Revenge of the Wild Kingdom: Animal Bites and Stings in Children

Author: Martha S. Wright, MD, Associate Professor of Pediatrics, Case Western Reserve University School of Medicine; Associate Director, Pediatric Emergency Medicine, Rainbow Babies and Children’s Hospital, Cleveland, OH.

Peer Reviewer: Steven M. Winograd, MD, FACEP, Attending Physician, Department of Emergency Medicine, Jeannette District Memorial Hospital, University of Pittsburgh Medical Center, PA.

Children are, by nature, playful, active, and curious—characteristics that frequently bring them into contact with members of the animal kingdom. On occasion, mammalian bites, arthropod stings and, less commonly, reptile envenomations are the outcome of these encounters. The spectrum of disease following these injuries includes clinical syndromes resulting from direct trauma, effects of toxins, immune phenomena, and transmitted infections. Understanding the determinants of disease and anticipating the clinical consequences prepare the clinician to evaluate and manage these injuries appropriately, whether they are caused by the bite of a highly evolved mammal or the sting of a flying insect.

Interestingly, despite the frequency with which these injuries occur, controversy has surrounded many aspects of evaluation and treatment. Debate continues over the use of prophylactic antibiotics after mammalian bites, indications for antivenom use in snakebites, and the appropriate wound management of brown recluse spider bites. In some cases, conflicting recommendations still exist in the literature. Presently, however, as the principles of evidence-based medicine are utilized to examine critically many of the limited studies and personal anecdotes on which management guidelines have been based, a clearer picture of what works and what doesn’t work is emerging. This article will describe for the emergency physician the clinical conditions caused by bites and stings, identify the clinical issues of greatest importance in the acute care setting, and emphasize treatment recommendations that are based on strong evidence of efficacy.— The Editor

Mammalian Bites

It is estimated that more than 5 million mammalian bites occur each year in the United States, with 15-20% of bite victims seeking medical attention.1,2 These injuries account for roughly 1% of all emergency department (ED) visits. Children are particularly at risk for mammalian bites, as well as for other serious bite injuries, because of their size and behavioral characteristics.

Dog Bites. Dogs are responsible for 80-90% of mammalian bites.1,2 The epidemiology of dog bites has been well studied. The typical pediatric victim is a boy between the ages of 5 and 9 years who provokes a family or neighborhood dog, although increasing numbers of unprovoked dog attacks are being reported.1,3 Medium- and large-breed dogs, including German shepherds, pit bulls, huskies, and rottweilers, are implicated more frequently than other breeds.4 In young children, more than three-quarters of bites involve the head and neck, while the extremities are the areas of the body most commonly injured in older children and adults. Children are at greatest risk for serious injury, with 70% of dog-bite-related fatalities occurring in victims younger than 10 years of age.4-7

The animal’s large teeth and jaw muscles, which can generate compressive forces of more than 400 pounds per square inch, are responsible for the observed patterns of injuries. Dogs tear and crush tissue, producing lacerations, abrasions, avulsions, and crush injuries. Wound infection occurs in 3-18% of bites, and other complications (e.g., sepsis, septic arthritis, osteomyelitis, tenosynovitis, endophthalmitis, rabies, and tetanus) have been reported.8 Dog-bite wounds to the head and face in young children have been associated with brain injury and meningitis.6 In addition, because of the predilection for bites to the face, children are at significant risk for scarring and disfigurement.

Cat Bites. In contrast to dog bites, cat bites are relatively uncommon in children. Cats are responsible for about 10% of reported animal bites annually, and cat-bite victims are more frequently female, older than dog-bite victims (mean age 19.5 years), and bitten by an unknown or stray animal.3,9 The cat’s sharp teeth and claws, and relatively weak jaw muscles predispose the victim to scratches and puncture wounds.10 In adults, more than 80% of cat bites are inflicted on the upper extremities and hands, while in pediatric patients, one-third of bites occur on the face and neck.9 Because they are typically small, deep punctures, cat bites are particularly prone to infection, with infection rates as high as 28-80% reported in some studies.8 Other complications are similar to those seen following dog bites. In addition, cats are the leading domestic carrier of rabies and are the reservoir for Bartonella henselae, the agent responsible for cat scratch disease.11

Human Bites. Human bites are even less common in the ED than dog and cat bites, but can be associated with complications. In the pediatric population, more than half of human bites occur during fights in children older than 10 years.12,13 Other causes of "tooth-skin" contact include sports events, play activities, and child abuse.12,14 While deep hand lacerations and avulsions predominate in adolescents and adults, human bite injuries in young children are usually abrasions involving the face and neck.13 Wound infection, tenosynovitis, osteomyelitis, amputation, and transmission of various infectious pathogens, including hepatitis B, human immunodeficiency virus (HIV), and syphilis, are known complications of human bites.

Rodent Bites. The characteristic rat bite is a puncture wound on the finger or hand that occurs during sleep or while attempting to handle the animal.15 Rat bites typically are seen in laboratory workers and among children living in poverty. Children younger than 10 years are at greatest risk, accounting for 69% of rat bites in one study.16 Rat bites result in wound infection in fewer than 10% of cases, although they may be responsible for transmission of a variety of diseases, including plague (bubonic, pneumonic, septicemic, and meningeal), rat bite fever, leptospirosis, melioidosis, and tetanus.11 Rabies transmission by rodents never has been reported in the U.S.17

Management. Although it is rare for a victim of a mammalian bite to require intervention for life-threatening injuries, this activity would be the priority in an acutely injured patient. Once the patient is stabilized, the primary goal of mammalian bite management is wound care that focuses on promotion of wound healing, detection of deep and/or occult injuries, and restoration of function of the injured area. (See Figure 1.) In addition, prophylaxis for a variety of potential viral and bacterial infections may be indicated, as determined by the clinical situation.

An appropriately directed history will provide information to facilitate clinical decision-making in the care of the bite victim. Information that should be obtained includes the type and immunization status of the animal responsible for the bite, report of unusual behavior in the animal, the time and circumstances of the injury, the immunization status of the victim, and any other victim characteristics that would predispose the patient to infection (e.g., immunosuppression).

Physical examination should include careful inspection and exploration of the bite wound, with special attention to altered neurovascular function, joint capsule integrity, and signs or symptoms of compartment syndrome.18 Radiologic studies may be indicated if concern exists for fracture, brain injury, or the presence of a foreign body in the wound (e.g., a tooth). Laboratory tests rarely are indicated in the evaluation of the acute, noninfected wound. Pretreatment cultures in this setting have a low predictive value for causative organisms in wounds that subsequently become infected.19 Wounds with evidence of infection, however, should be cultured both aerobically and anaerobically.

Although current literature lacks large prospective studies to support many of the recommendations made for wound preparation, wound closure, and use of prophylactic antibiotics, most experts agree that the mainstays of bite wound management are cleansing, copious irrigation, and debridement of devitalized tissue.19-22 Initial cleansing with soap and water has been shown to decrease the incidence of rabies infection.17 Irrigation should be accomplished with sterile saline, a 19-gauge catheter, and a 20-30 cc syringe to generate adequate pressure to dislodge foreign or devitalized material without harming viable tissue. Tetanus immunization status should be updated according to standard guidelines.

Surgical closure of bite wounds remains a controversial topic, but a recent study suggests that it can be accomplished safely without apparent increase in infection risk in low-risk wounds.23 It is discouraged, however, in wounds with a high risk for infection.19,20 These include cat puncture wounds, closed fist, and other hand injuries from humans, dogs, or cats; significant crush or puncture wounds; and all bites in immunocompromised patients. Delayed primary closure or healing by secondary intention is recommended for bites such as these.

The use of prophylactic antibiotics in both high- and low-risk bite wounds has been studied, but consensus regarding efficacy is lacking because of numerous study limitations.24-30 Of the randomized clinical trials published to date, the majority suffer from small sample size, high lost-to-follow-up rate, lack of standardized wound preparation, and failure to document patient compliance.31 While the limited available evidence suggests possible benefit from antibiotic prophylaxis in human and hand bites only, there appears to be no effect in uninfected, low-risk, carefully prepared wounds.31,32 However, most experts are more liberal in their recommendation for antibiotic use, encouraging their use for most high-risk bites.19,21 When indicated, recommended antibiotics include those with a spectrum that can address the expected organisms, specifically Pasturella multocida, the pathogen cultured most commonly from dog and cat bites, as well as anaerobes, staphylococcus species, and streptococcus species.8,19,21,33 While a variety of antibiotic combinations will provide appropriate coverage, amoxacillin/clavulanate is recommended most often. (See Table 1.) In the penicillin-allergic patient, azithromycin or doxycycline may be used in children older than 8 years.19,20,21 While fluoroquinones have demonstrated activity against the most likely bite-related pathogens, their use is not recommended in children.

All infected wounds require antibiotic therapy. The broad-spectrum intravenous agents ampicillin/sulbactam, cefoxitin, and ceftriaxone provide coverage for the most common organisms in severe wound or invasive infections. They are reasonable empiric choices before culture identification of the infective pathogens is available.

Concern for rabies infection prompts many people to seek medical attention following animal bites. Risk for rabies is greatest after wild animal exposure, particularly to raccoons, skunks, and bats, although most post-exposure rabies prophylaxis given in the United States follows dog or cat bites. A recent report suggests that post-exposure rabies prophylaxis in the United States often is administered or withheld inappropriately, and the authors of the report encourage improved physician compliance with the current Centers for Disease Control and Prevention guidelines.34 Current recommendations for rabies immunoprophylaxis are outlined in Table 2 and Table 3.

Arthropods

The bites or stings of arthropods may cause injury as minor as local pruritus or as serious as anaphylaxis.35 Of the 1 million species in the insect kingdom, the order Hymenoptera and the class Arachnida contain the few members that pose the greatest medical threat to humans. Luckily, most of these injuries are minor and require only supportive care. Awareness of the potential for severe reactions is important, however, as in rare situations aggressive intervention may be life-saving.

Hymenoptera. Honeybees, wasps, yellow jackets, and fire ants are found throughout the United States and are responsible for the largest number of insect bites brought to medical attention.35 These insects envenomate their victims with immunoreactive substances that cause annoying local reactions and, in some cases, trigger synthesis of IgE antibodies that can mediate systemic anaphylaxis upon subsequent reexposure to the venom. Non-IgE immune mediated reactions also may follow exposure to hymenoptera venom, and include a serum sickness-like syndrome, Guillain-Barré syndrome, acute glomerulonephritis, thrombocytopenic purpura, and transverse myelitis.

Bees. A bee sting causes immediate pain and gradual development of local swelling, erythema, and pruritus. On occasion, these local reactions can be quite impressive, causing significant redness, warmth, and edema extending beyond the sting site and mimicking cellulitis. Non-anaphylactic systemic reactions, including nausea, vomiting, diarrhea, and fever, have been noted in adults following attacks by swarms. Bees attack their victims with barbed stingers, to which the venom glands are attached. The stinger remains in the wound and continues to inject venom for 10-20 seconds after the initial sting. Rapid removal of the stinger by flicking it from the skin (a credit card often is recommended as the instrument of choice) is important to prevent further envenomation, infection, or a foreign body reaction at the sting site.36

Wasps, Hornets, and Yellow Jackets. These insects have smooth stingers that typically are not retained in the wound, and therefore, can be used to inject venom repeatedly. Local and systemic reactions are similar to those seen following bee stings.

Fire Ants. Fire ants (Solenopsis invictus, Solenopsis ricteri) are found throughout the southern United States. These aggressive insects swarm from their hill when disturbed and attack the victim en masse, injecting venom that causes severe burning pain.37 Each ant sting typically produces a small erythematous wheal surrounding a sterile pustule. Large local reactions are reported in 17-56% of patients, and may be mistaken for cellulitis. Anaphylaxis is estimated to occur in up to 1% of stings.35,37

Management. Treatment of Hymenoptera bites and stings primarily involves attention to local wound care and relief of pain and pruritus.35 In addition, the clinician must be prepared to treat anaphylaxis, the potentially life-threatening immune reaction to hymenoptera venom. There are 40-150 deaths from insect sting-induced anaphylaxis yearly (although these occur mostly in adults), and it is estimated that 0.5-5% of the U.S. population has had a significant allergic reaction to bee stings.35,38

On presentation, the sting victim should be assessed for cardiovascular or respiratory dysfunction or other signs of anaphylaxis. Historical information, such as knowledge of previous allergic reactions, insect type, time and circumstances of the sting, and development of symptoms, will guide patient treatment. If the patient is stable, local wound management may proceed with inspection for and removal of the stinger in the case of bee stings, wound cleansing, application of ice, and administration of an oral antihistamine (e.g., diphenhydramine).

Anaphylaxis is the syndrome resulting from antigen-triggered, IgE-mediated release of histamine and other vasoactive substances from mast cells.39 The clinical syndrome develops within 30 minutes of a sting and is characterized by symptoms in two or more organ systems. Life-threatening symptoms typically affect the cardiorespiratory systems, and include laryngeal edema with airway obstruction, bronchospasm, hypotension, or shock. Anaphylaxis symptoms manifested by other organ systems include urticaria, angioedema, vomiting, diarrhea, and altered mental status. Death results either from hypoxemia secondary to airway obstruction or from cardiac failure secondary to shock.

Anaphylaxis therapy is directed at relieving systemic effects of histamine and other mediators, suppressing further histamine release and mediator synthesis, and blocking histamine tissue receptors.39 In dermal cases, patient comfort and relief from pruritus is achieved using antihistamines. In severe cases, however, cardiovascular and respiratory support may be required. The mainstays of therapy for anaphylaxis are rapid administration of epinephrine, antihistamines, corticosteroids, and fluid resuscitation. Anaphylaxis can have a biphasic clinical course, in which the patient’s initial histamine-related symptoms resolve only to return several hours later.40 These late symptoms are due to synthesized mediators like prostaglandins, leuko-trienes, and kinins. Because of the risk for relapse following a significant anaphylactic reaction, patients should be admitted to the hospital for 24 hours of observation, regardless of their initial response to therapy.

Patients experiencing Hymenoptera sting anaphylaxis of any severity should be considered for referral for for skin testing and desensitization therapy. Progressive desensitization is highly effective at preventing future anaphylactic reactions from Hymenoptera stings.41 In addition, on discharge patients should be provided with prescriptions and instructions for epinephrine self-injectors, and be advised to wear Medic Alert bracelets.

Arachnidae. The family Arachnida includes spiders, ticks, and scorpions. Several members of this family can cause illness or injury in humans.

Black Widow Spider. The black widow spider (Lactrodectus mactans, Lactrodectus hesperus) is a nonaggressive insect that lives under rocks and in woodpiles throughout the continental United States. Only the female, which injects a potent neurotoxin at the bite site, is poisonous to humans. This spider measures 3-4 cm, and has a shiny black body, and has the characteristic red "hourglass" marking on her abdomen.

Although the bite itself usually is painless, patients may describe a vague burning sensation at the site, followed by regional lymph node tenderness.42,43 Within 30-90 minutes after envenomation, severe muscle spasms of the abdomen, back, and chest develop, accompanied by restlessness and hypertension. Cholinergic symptoms may be present and include diaphoresis, increased salivation, lacrimation, vomiting, and diarrhea. These symptoms, which are due to venom-mediated synaptic acetylcholine and norepinephrine release, generally resolve in 24-72 hours. As the spider rarely is recovered for identification and the bite may be undetected, the diagnosis is based on clinical features. The observed symptom complex must be differentiated from appendicitis, peritonitis, renal colic, electrolyte disturbances, and cholinergic crisis from organophosphate poisoning or other toxins.

Management. Treatment is directed at circulatory support and muscle spasm relief. Mild symptoms may be managed with oral analgesics. More severe symptoms will require parenteral narcotics for pain and benzodiazepines for muscle spasms and, rarely, respiratory support. Most children with moderate to severe symptoms will require hospital admission for supportive care. Calcium gluconate, long touted as the antidote for symptoms related to black widow spider envenomation, has been found to be ineffective, as have methocarbamol and dantrolene.35 In general, pain and spasm relief alone will relieve hypertension, but antivenin is available and indicated for hypertension or tachycardia that does not respond to supportive treatment. Skin testing should precede antivenin administration, as it is a horse-serum derived product, and anaphylaxis can result from its use. Wound care, if the wound is identified, includes local cleansing and tetanus prophylaxis.

Brown Recluse Spider. The brown recluse spider (Loxsceles reclusa) is the most familiar representative of a group of spiders responsible for the syndrome of "necrotic arachnidism."35,43 These spiders inject proteolytic enzyme-rich venom into the bite site, which can cause extensive local skin necrosis and a variety of systemic symptoms.

The brown recluse spider is found in the Southeastern and Midwestern United States, especially Missouri, Arkansas, Oklahoma, and Kansas, where it lives in dark areas under rocks and in woodpiles. It is not aggressive, but bites defensively when disturbed. This nondescript, brown spider is 2-3 cm in diameter and displays a characteristic violin-shaped marking on its back.

The bite of a necrotizing spider frequently goes unnoticed by the victim for several hours, until local itching, redness, and pain occur at the site.44 A blister soon develops, and during the next several days, the center of the lesion turns black, leading to a slowly healing ulcer that remains after the eschar sloughs. Nausea, vomiting, fever, headache, arthralgias, and myalgias are common systemic features of this syndrome. Severe hemolytic anemia, seizures, renal failure, and shock are reported rarely. Children are bitten more frequently than adults and are more likely to develop systemic manifestations, especially hemolytic anemia.

Management. Treatment of brown recluse spider bites requires conscientious wound care, including ice to the bite site during the acute phase (which may limit necrosis by decreasing the enzymatic activity of the toxin), local cleansing, and tetanus prophylaxis, as well as management of systemic symptoms.35,43,44 Skin grafting may be necessary for some lesions once the wound has stabilized. Specific modalities such as local steroid injection, systemic corticosteroids, early wide excision of the lesion, local infiltration with phentolamine, hyperbaric oxygen, and use of oral dapsone, which decreases the local infiltration of neutrophils into the envenomated area, have been advocated, but none have been found to improve the outcome of the lesion.35 While routine laboratory testing typically is unhelpful, a complete blood count is recommended to evaluate for hemolytic anemia in children. Systemic steroids are useful in the management of hemolytic anemia resulting from envenomation.

Scorpions. Of the 650 species of scorpions in the world, only one species dangerous to humans is found in the United States. The scorpion Centruroides exilicauda makes its home in Arizona, Texas, Southern California, and Northern Mexico, and is responsible for the majority of deaths reported from scorpion envenomation. The scorpion is an insect that contains a potent neurotoxin in specialized glands at the base of its tail. Humans are stung when they disturb the scorpions in their hiding places (under rocks or logs), or in clothing or shoes. Children especially are vulnerable to the effects of the venom.

Scorpion venom causes acetylcholine and catecholamine release and calcium channel dysfunction. Following a sting, there is vague discomfort, tingling, and hyperesthesia at the site.45 Within 60 minutes, hyperactivity, restlessness, roving eye movements, tachycardia, hypertension, and cholinergic symptoms of salivation, lacrimation, vomiting, bronchorrhea, and wheezing develop, persisting as long as 36 hours. In the absence of a bite history, the marked agitation and restlessness may suggest other etiologies, such as encephalitis, phenothiazine toxicity with dystonia, and seizure or movement disorders, while the cholinergic symptoms are suggestive of organophosphate intoxication.46

Management. Treatment is directed at supporting cardiorespiratory function and pain control. While most stings can be treated with oral analgesics, more severe systemic symptoms, especially in young children, may require more aggressive therapy. Bronchorrhea and impaired respiratory mechanics may necessitate airway protection and mechanical ventilation. Agitation and pain may require parenteral narcotics and benzodiazepines. Young children frequently will require hospitalization, monitoring, and sedation as their symptoms resolve. Non-FDA-approved goat serum antivenin is available in Arizona and has been shown to result in rapid resolution of life-threatening symptoms, but is associated with both anaphylactic and delayed hypersensitivity reactions.45,47 It is recommended that its use be reserved for those patients with severe systemic symptoms.45,47 Wound care should include local cleansing and tetanus prophylaxis.

Ticks. Ticks threaten human health as vectors for a variety of rickettsial, bacterial, and spirochetal diseases, most notably Lyme disease and Rocky Mountain spotted fever, and the toxin-mediated syndrome of tick paralysis.48,49 These arthropods inhabit grassy fields throughout the United States. The bite itself is rarely cause for alarm, although granuloma formation is known to occur at the site. Generally, tick bites go unnoticed, and only about 50% of patients with proven tick-borne diseases relate a tick bite history.

Tick paralysis is characterized by motor weakness or acute ataxia that progresses into an ascending flaccid paralysis. Due to a neurotoxin elaborated at the bite site that blocks acetylcholine release at the neuromuscular junction, clinical symptoms disappear when the tick is removed. These neurologic symptoms must be distinguished from Guillain-Barré syndrome, poliomyelitis, spinal cord compression syndromes, and botulism.

Management. Management of tick bites most often involves tick removal, local wound care, and a decision regarding antibiotic prophylaxis for Lyme disease. The first two tasks are relatively straightforward, but the third is surrounded by controversy. While other methods of tick removal have been recommended, the most effective technique involves grasping the tick with forceps as close to the skin surface as possible and pulling with steady, gentle pressure until the tick releases.50 This method is least likely to leave mouthparts behind or cause tick regurgitation into the wound, which may increase the risk of transmitted infection. The wound should be cleansed routinely, and tetanus prophylaxis provided if indicated.

At present, routine antibiotic prophylaxis for Lyme disease is not recommended.51,52 The likelihood of developing Lyme disease after the bite of an Ixodes (deer) tick is estimated at 1-3.4%, and the disease can be treated effectively at the onset of the characteristic rash, erythema chronicum migrans. If, however, the decision is made to use prophylactic antibiotics because of endemicity of the disease, parental anxiety, or duration of tick attachment, amoxicillin (40 mg/kg/d divided TID for 10 days) in younger children or a single dose of doxycycline (200 mg) in children older than 8 years are the regimens of choice.51-53

Snakebites

Of the 45,000 snakebites reported each year in the United States, approximately 8000 are caused by venomous snakes.54 Although the two families of indigenous poisonous snakes—Viperidae, subfamily crotalinae (pit vipers) and Elapidae—are distributed throughout the continental United States, most of these attacks occur in the Southeastern and Southwestern states. Pit vipers (rattlesnakes, water moccasins, and copperheads) are responsible for 90% of poisonous snakebites in the United States, with coral snakes (Elapidae) accounting for 3%.54 Increasingly, exotic snakebites, which account for 5% of reported bites, are presenting to medical attention, although not commonly in children.54

The majority of pediatric snakebite victims are 5- to 19-year-old males who are bitten on the hands or upper extremities while handling the snakes.55 Younger children may present with bites to the feet or legs when they accidentally come into contact with a snake on the ground. Only 10-15 deaths are recorded yearly from snakebites, but while fewer than 10% of poisonous bites occur in children, 20% of the fatalities occur in the pediatric age group.54,55 This presumably is due to the child’s smaller size and the proportionately larger venom dose per kilogram.

Pit Vipers. Crotalid venoms are snake-specific combinations of hemo-, neuro-, nephro- and cardiotoxic peptides and necrotizing proteinases that allow a snake to immobilize, kill, and then digest an animal meal.56 It is these venom components that are responsible for the multiple organ system dysfunction seen in the unfortunate human victim of a snake encounter.

An envenomated pit viper bite will be immediately painful, with erythema and swelling developing at the site in minutes.54,56 Over the next several hours, vesicles and hemorrhagic bullae develop, and the swelling increases, in some cases progressing to involve the entire limb and trunk. Systemic manifestations of moderate envenomation include weakness, paresthesias, tachycardia, and hypotension; laboratory abnormalities include hemoconcentration, low fibrinogen level, and thrombocytopenia. In severe envenomation, the patient may develop shock from hypovolemia secondary to toxin-mediated endothelial leakage, hemorrhage, and respiratory distress, as well as anemia, acidosis, and toxin -mediated coagulopathy. In the absence of a snakebite history, the local reaction to pit viper envenomation can be mistaken for cellulitis, wound infection, deep venous thrombosis, or necrotic arachnidism, while the systemic effects may mimic septic shock, severe hemolytic anemia, or hemolytic-uremic syndrome.56

Elapidae. In contrast to crotaline venom, the primary constituents of coral snake venom are neurotoxins.56 As a result, the clinical picture following envenomation by this snake is one of gradual weakness and paresthesias that may progress to flaccid paralysis. Because of an absence of proteolytic enzymes in the venom, these symptoms occur without local tissue destruction or pain at the bite site. The onset of neurologic symptoms may be delayed, with a sudden deterioration following a latent period of more than 12 hours reported in some cases. Ventilatory failure secondary to respiratory muscle weakness is the major complication of coral snake envenomation. In the absence of a snakebite history, the weakness and flaccid paralysis of coral snake envenomation may be mistaken for the neurologic manifestations seen in botulism, polio, Guillain-Barré syndrome, transverse myelitis, or spinal cord compression syndromes.

Management. The challenge for clinicians treating snakebite victims is first ascertaining that a poisonous snake inflicted the bite, and then determining if envenomation occurred. The differentiation of poisonous from non-poisonous snakes can be done by directly inspecting the (preferably dead) snake or from a witness’s description. Nonpoisonous snakes have round pupils, small teeth instead of fangs, a rounded snout, and no rattle on the tail. The characteristics of the snake’s coloration as illustrated in the mnemonic "Red on yellow, kill a fellow, red on black, venom lack" may help determine whether, in fact, a coral snake or another striped, non-poisonous snake inflicted the bite. Other information that will influence the patient’s management includes time elapsed since the bite, therapy rendered in the field, development of symptoms, and victim characteristics such as tetanus immunization status.

Inspection of a crotaline bite site usually will reveal if envenomation has occurred. However, 20% of pit viper bites are "dry" and will require nothing more than wound care. It is recommended that a patient be observed for 6-12 hours for any signs of envenomation before concluding that the bite is minor or dry.54,56 Envenomation by a coral snake is confirmed by the development of neurologic symptoms. In addition to wound inspection, these victims require a complete physical and laboratory evaluation. Laboratory testing of the patient with an envenomated snakebite should include complete blood count, coagulation studies, type and cross match, serum electrolytes, blood urea nitrogen/creatinine, and urinalysis.

The goals of snakebite therapy include the treatment of systemic and local venom effects, venom inactivation, and prevention of long-term disability. An approach combining supportive care, conscientious wound management, and the appropriate use of antivenin will be most effective. (See Figure 2.) Very little controlled scientific data on methods of treatment exist, and many of the current recommendations are based on anecdotal reports.

Following a snakebite, the patient should be transported rapidly to a medical facility. In the prehospital environment, supportive care, including splinting the injured extremity, removing constricting clothing or jewelry, minimizing patient movement, and providing analgesia, is indicated.57 Controversy surrounds the administration of other first aid measures such as the use of constriction bands (2- to 4-cm bands placed loosely above the bite to restrict lymphatic flow while allowing arterial and venous blood flow) and the use of continuous suction over the wound. Although an animal study has demonstrated some benefit from constriction bands, concern for arterial compression and ultimate neurovascular compromise as tissue edema progresses, has limited their use.58 Regarding continuous suction, animal studies have demonstrated that when using appropriate equipment within 5-10 minutes of a bite, suction can remove 30-50% of radiolabeled venom.59 However, more recent reports suggest that marketed suction devices are not large enough to cover both fang marks in many crotaline bites, and skin necrosis at the bite site has been observed.60 Fang mark incisions no longer are advocated, as these do not hasten venom removal and can cause additional tissue and tendon damage if improperly performed. Arterial tourniquets (in contrast to constriction bands) are contraindicated.

In a medical facility, assessment of the wound and major organ function are the first priorities. Treatment of cardiovascular and respiratory dysfunction must be performed urgently. Following stabilization, wound care should proceed with irrigation, loose dressing, splinting for comfort, and tetanus immunization. Prophylactic use of broad-spectrum antibiotics has not been studied in randomized trials and remains controversial, although the available studies suggest a low incidence of infection in untreated wounds.54 Fasciotomies are rarely necessary despite the impressive nature of the swelling.61 Previously recommended therapies, including early wide excision of the wound and use of steroids, have not been shown to improve outcome, while cryotherapy and electroshock therapy have proven harmful.61,62

Treatment with antivenin depends on the type of snakebite. Use of Micrurus fulvius antivenin (Wyeth-Ayerst Pharmaceuticals, Philadelphia, PA) after known or suspected Eastern coral snakebite is advocated regardless of the wound characteristics.56 Administration of three to five vials of antivenin given intravenously after skin testing neutralizes the maximum amount of venom injected by this snake and should be given prior to the progression of neurologic signs. Because the antivenin is dosed to neutralize an estimated quantity of venom, the same dose is administered to children as adults. There is no antivenin available for the treatment of Arizona coral snake bites. At present, an ovine-derived antibody fragment (Fab) antivenin to Micrurus fulvius is being evaluated and may prove more effective and safer than the presently available antivenin.63

Historically, the use of antivenin for pit viper envenomation has been a more controversial subject.64 For the last 50 years, a single polyvalent horse-serum based antivenin, effective against all indigenous crotaline species (Antivenin [Crotalidae] polyvalent, Wyeth-Ayerst, Philadelphia, PA) has been the only antivenin available. Dosage is based on wound appearance, presence of systemic symptoms and coagulation abnormalities. Its use is associated with reduced swelling, reduced tissue damage, and reversal of coagulopathy. Unfortunately, the benefits of its use must be balanced against the 9-33% risk of immediate hypersensitivity reactions and nearly 100% incidence of delayed hypersensitivity reactions.54

Recently a new, safer product has become available that may make the clinical decision to administer antivenin easier as experience with the product increases.64,65 This sheep serum derived (ovine) polyclonal, polyvalent antibody fragment (Fab) affinity-purified antivenom (FabAV (CroFabTM), Savage Laboratories, Melville, NY) has been found effective in treating mild to moderate envenomations with fewer adverse reactions. The reported immediate hypersensitivity rate is 14% (with only mild to moderate reactions noted) and delayed hypersensitivity reactions developed in only 16% of study patients.64 This product is delivered at a standard initial dose of 4-6 vials, and then re-dosed hourly until the envenomation symptoms have stopped progressing.66 After stabilization, subsequent two-vial doses are delivered either based on recurrence of symptoms or on a scheduled basis. Admission to a critical care unit usually is necessary for patients with moderate to severe envenomation syndromes to ensure close monitoring of wound characteristics and coagulation parameters as well as timely administration of antivenin.

Conclusion

Mammal, snake, and insect bites and stings are common in children. Some of these injuries or their complications may be severe and require aggressive intervention. The initial management of all patients should employ the familiar principles of advanced life support, supportive care, and wound management. In addition, some patients will benefit from bite-specific therapeutic interventions such as antivenin or antibiotics. Familiarity with the most current evidence-based recommendations and modalities is important to providing optimal care for these patients.

References

1. Weiss HB, Friedman DI, Coben JH. Incidence of dog bite injuries treated in emergency departments. JAMA 1998;279:51-53.

2. Sacks JJ, Kresnow M, Houston B. Dog bites: How big a problem? Inj Prev 1996;2:52-54.

3. Patrick GR, O’Rourke KM. Dog and cat bites: Epidemiologic analyses suggest different prevention strategies. Public Health Rep 1998;113:252-257.

4. Sacks JJ, Lockwood R, Hornreich J, et al. Fatal dog attacks, 1989-1994. Pediatrics 1996;97:891-895.

5. Centers for Disease Control and Prevention. Dog-bite-related fatalities—United States 1995-1996. MMWR Morbid Mortal Wkly Rep 1997;46:463-467.

6. Brogan TV, Bratton SL, Dowd MD, et al. Severe dog bites in children. Pediatrics 1995;96:947-950.

7. Calkins CM, Bensard DD, Partrick DA, et al. Life-threatening dog attacks: A devastating combination of penetrating and blunt injuries. J Pediatr Surg 2001;36:1115-1117.

8. Talan DA, Citron DM, Abrahamian FM, et al. Bacteriologic analysis of infected dog and cat bites. N Engl J Med 1999;340:85-92.

9. Wright JC. Reported cat bites in Dallas: Characteristics of the cats, the victims, and the attack events. Public Health Rep 1990;105:420-424.

10. Dire DJ. Cat bite wounds: Risk factors for infection. Ann Emerg Med 1991;19:973-979.

11. Glaser C, Lewis P, Wong S. Pet-, animal- and vector-borne infections. Pediatr Rev 2000;21:219-232.

12. Baker MD, Moore SE. Human bites in children: A six year experience. Am J Dis Child 1987;141:1285-1290.

13. Marr JS, Beck AM, Lugo JA. An epidemiologic study of the human bite. Public Health Rep 1979;94:514-521.

14. Schweich P, Fleisher G. Human bites in children. Pediatr Emerg Care 1985;1:51-53.

15. Hirschhorn RB, Hodge RR. Identification of risk factors in rat bite incidents involving humans. Pediatrics 1999;104:e35.

16. Ordog GJ, Balasubramanium S, Wasserberger J. Rat bites: 50 cases. Ann Emerg Med 1985;14:126-130.

17. Centers for Disease Control and Prevention. Rabies prevention-United States, 1999. MMWR Morbid Mortal Wkly Rep 1999;48(RR-1):1-21.

18. Anderson PJ, Zafar I, Nizam M, et al. Compartment syndrome in victims of dog bites. Injury 1997;28:717.

19. Abrahamian FM. Dog bites: Bacteriology, management and prevention. Curr Infect Dis Rep 2000;2:446-453.

20. Fleisher G. The management of bite wounds. N Engl J Med 1999;340:138-140.

21. Smith PF, Meadowcroft AM, May DB. Treating mammalian bite wounds. J Clin Pharm Ther 2000;25:85-99.

22. Dire DJ. Emergency management of dog and cat bite wounds. Emerg Med Clin North Am 1992;10:719-36.

23. Chen E, Hornig S, Shepherd SM, et al. Primary closure of mammalian bites. Acad Emerg Med 2000;7:157-61.

24. Boenning DA, Fleisher GR, Campos JM. Dog bites in children: Epidemiology, microbiology, and penicillin prophylactic therapy. Am J Emerg Med 1983; 1:17-21.

25. Dire DJ, Hogan DE, Walker JS. Prophylactic oral antibiotics for low risk dog bite wounds. Pediatr Emerg Care 1992;8:194-199.

26. Elenbaas RM, McNabney WK, Robinson WA. Prophylactic oxacillin in dog bite wounds. Ann Emerg Med 1982;11:248-251.

27. Elenbaas RM, McNabney WK, Robinson WA. Evaluation of prophylactic oxacillin in cat bite wounds. Ann Emerg Med 1984;13:155-157.

28. Jones D, Stanbridge T. A clinical trial using cotrimoxazole in an attempt to reduce wound infection rates in dog bites. Postgrad Med J 1985;61:593-594.

29. Rosen RA. The use of antibiotics in the initial management of recent dog-bite wounds. Am J Emerg Med 1985;3:19-23.

30. Skurka J, Willert C, Yogev R. Wound infection following dog bite despite prophylactic penicillin. Infection 1986;14:134-135.

31. Medeiros I, Saconato H. Antibiotic prophylaxis for mammalian bites. (Coch-ran Review). Cochrane Database Syst Rev 2001;2:CD001738.

32. Cummings P. Antibiotics to prevent infection in patients with dog bite wounds: A meta-analysis of randomized trials. Ann Emerg Med 1994;23:535-540.

33. Brook I. Microbiology of human and animal bite wounds in children. Pediatr Infect Dis 1987;6:29-32.

34. Moran GJ, Talan DA, Mower W, et al. Appropriateness of rabies post-exposure prophylaxis treatment for animal exposures. Emergency ID Net Study Group. JAMA 2000;284:1001-1007.

35. Diekma D, Reuter D. Arthropod bites and stings. Clin Ped Emerg Med 2001;2:155-167.

36. Visscher P, Vetter R, Camazine S. Removing bee stings. Lancet 1966;348:301-302.

37. deShazo R, Butcher B, Banks W. Reactions to the stings of the imported fire ant. N Engl J Med 1990;323:462-466.

38. Neugut AI, Ghatak AT, Miller RL. Anaphylaxis in the United States: an investigation into its epidemiology. Arch Intern Med 2001;161:15-21.

39. Uram R. What every pediatrician must know about anaphylaxis and anaphylactoid reactions. Pediatr Ann 2000;29:737-742.

40. Lee J, Greenes D. Biphasic anaphylaxis reactions in pediatrics. Pediatrics 2000;106:762-766.

41. Valentine M, Schuberth K, Kagey-Sobotka A, et al. The value of immunotherapy with venom in children with allergy to insect stings. N Engl J Med 1990; 323:1601-1603.

42. Clark R, Wethern-Kestner S, Vance M, et al. Clinical presentation and treatment of black widow spider envenomation: A review of 163 cases. Ann Emerg Med 1992;21:782-787.

43. Bond G. Snake, spider, and scorpion envenomations. Pediatr Rev 1999;20:147-151.

44. Wright S, Wrenn K, Murray L, et al. Clinical presentation and outcome of brown recluse spider bite. Ann Emerg Med 1997;30:28-32.

45. Sofar S, Shahak E, Gueron M. Scorpion envenomation and antivenom therapy. J Pediatr 1994;124:973-978.

46. Berg R, Tarentino M. Envenomation by the scorpion Centruroides exilicauda: Severe and unusual manifestations. Pediatrics 1991;87:930-933.

47. Bond G. Antivenin administration for Centruroides scorpion sting: Risks and benefits. Ann Emerg Med 1992;21:788-791.

48. Spach D, Liles W, GL Campbell GL, et al. Tick-borne disease in the United States. N Engl J Med 1993;329:936-947.

49. Parola P, Raoult D. Ticks and tickborne bacterial diseases in humans: An emerging infectious threat. Clin Infect Dis 2001;32:897-928.

50. Needham G. Evaluation of five popular methods of tick removal. Pediatrics 1985;75:997-1002.

51. American Academy of Pediatrics. Committee on Infectious Diseases. Prevention of Lyme disease. Pediatrics 2000;105:142-147.

52. Poland G. Prevention of Lyme disease: A review of the evidence. Mayo Clin Proc 2001;76:713-724.

53. Nadelman R, Nowakowski J, Fish D, et al. Prophylaxis with single-dose doxycycline for the prevention of Lyme disease after an Ixodes scapularis tick bite. N Engl J Med 2001;345:79-84.

54. Bond G. Controversies in the treatment of pediatric victims of crotalinae snake envenomation. Clin Ped Emerg Med 2001;2:192-202.

55. LoVecchio F, DeBus DM. Snakebite envenomation in children: A 10-year retrospective review. Wilderness Environ Med 2001;12:184-189.

56. Walter F, Bilden E, Gibly R. Envenomations. Crit Care Clin 1999;15:353-386.

57. McKinney P. Out-of-hospital and interhospital management of Crotaline snakebite. Ann Emerg Med 2001;7:168-174.

58. Burgess J, Dart R, Egen N, et al. Effects of constriction bands on rattlesnake venom absorption: A pharmacokinetic model. Ann Emerg Med 1992;21: 1086-1091.

59. Bush S, Hegewald K, Green S, et al. Effects of negative pressure venom extraction device (Extractor) on local tissue injury after artificial rattlesnake envenomation in a porcine model. Wilderness Environ Med 2000;11: 180-188.

60. Zamudio K, Hardy D, Martins M, et al. Fang tip spread, puncture distance and suction for snake bite. Toxicon 2000;38:723-728.

61. Hall E. Role of surgical intervention in the management of crotaline snake envenomation. Ann Emerg Med 2001;37:175-180.

62. Dart R, Gustafsen R. Failure of electric shock treatment for rattlesnake envenomation. Ann Emerg Med 1991;20:659-661.

63. Rawat S, Lang G, Smith D, et al. A new antivenom to treat Eastern coral snake (Micrurus fulvius) envenoming. Toxicon 1994;32:185-190.

64. Dart R, McNally J. Efficacy, safety, and use of snake antivenin in the United States. Ann Emerg Med 2001;37:181-188.

65. Dart R, Siefert S, Carroll L, et al. Affinity-purified, mixed monospecific crotalid antivenom ovine Fab for the treatment of crotalid venom poisoning. Ann Emerg Med 1997;30:33-39.

66. Package insert and product information for AVFab (CROFAB™ Crotalid polyvalent immune Fab (ovine)), Protherics Inc. Nashville, TN. (www.protherics.com/CroFab_PI_0301.pdf; Accessed 4/16/2002.)