity with centimeters of edema;12,13 however, this model fails in pediatric patients because proportionally larger areas are involved for any given measurement. Envenomation scales based primarily on local swelling may underestimate a severe envenomation presenting with mild local effects, as in Mojave rattlesnake envenomations. Snake species and size may affect envenomation severity but are frequently unknown in pediatric cases. The possibility of "dry bites" should be considered when evaluating envenomations. The clinical course dictates when antivenom is given. While many grading scales are based predominantly on local effects with some correlation of systemic and laboratory abnormalities,12 effects of envenomation should more appropriately be divided into three separate parameters: local effects, systemic effects, and laboratory abnormalities. Severity of envenomation may be reflected by a single parameter without significant changes in the others; therefore, envenomation should be graded according to the most severely affected parameter. Initial antivenom dose is then based on this grade of envenomation.
Swelling should be quantitated in relation to involvement of an extremity, since most bites occur on an extremity. Bites to the head, neck, or trunk may require more aggressive treatment due to potential complications involving vital structures. While only local and systemic effects are immediately apparent for initial grading, additional antivenom should be given as mandated by laboratory data and a changing clinical course until abnormalities in the affected parameter(s) stabilize.
Guidelines for grading pediatric envenomations have been compiled from previous recommendations.2,7,33 Choice of initial antivenom dose is based on grade of envenomation and should be guided by laboratory data and a changing clinical course. No antivenom should be given for a minimal envenomation, while 5-10 vials of antivenom should be given initially for moderate envenomations. Patients with severe envenomations should be given 15 vials of antivenom with additional doses given as needed for progression of severity or a lack of improvement in signs of envenomation. The importance of serial examinations and laboratory evaluation is emphasized, as envenomation is a dynamic process. Until abnormalities reverse, additional antivenom should be given as necessitated by the changing clinical course. Repeat doses may be given every 30 minutes to two hours as needed.2 More aggressive antivenom therapy may be initially required for cases of suspected Mojave rattlesnake bite.3,7 Antivenom is most effective if given as soon as possible after the snakebite, but may reverse coagulation defects even after 72 hours.3
Many complications of snakebite can be prevented with the use of aggressive antivenom therapy. Antivenom is the first line of treatment of coagulation defects. Treatment with blood products should be reserved for severe anemia or serious bleeding that persists after antivenom administration.25 Surgical intervention for compartment syndrome may be avoided with sufficient antivenom therapy.34 If compartment pressure remains elevated despite antivenom, surgical consult for fasciotomy may be needed.21,33 However, local wound excision and routine fasciotomy are no longer recommended.
Neurologic effects have been shown to correct with antivenom.28 Antivenom may also treat myoglobinuric renal failure, along with other measures, such as hydration, diuresis, and possibly alkalinization of urine.
Antivenom and Adverse Reactions. Complications of antivenom administration include anaphylaxis and serum sickness. Anaphylaxis, an immediate, potentially life-threatening allergic reaction, is characterized in its most severe form by urticaria, bronchoconstriction, vomiting, and hypotension. Wyeth Antivenin (Crotalidae) Polyvalent is derived from horses immunized to the venoms of two U.S. snakes, Eastern and Western diamondbacks (C. adamateus and C. atrox, respectively), and two South American snakes, the Tropical rattlesnake (C. durissus) and Fer-de-lance (Bothrops atrox). Due to the variety of heterologous proteins in hyperimmune equine serum, anaphylaxis may occur in as many as 25% of patients who receive antivenom.35
Preparations to treat anaphylaxis should be made prior to administration of antivenom. If anaphylaxis occurs, stop the infusion and treat as needed with airway control, epinephrine, H1 and H2 blockers, and steroids. In severe envenomations, antivenom may need to be continued despite anaphylaxis.28,36 Some authorities recommend pretreatment for anaphylaxis with H1/H2 blockers and steroids before antivenom is administered.2
Crotalid antivenin is dissolved in 10 mL of any sterile warm diluent and may be diluted 1:2 in normal saline (for example, 5 vials would be dissolved in 50 cc, then diluted into a total volume of 100 cc). Start mixing the antivenom as soon as possible after the decision is made to administer, as it takes about 20 minutes of gentle agitation to go into solution. Start the infusion slowly (at a rate of 1 mL/min) for the first several minutes, with close observation for signs of allergic reaction. If there is no allergic reaction, administer at a rate of 20 mL/kg/h. The initial dose should be administered over 1-4 hours if no allergic reaction occurs after 10 minutes.2,3,37 Children seem less likely to suffer anaphylaxis than adults.4
Serum sickness (manifested as urticaria, arthralgias, and fever) is almost certain to develop 1-4 weeks after treatment when eight or more vials of antivenom are given.7,35 For this reason, where effects of envenomation are judged to be less severe than potential complications of serum sickness, fewer than eight vials of antivenom should be given. The treatment for serum sickness is antihistamines and steroids given regularly until all signs and symptoms have subsided for 24 hours, followed by gradual tapering.
An experimental affinity purified Fab antivenin derived from sheep serum has recently been produced that may significantly reduce the allergic complications of the existing polyvalent Crotalid antivenin.38,39 The new antivenom may better neutralize Mojave toxin (Venom A) than the currently available antivenom, but this has not been studied.
Skin Testing. Skin testing is only potentially useful for variably predicting immediate hypersensitivity in moderately envenomated patients in whom there is a question whether the need for antivenom outweighs the risk of anaphylaxis. The test itself is unreliable in its prediction of allergy to antivenom. This may be secondary to the use of pure horse serum for the test followed by administration of antivenom, which contains many different heterologous proteins. The reliability of the test may be improved if antivenom is used for the skin test, but this has not been studied.2 An option entails slowly infusing the first vial of dilute antivenom while being immediately prepared to treat anaphylaxis.
Skin testing is not indicated for minimal envenomations as it may sensitize individuals to future exposures to antivenom or even precipitate anaphylaxis.19 It also is not necessary for severe envenomations where antivenom is clearly needed except for medico-legal purposes. Even if the test is positive, antivenom is still indicated for severe envenomations. Since anaphylaxis may occur in up to one-quarter of all patients receiving antivenom, preparative and preventative measures, including possible pre-treatment and airway/epinephrine at bedside, should always be exercised when antivenom is given.4,35
Disposition. Patients with mild-to-moderate envenomations may need hospital admission or extended ED observation with close follow-up for delayed progression of envenomation severity, as there are many reports of delayed complications.40-42 Some authorities recommend admission for all children with envenomations. Patients receiving antivenom should be admitted and monitored in an intensive care setting during infusion of antivenom.33 Severely envenomated patients and patients suffering anaphylaxis to antivenom should be admitted to an intensive care unit, and admission should be strongly considered for children with confirmed Mojave rattlesnake bites.
Antibiotics. Although infectious microorganisms (such as Pseudomonas, Proteus, Clostridium, and Bacteroides) are known to inhabit snakes’ mouths, there is a low incidence of wound infections.29 This may be due, in part, to the antibacterial activity of crotalid venom. However, even nonvenomous snakebites without complicating factors (such as a retained tooth) seldom become infected.30 Although widely prescribed, prophylactic antibiotics are probably not necessary. Local wound care, including irrigation and exploration, may preclude the need for antibiotics. Antibiotics such as ceftriaxone are indicated for infected bites.43 Up-to-date tetanus prophylaxis is indicated.
Prevention. The pediatric and adolescent population may benefit from education on how to prevent snakebites. Preventative measures, such as wearing protective clothing while in the snakes’ environment and not reaching blindly into areas where snakes may hide, may reduce the incidence of snakebites.18 Children and adolescents should be taught not to harass snakes or keep venomous snakes as pets. Important facts to understand include that a snake can strike up to two-thirds of its body length, a rattlesnake does not always rattle its tail as a warning before striking, and venomous snakes have the capability of envenomating from birth.
The copperheads and cottonmouths (Agkistrodon sp.) account for 25% and 10% of all venomous bites in the United States, respectively.18 Small children may be more at risk for severe envenomation requiring antivenom from copperheads and cottonmouths.18,21 However, most envenomations are mild, requiring only tetanus prophylaxis and pain control,3,21,44 and there are no deaths reported in the medical literature from copperheads.14 If an envenomation is more severe, antivenom is indicated, and further treatment is identical to that of rattlesnake envenomations.
The coral snakes (Micrurus and Micruroides) include the eastern (including Texas and South Florida) coral snakes and the Arizona (also known as Sonoran or western) coral snake. Coral snakes make up only 1-6% of all snakebites in the United States per year, and only 13 bites were reported in children and adolescents in 1995.1,2,45 Although there are no deaths reported in the United States in almost 30 years, eastern coral snakes are capable of delivering a lethal envenomation in adults, with mortality estimated at 10%.2,46 There has never been a death reported after an Arizona coral snakebite.2 The eastern coral snakes are indigenous to the southeast and Texas. The Arizona coral snake is found in Arizona and New Mexico.45 Coral snakes are characterized by an alternating sequence of yellow, red, and black bands, with a black snout. Coral snakes can usually be distinguished from nonvenomous mimics (such as kingsnakes and milksnakes) by their band pattern. Coral snakes in the United States have red bands are adjacent to yellow bands, whereas red bands are adjacent to black bands in mimic snakes. The mnemonic "red touch yellow, kill a fellow" may be helpful in remembering this color scheme. They have round pupils and subcaudal scales in a double row.18,33 Unlike pit vipers, coral snakes have short, fixed, anterior fangs. When a coral snake bites into a victim’s finger, toe, or web space, its venom is inefficiently delivered to the systemic system. Between 40% and 75% of all bites result in significant envenomation.21,46
The venom lacks proteolytic enzyme function, which makes local signs of envenomation rare following a bite. There are even reports of envenomation without visible fang marks.47 Local necrosis does not occur. Coral snake venom does not appear to cause hemolytic coagulation abnormalities or life-threatening arrhythmias.47 However, rhabdomyolysis has been observed.46 Systemic symptoms include drowsiness, fasciculations, tremors, nausea and vomiting, slurred speech, paresthesias, miosis, ptosis, diplopia, dysphagia, stridor, excessive salivation, and eventual respiratory paralysis. Signs of systemic envenomation usually present within three hours, but may be delayed greater than 13 hours after the bite.3,5,33,46 The predominant component of its venom is a neurotoxin that causes a curare-like, postsynaptic, nondepolarizing blockade at the neuromuscular junction by binding competitively to the acetylcholine receptor.48 Children are prone to seizures, probably because of the cerebral hypoxia secondary to respiratory failure.47
Prehospital treatment should include protection of the airway, breathing, and circulation. Venom extraction may be of benefit if immediately available, as above. Constriction bands or pressure immobilization techniques, as described for elapid bites in Australia, may be useful for field first aid for coral snake bites, but their use has not been well-studied.47,49,50
In administering Wyeth Antivenin (Micrurus fulvius) (equine), physicians must consider precautions for anaphylaxis and serum sickness, as with rattlesnakes. If the patient is bitten by a coral snake, he or she may need to be given antivenom before symptoms appear in order to prevent respiratory failure.46,47 Patients who develop respiratory paralysis may require ventilatory support for several days to weeks.3,51 Skin testing is controversial, as above. Recovery has been shown in patients without using antivenom. Some recommend treating patients with possible allergy to antivenom with supportive care only.47,49 There is no antivenom for bites from the Arizona (Sonoran) coral snake, and treatment is supportive.
Children may require more antivenom than adults. Early treatment with antivenom is indicated for a positively identified coral snake bite with fang marks and a negative skin test46,47 and may be indicated in other less well-defined situations. Three to 10 vials of antivenom are recommended for pediatric patients diluted in NS and delivered over two hours.3,33,46 For those presenting late with symptoms, signs of bulbar paralysis may imply impending respiratory failure. Elective intubation should be considered to prevent aspiration.49 Any child suspected of being bitten by a coral snake should be admitted to the ICU for at least 24 hours.5,47
Almost 24,000 spider bites were reported to the AAPCC in 1995, one-third of which were in children and adolescents.1 These data may represent overreporting, since many unexplained lesions are attributed to spiders. No deaths were reported from spiders.
All but two species of spiders in the United States are venomous. However, only about 50 species have fangs large enough to penetrate human skin, and only a few of these deliver a potent enough venom in sufficient quantity to be considered medically significant. Only the widow and brown spiders are considered dangerous to humans.17,56 Widow spiders are distributed throughout the United States except in Alaska. In the United States, bites occur most often in the southern and western states and are more common in the warm months, when spiders are more active.56 Brown spiders exist all over the world.
Pediatric Considerations. More aggressive treatment and hospitalization has been recommended by some for children envenomated by widow spiders;57 however, other sources suggest that children may actually suffer less morbidity than adults.58 The diagnostic challenge of young children with unexplained crying may represent spider envenomations.
Description. Of the five species of widow spider (Latrodectus sp.) found in the United States, only three species are black. The female black widow spider, which is the most common and well-known widow spider, is shiny black in color with a red spot on the ventral surface of the abdomen, often in the shape of an hourglass. Other widow spiders may be brown and have irregular red markings. The male spider is brown, much smaller than the female, and is not capable of envenomating humans.
Widow spiders spin irregular webs in dark, secluded areas such as woodpiles, basements, and garages and may be found in old furniture, shoes, or clothing. The spiders are not aggressive and bite in self-defense when a web is disturbed.
Pathophysiology. Venom. Widow spider venom is one of the most potent venoms by volume, even more so than that of pit vipers.59-61 Venom consists of six active components, with alpha-latrotoxin being the main component producing systemic symptoms.62 The proposed latrotoxin mechanism of action occurs through glycoprotein and ganglioside binding on neuromuscular pre-synaptic membranes. This opens cation channels, allowing release of acetylcholine and catecholamines, and inhibits re-uptake of choline. These biochemical changes result in excessive stimulation of the motor end plate.63-65 The resulting envenomation produces neurotoxic and autonomic symptoms.
Clinical Effects. Local Effects. The initial widow spider bite may be painful at the site or go unnoticed.56 Children, particularly at preverbal ages, may present with unexplained crying as early as 30 minutes post bite, while adults may present as late as 12 hours post bite.57,61,66 The average time in all patients from envenomation to onset of symptoms is between one and two hours.57 Within 20 minutes to one hour, a local erythematous reaction or halo-like target lesion with two small puncture wounds (1-2 mm apart) may be seen. The target lesion has been used as a reliable sign of envenomation in certain studies.63
Systemic Effects. The earlier the systemic symptoms, the more severe the envenomation. Systemic symptoms can be grouped into muscle pain and general autonomic disturbances. Patients complain of abdominal, thigh, and back pain from increased spasm of the large muscle groups regardless of bite location.8,66 Pediatric patients may present with refusing to bear weight and difficulty walking.58 Cholinergic symptoms include local or generalized diaphoresis, vomiting, salivation, lacrimation, and bronchorrhea.62 Other symptoms include weakness, fasciculations, ptosis, hyperreflexia, and seizures, fever, tachycardia, and hypertension.
The clinical course of widow spider bites in children is reported to be potentially more severe because of the smaller volume for the venom distribution.67 Status asthmaticus has been described, which may be due to bronchial smooth muscle contraction.68 Unusual pediatric clinical findings include priapism and hypertension.69 Widow spider bites are one of the rare occasions in which a child can present in hypertensive crisis. This can result in renal problems, seizures, or cerebral hemorrhage.67 In a recent review of pediatric spider bites, 92% of cases developed severe hypertension but no complications were reported.58 Seizures resulting from widow envenomation are thought to be secondary to hypertension. Normotensive seizures have not been described.56
A clinically significant effect of the muscle cramping associated with widow spider envenomations is muscle fatigue that results in respiratory difficulties. Respiratory failure has been described as one of the main causes of death due to widow spider envenomation. An expiratory grunt thought to be an effort to keep from moving the abdominal wall has been described and was seen more commonly in pediatric patients.58,66
An unusual clinical feature described in widow spider envenomation is diaphoresis at the bite site, face, and nose, with the rest of the body being dry. General diaphoresis may be associated with a more severe envenomation.8,63 There also can be a gradual onset of periorbital edema without other signs of angioedema or anaphylaxis.
Emergency Department Treatment and Disposition. Prehospital Care. Maintaining the airway, breathing, and circulation, along with careful observation of respiratory status, is the priority for prehospital care. Seizure precautions may also be indicated.
Grading of Envenomations. A three-class grading system for bites has been developed.63 (See Table 4.) Grade I is relatively asymptomatic with mild local pain. Grade II has progression of pain to localized muscle pain, while Grade III has generalized muscle pain, systemic symptoms, and abnormal vital signs.
Pain Control. Calcium gluconate has traditionally been recommended for pain control of widow spider bites since it has been thought to replenish calcium stores in the sarcoplasmic reticulum of muscles that are depleted by repetitive stimulation. However, calcium gluconate has been reported to be only 4% effective in a more recent study in comparison with a combination of IV opioids and benzodiazepines.63 Most human experience with calcium is anecdotal, with symptoms often recurring within 20 minutes of calcium infusion. Thus, calcium gluconate is no longer recommended as first-line treatment for widow spider bites.63
Dantrolene sodium is controversial therapy for widow spider bites. Plasma concentrations are variable in children, and there is a potential delay in achieving therapeutic levels via the oral route.67
Benzodiazepines, such as lorazepam and diazepam, have been used in treatment of widow spider bites with favorable results along with the added benefits of sedation, amnesia, and anxiolytic effects. Muscle relaxants, such as methocarbamol, have also been used, but have been reported to be even less effective than calcium.70
Narcotics, such as morphine sulfate and meperidine, are commonly used for widow spider bites. In conjunction with benzodiazepines, this is recommended as the therapy of choice in patients who are not candidates for antivenom.63
Antivenom. Latrodectus Antivenin (Merck & Company) has been shown to rapidly and completely relieve symptoms of widow spider envenomation.58,63 The dose is one vial of antivenom mixed in 50-100 mL of normal saline and infused over 30-60 minutes. This dose may be repeated if needed. Because pediatric patients have been reported to suffer more morbidity from widow spider bites, more aggressive use of antivenom has been recommended.57 Although effectiveness of the antivenom is supported by the literature, its use is limited by concerns over anaphylaxis, since it is a horse serum derivative.67 Although there have been no deaths reported from widow spider envenomation in over 30 years,58 fatality has been reported from anaphylaxis after administration of Latrodectus Antivenin.63 Skin testing, as previously mentioned, has variable predictability in identifying immediate hypersensitivity. Serum sickness may occur,64 but because of the relatively small amount of antivenom used, it is less common than with snakebite antivenom.
Widow spider envenomation has been described as a disease of discomfort rather than a deadly one, even in children.58 Symptoms of widow spider envenomation usually do not require antivenom as most are self-limited, often resolving within a few hours.64 Occasionally symptoms are prolonged but have been shown to "dramatically" respond to administration of antivenom as late as 30 hours after envenomation.71 Antivenom should be considered for severe envenomations when symptoms persist despite adequate administration of parenteral narcotics and benzodiazepines, in children without allergic contraindications, or for children with life-threatening complications associated with envenomation.58,63
Disposition. Although antivenom may not change outcome after widow spider envenomation,64 patients receiving antivenom appear to require less hospitalization.58,63 If high-dose narcotics and benzodiazepines are required to control persistent pain or abnormalities in vital signs persist, hospital admission is recommended.58 Symptoms from widow spider envenomations may last for several days. Antivenom may resolve pain within the two hours it takes to infuse.58 Such patients may be discharged home from the ED with good follow-up, preventing hospitalization. Patients suffering anaphylaxis due to antivenom or significant complications to the envenomation itself should be admitted.63
Antibiotics. Wound care considerations include cleansing of the wound and tetanus prophylaxis. Prophylactic antibiotic therapy is not routinely indicated.43
Description. The brown recluse spider is the most prevalent of the 13 species of brown spiders (Loxosceles) distributed throughout the United States. The brown recluse is found in the south central United States, and desert species are distributed in the southwest. All brown spiders cause a similar local reaction, but the brown recluse is thought to cause more severe local and systemic symptoms.72 Brown spiders are light to dark brown in color and are approximately 1-2 cm long with a 3 cm leg span. Many have an identifying violin or fiddleback marking on the dorsal cephaothorax, although this marking may be faint or even absent on several species.73 These spiders are reclusive, nocturnal hunters found under woodpiles, rocks, and in garages.74 Envenomations occur in spring and summer, often when a spider is trapped against the skin. Unlike the black widow spider, both the male and female spider are capable of envenomating humans.15 Although this discussion focuses on brown spiders, other spiders are capable of causing a necrotic lesion, referred to as necrotic arachnidism.8,77
Pathophysiology. Venom. Brown spider venom produces a dermonecrotic reaction secondary to proteolytic enzymes designed to initiate digestion of the prey’s tissue.78 The venom is a complex cytotoxin consisting of at least eight separate components (e.g., hyaluronidase, protease, sphingomyelinase D, hemolysins). Several reports identify sphingomyelinase D as the major cytotoxic factor of Loxosceles venom.73,78,79
Sphingomyelinase D destroys sphingomyelinase in cell-wall membranes and causes release of inflammatory mediators that damage the endothelium of local arterioles and venules. This lyses erythrocytes and activates platelets, which leads to thrombosis, infarction, and necrosis. Further tissue damage may be due to activity of complement and destruction of leukocytes, leading to the release of kinins, enzymes, and histamine.73,78
Clinical Effects. Local Effects. Local effects from brown spider envenomation are much more common than systemic effects. Initially, the brown recluse spider bite causes little or no pain and may go unnoticed. Fewer than 10% of lesions progress to form large ulcerations.78,81 In wounds that do progress, a burning sensation occurring 30-60 minutes after the bite has been identified in as many as 90% of bites in one series.73 The immediate area of bite becomes erythematous. After several hours, a blister forms within a central ischemic ring surrounded by an eccentric ring of erythema, which is sometimes called a "target lesion." Within 3-4 days, a bleb forms with induration and swelling that later ruptures, forming a central necrotic ulcer. The ulcer enlarges and may be covered with an extensive eschar (up to 15 cm). Necrosis may be superficial or involve muscle and fascial layers.73,82 Fatty areas such as the abdomen, thighs, and buttocks form more extensive necrotic lesions due to the tenuous blood supply to these regions. Ulcerations can require months to heal and may need skin grafting.
Other lesions may resemble the wounds caused by brown spiders, and spiders are probably not responsible for many of the injuries they are thought to have caused. Unless the spider is identified, diagnosis based upon the lesion alone may be inaccurate.72 In addition, patients may present late because of the insidious progression of the wound, and may not recall being bitten.79,83
Systemic Effects A rare systemic reaction has been described associated with brown spider envenomation. Children may experience arthralgias, chills, nausea, vomiting, and rash.73,79 The combination of high fever and scarlatiniform rash, together with a typical bite lesion, may suggest loxoscelism.73 Other reported pediatric systemic effects include hemolytic anemia, epiglottis swelling, and disseminated intravascular coagulation.75,76,80,84 Systemic envenomation may progress to hemolysis, thrombocytopenia, hemorrhage, shock, jaundice, and renal failure. Systemic symptoms are proportional to the amount of venom injected and not necessarily to the size or appearance of the bite.
Emergency Department Treatment and Disposition. Treatment of brown spider envenomation is controversial, and there are no controlled human studies to evaluate different treatment modalities. Tetanus prophylaxis and wound cleansing are recommended to avoid later secondary infection, but no evidence has linked decreased tissue loss with any specific local therapy.73
Although some recommend local surgical excision,85,86 other sources suggest excision of the lesion has not been shown to aid in healing and may even be detrimental.79 Untreated, many of the envenomations will regress and form a smaller final cosmetic lesion than if excised.8
Dapsone has been thought to decrease skin necrosis by inhibiting polymorphonuclear chemotaxis, lessening the inflammatory reaction. It has been anecdotally reported to resolve the ulceration from brown spider bite73 and eliminate the need for surgical debridement.83 However, dapsone has recently been shown to have no more effect on lesion size or histopathological response than control in an animal model and is not currently recommended.81,87 In addition, dapsone is associated with serious side effects, such as hemolytic anemia, methemoglobinemia, and toxic hepatitis. Dapsone is contraindicated in pregnancy, G6PD deficiency, and patients allergic to sulfa.
Hyperbaric oxygen (HBO) therapy is thought to cause neovascularization in necrotic tissues and inactivate enzymes that contain sulfa-hydryl groups, although it has also been shown in animal studies to have no benefit over controls.81,87
Antivenom to certain brown spiders has been produced, although there is no commercially available antivenom in the United States.54 Antivenom may be effective if given early to prevent the activity of sphingomyelinase enzyme but has been reported to be less effective once the inflammatory reaction has developed.83 This would require earlier and more accurate recognition of brown spider envenomation than currently available.
Systemic steroids have been recommended for systemic envenomations to prevent further hemolysis, although there has been no proof of benefit.73,81
Other anecdotal treatments without proven benefit that are possibly dangerous include electric shock, local steroids, heparin, colchicine, cyroheptadine (serotonin antagonist), and vasodilators. Analgesics and antihistamines may provide symptomatic relief. Antibiotics may be needed for secondary infection.86
Laboratory tests for evaluation of systemic toxicity include complete blood count with platelets, electrolyte, BUN, creatinine, and baseline clotting parameters. All patients with signs of systemic envenomation should be admitted to the hospital for evaluation for hemolysis, coagulopathies, and renal failure. Patients with local effects from brown spider envenomation should be followed closely as outpatients with wound care instructions and good follow-up. Patients with systemic infections or underlying debilitating disease should be admitted.
Pediatric patients accounted for a little more than one-fourth of the 11,000 scorpion exposures in 1995.1 No deaths have been reported from scorpion stings since 1968.88 The bark scorpion (Centruroides) is the only U.S. scorpion considered dangerous to humans. All other U.S. scorpions cause local burning pain and swelling but no systemic symptoms.59,88
Bark scorpions are nocturnal and dwell in trees. They are distributed mostly in Arizona but may also be found in parts of California, Texas, New Mexico, and Nevada.59,89 Envenomations have occurred in other areas when scorpions are unknowingly transported in personal belongings.90,91
Description. Scorpions have a segmented cephalothorax, abdomen, and tail. They have eight legs and two pincers. Bark scorpions are yellow or brown and about 5 cm in length. They can be distinguished from other scorpions by a small tubercle just below the base of the stinger, slender pincers, a triangular rather than pentagonal central sternal plate, and a rectangular rather than square proximal tail segment.59,88,92
Pediatric Considerations. Children suffer greater morbidity and mortality from scorpion envenomation than adults.33,88,89,92 Prior to modern intensive care units and development of antivenom, death occurred more often in pediatric patients.88 Young children suffer more from respiratory compromise than adults envenomated by bark scorpions. Although death has not been reported in almost 30 years in the United States from scorpion envenomation, morbidity may be severe; one such case led to quadriparesis.89 Most authorities agree on more aggressive treatment and admission of children with bark scorpion stings.
Pathophysiology. Venom Apparatus and Venom. Scorpions attack humans when threatened, thrusting their tail over their body while grasping with pincers and repeatedly stinging.59 The segmented tail ends in a vesicle containing venom glands, which contract and eject venom during the scorpion sting.59,90,91 Bark scorpion venom is primarily neurotoxic. Since there are no enzymes to produce tissue destruction, there is minimal inflammatory response.90,91 The protein neurotoxins activate sodium channels with prolongation of the action potential as well as spontaneous depolarization of the nerves, which enhances repetitive firing of the neurons.59,90,91 This autonomic stimulation results in catecholamine release.
Clinical Effects. Local Effects. Children may have more severe envenomation because the severity of sting symptoms is weight-dependent.93 After the sting, symptoms of pain and paresthesias begin immediately and progress to maximum severity in about five hours.88 The area of the sting is very sensitive, and tapping over the site can accentuate the pain, resulting in a positive "tap test."24,88 Diagnosis in young children may be difficult if the sting is unwitnessed due to the absence of local signs. The only sign of envenomation may be agitation or unexplained crying.94
Systemic Effects. Local pain progresses to generalized symptoms that may last up to 30 hours.88,89 Systemic symptoms are produced by both sympathetic and parasympathetic stimulation. Sympathetic symptoms can be described by the typical sympathetic "overdrive" syndromediaphoresis, tachycardia, hypertension, pulmonary edema, and seizures. Parasympathetic symptoms include the "SLUDGE" syndrome (salivation, lacrimation, urination, defecation, gastric emptying), bradycardia, and hypotension.59 Patients may complain of trouble swallowing.90,91
Airway secretions are an important consideration in the treatment of scorpion envenomations. Excessive drooling can be seen, particularly in children, and may be a combination of increased salivation and difficulty in swallowing.90,91 Fatalities due to scorpion envenomations in infants and children have been attributed to respiratory arrest.88
Cranial nerve dysfunction can be described as "roving" eye movements, blurred vision, tongue fasciculations, and difficulties with pharyngeal muscles resulting in stridor and contributing to respiratory arrest.
Excessive somatic muscular activity can be mistaken for seizure activity as the extremities can have uncontrollable jerking. However, unlike seizures, the patient remains awake and alert.90,91 True seizures are generally not found with bark scorpion envenomation.88
Cardiac dysfunction has been described and is thought to be due to catecholamine effects on myocardial contractility and perfusion causing increasing myocardial oxygen demand in excess of supply.95
Emergency Department Treatment and Disposition. Prehospital. Extractor devices may be beneficial but are not well-studied for scorpion envenomations. A lymphatic band with elastic wrap may delay venom absorption.
Supportive care with airway control is the number-one priority in treatment of scorpion envenomations. All patients should have intravenous access and continuous monitoring. No laboratory findings are specific for scorpion envenomation. Laboratory studies specific to the patient’s supportive care, particularly respiratory status, should be obtained. Creatinine kinase may need to be obtained to evaluate for possible rhabdomyolysis. Treatment of scorpion envenomation is based on correct identification, quantification of poisoning, and comparison of clinical picture with a graded scale of treatment.59
Grading and Antivenom Administration. Criteria for estimating the severity of scorpion envenomation have been developed.90,91 (See Table 5.) Grade I includes local pain and paresthesias and grade II envenomations have symptoms progressing to sites remote from the sting site. Grade III envenomations include cranial dysfunction or somatic neuromuscular dysfunction; grade IV includes both.
Grades I and II are subjective and may be combined for young children.90,91 The majority of grade IV scorpion envenomations occur in children less than 11 years of age. Infants have been reported to reach grade IV envenomations in 15-30 minutes.
Symptomatic relief of local pain and burning can be provided with analgesics and local wound control. Tetanus prophylaxis is indicated. Most grade I and II envenomations have spontaneous resolution of symptoms. Symptoms abate at a rate dependent on the age of victim and grade of envenomation.88 Pain and paresthesias can persist for as long as two weeks post envenomation.88,90,91 In grade III envenomations, illness severity can range from mild tongue fasciculations to severe cranial nerve dysfunction. Patients with grade IV envenomations typically appear ill.90,91
Analgesics are recommended for pain control. Corticosteroids, antihistamines, calcium, and sympathomimetics have all been administered for symptomatic relief but have no scientific support.59 Historically, barbiturates have been recommended for neuromuscular activity control in severe envenomations but may be dangerous for patients with airway difficulties. The physician must provide careful respiratory monitoring and support if using them. Barbiturates have been associated with complications and have not been shown to shorten illness duration.90,91
USA-APL Scorpion Antivenin for bark scorpion envenomation may be obtained in Arizona but is not approved by the Food and Drug Administration. Developed by Arizona State University, it is a goat serum derivative. Bark scorpion antivenom has not been well-studied but has been reported to have beneficial clinical effects.90,91,93,95 Antivenom has been shown to benefit patients with grade III and IV envenomations by rapidly resolving symptoms and shortening clinical course. Some physicians prefer hospitalization, sedation, and supportive care.90,91 Benefits of antivenom, including immediate symptom resolution and avoidance of sedation, paralysis, intubation, and possibly even hospitalization, must be weighed against allergic complications.89
Antivenom dose is one vial diluted in 50 cc normal saline intravenously over 15-30 minutes; this may be repeated after one hour. Improvement in severe neurologic symptoms can be seen within minutes, but skeletal symptom resolution can take longer.88,90,91 Risk of anaphylaxis and serum sickness is present but is less common, probably because antivenom is derived from goat serum and small volumes are given. Some experience with antivenom has suggested that if full symptom resolution occurs rapidly, the patient may be safely discharged home, avoiding a costly hospitalization and an intubation with sedation.89 Without antivenom, admission or extended critical care observation should be strongly considered, especially for young children with bark scorpion envenomations.
While the bites and envenomations of snakes, spiders, and scorpions are less common than some presenting pediatric emergencies, they are nevertheless a potential challenge to the clinician. Once the precarious process of recognition and diagnosis is overcome, the clinician is still faced with demanding therapeutic decisions that at times are as risky as the injury itself. This review of the agents of envenomation, the associated pathophysiology, and the available treatments for snake, spider, and scorpion envenomations helps clarify the decision making for the clinician.
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Physician CME Questions
1. What features best distinguish pit vipers from nonvenomous snakes and coral snakes?
A. A round pupil
B. Divided subcaudal scales
C. A heat-sensing organ
2. What is the best treatment for children who suffer coagulopathy from crotalid envenomation?
A. Vitamin K
B. Antivenom
C. Transfusion
3. Which prehospital therapy/first aid is safe and may be beneficial in the treatment of pediatric envenomations?
A. Electric shock
B. Tourniquet
C. Venom extraction
4. Children may present with which of the following after widow spider envenomation?
A. Unexplained crying
B. Diaphoresis
C. Muscle cramping
5. What is the best treatment for children with brown spider envenomation?
A. Local wound care
B. Hyperbaric oxygen
C. Dapsone
6. Children are at increased risk for which complication following bark scorpion envenomation?
A. Necrosis
B. Infection
C. Rhabdomyolysis
D. Respiratory paralysis
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