Authors
Maria Ortega Tsiu, MD, MBA, Resident Physician, Stanford/Kaiser Emergency Medicine Residency, Stanford University Medical Center, Department of Emergency Medicine, Stanford, CA
Robert L. Norris, MD, Stanford University Medical Center, Department of Emergency Medicine, Stanford, CA
N. Ewen Wang, MD, Professor of Emergency Medicine, Associate Director Pediatric Emergency Medicine, Stanford School of Medicine, Stanford, CA
Peer Reviewer
John Cheng, MD, Pediatric Emergency Medicine Associates, LLC, Atlanta, GA
To reveal any potential bias in this publication, and in accordance with Accreditation Council for Continuing Medical Education guidelines, we disclose that Dr. Tsiu (author), Dr. Norris (author), Dr. Wang (author), and Dr. Cheng (peer reviewer) report no relationships with companies related to the field of study covered by this CME activity.
EXECUTIVE SUMMARY
- Antibiotics are not indicated for all bite wounds, but are recommended for human bites and high-risk bite wounds from cats and dogs.
- Fight bites should be treated with antibiotics and washed out in the operating room.
- An intercanine distance of > 3 cm on a human bite wound found on a child should raise the clinician’s suspicion for non-accidental trauma.
- The two families of terrestrial venomous snakes in North America are Viperidae (subfamily Crotalinae — the pit vipers [rattlesnakes, cottonmouth water moccasins, copperheads]) and Elapidae (coral snakes).
- The diagnosis and treatment of spider envenomations is clinical. Black widow spider antivenom should be administered with caution. In North America, there is no antivenom available for brown recluse spiders.
“When the dog bites, when the bee stings / When I’m feeling sad, I simply remember my favorite things, And then I don’t feel so bad.”
– Oscar Hammerstein II
Case Study
A 4 year-old girl presents to the emergency department (ED) with a laceration through her upper lip that was caused by a bite from a stray dog. She is otherwise well-appearing and is playing with a toy. What is your management plan? What medications will you administer? Is the patient at risk for infection?
Introduction
As a consequence of their playful and curious nature, children not uncommonly present to the ED with bite injuries; in fact, more than half of bite victims in the ED are children.1 Although envenomations are infrequent, the relatively high dose of venom per body weight in a young child can lead to significant effects. This article will discuss the key clinical features and management of bites from dogs, cats, and humans, as well as envenomations from snakes and spiders. Although not exhaustive, this review will provide a framework for the care of children who have sustained a bite or possible envenomation.
Dog, Cat, and Human Bites
Epidemiology. With pet ownership so widespread, the ED provider will frequently care for children with cat or dog bites. Recent sources have cited that 36.5% of households in the United States own at least one dog and 30.4% own at least one cat.1 An estimated 4.5 million dog bite-related injuries occur in the United States each year, and there are approximately 20-30 fatal dog injuries each year.1-3 These dog bite injuries are more common in children, frequently involve the patient’s extremities, and most commonly result from the family pet.1,4 It is estimated that there are approximately 300,000 cat bites per year in the United States.5 Patients are thought to be less likely to seek medical care for cat bites than dog bites.1,6
Human bites are considered to be the third most common mammalian bite, although true incidence is unknown, as it is thought that they are likely underreported.1,5 In children, human bite injuries have a bimodal distribution — most commonly occurring in toddlers and early teenagers.5 Toddlers may bite other toddlers and family members, while school-age children may sustain human bites as a result of play and sports injuries, and adolescents possibly as a part of sexual activity.5 These injuries may also be the result of non-accidental trauma. Approximately 1-3% of human bites are considered to be secondary to child abuse.7 Certain clinical features should increase the physician’s suspicion for non-accidental trauma, including bite size and location, especially if near genitalia. The bite was likely caused by an adult if the intercanine distance is > 3 cm (distance between cuspid tips found on the wound), and appropriate authorities should be involved as indicated.7,8 Human bites in children are usually on the face, upper extremities, or trunk, but a careful examination of all skin surfaces should be conducted.7 Special attention should also be made to hand wounds including the possibility for a “fight bite” injury (discussed below).
Pathophysiology. Bites cause obvious mechanical damage, but also have a risk of infection due to inoculation with mouth flora. The risk of infections depends on factors such as 1) the mechanism (cat bites tend to involve more puncture-type inoculation whereas dog bites tend to cause lacerations and/or macerated tissue), 2) the location of the bite, and 3) the possible pathogens. This article will not discuss the management of extensive tissue damage and mauling, but rather, the assessment and initial treatment of relatively simple cat, dog, and human bites.
The most commonly isolated microbes from dog bites are Pasteurella spp, with other common aerobic isolates including Streptococcos spp, Staphylococcus spp, Moraxella, and Neisseria. Pasteurella is also the most commonly isolated pathogen from cat bites, although Streptococcus and Staphylococcus spp are also common.5,9 Human bites commonly involve Eikenella, Streptococcus viridans, Staphylococcus spp, and Corynebacterium. With high-risk human bites, based on history (outside the scope of this article), the possibility of transmission of viral infections including hepatitis B virus, hepatitis C virus, and human immunodeficiency virus (HIV) must also be considered.5
Clinical Presentation. In mammalian bites, the ED provider must assess the extent of trauma (including the possibility for tendon, vascular, and nerve injury), penetration of bony cortex or fracture, penetration of the joint space, and non-accidental trauma. A “fight bite” injury results from a clenched fist impacting the mouth/teeth and may appear to be an innocuous laceration/abrasion over the dorsal metacarpalphalangeal (MCP) joint, when in fact it is a deep injury with risk for septic arthritis. If penetration of the flexor sheath occurs from a bite, this can result in flexor tenosynovitis, and depending on the timing of presentation, the patient may present with Kanavel’s signs in the affected finger: 1) held in slight flexion, 2) tenderness of the synovial sheath, 3) fusiform swelling of the digit, and 4) pain on passive extension.5,10 Key components of the history of present illness include documenting when the injury occurred, whether the animal was known, and the context in which the bite occurred. Immunization status of both the animal and the patient and whether the patient has any comorbidities will also guide management.
Diagnostic Testing. Laboratory tests are rarely helpful in guiding management of the mammalian bites discussed here. Radiography, however, is useful and should be used liberally in nearly all types of pediatric bite wounds given the potential for significant morbidity for infections involving bones or joints.5 Although up to 70% of radiographs taken to evaluate fight bites demonstrated foreign bodies, fractures, joint space narrowing, and air, approximately 16.5% of fight bites had negative results on exam and radiography despite joint penetration.5
In the rare case of severe human bites (deep with significant tissue damage), transmission of blood-borne diseases, such as HIV and hepatitis viruses, should be considered; however, these are out of the scope of this article.
Treatment and Management. Wound Care. Local wound management should include analgesia, thorough irrigation, debridement as needed, and closure if appropriate. Analgesia can greatly facilitate wound irrigation and can come in several forms — local infiltration of anesthetic, intravenous, or intranasal opioids or sedatives, oral analgesics, and in some cases dissociative agents such as ketamine or nitrous oxide. The choice of agent depends on the clinical situation and the provider’s comfort with each medication. The importance of wound irrigation cannot be emphasized enough for any bite wound. Wounds can be irrigated with any clean solution. Although normal saline is often used, studies show no increase in infection from tap water irrigation. There is no need to add antiseptic solutions to the irrigation fluid. General consensus is that pressure irrigation should be used for bite wounds from mammals unless it is a puncture wound.11 Generally, irrigation with 50-100 mL of clean solution per cm of laceration length via a large-volume syringe attached to an 18-gauge catheter/needle (pressure of 11-31 pounds per square inch) is sufficient. Manually squeezing punctured irrigation solution containers is considered to be inadequate for pressure irrigation.12
Wound closure in bites increases the risk of infection; thus, the risks and benefits of wound closure should be carefully discussed with the parents and patient.5,13 Some wounds may be able to be well-approximated with adhesive strips, but in situations where this is not the case and there are important cosmetic considerations (e.g., the face), wound closure with sutures is likely indicated. Fortunately, face wounds seldom become infected, unlike hand wounds — all of which should be discussed with the patient.11 Another option for wound repair in a high-risk bite is delayed primary closure.13,14 Following wound care, the wound should be dressed and, in the case of an extremity wound, immobilized. All patients should have their wounds reexamined within 1-2 days.5
Antibiotic Prophylaxis. Appropriate wound care decreases the infection risk of bites substantially.9 Prophylactic antibiotics should be prescribed to patients in the following situations: older (age > 50 years), chronic alcohol users, asplenia (functional or anatomical), immunocompromised, including diabetic, preexisting edema in the area of the bite, underlying vascular disease, bite that occurred more than 12 hours prior to presentation, bite over a high-risk location (on a hand, joint space, foot, or genitals), human bites, or puncture wounds (often seen with cat bites).15-18 Antibiotics are also advised when bite wounds are closed primarily, but are not routinely necessary for bites allowed to heal by secondary intention.1,14,16,19
Fight bites penetrating the MCP joint and wounds penetrating a flexor tendon sheath have the potential for significant infectious morbidity. Studies have shown that local wound care alone is often inadequate for these injuries.20 Aside from thorough irrigation, antibiotics should be administered promptly, and orthopedic consultation is recommended, as surgical exploration is often indicated (see Table 1). There is insufficient evidence to recommend starting parenteral vs oral antibiotics, but given the theoretical potential that effective tissue levels of the antibiotic could be reached faster with parenteral antibiotic therapy, giving at least the first antibiotic dose parenterally should be considered.7,20-22
Prophylactic antibiotics should cover the common pathogens associated with dog, cat, and human bites, and for that reason, amoxicillin-clavulanate is often chosen (see Table 1).11 For patients with a true penicillin allergy (systemic reaction, allergic reaction rather than side effect), clindamycin plus trimethoprim-sulfamethoxazole can be substituted.11,13,15
Table 1. Common Mammalian Bite Pathogens and Antibiotics |
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Most Commonly Isolated Pathogens5,9 |
Antibiotic Therapy11,13,15 |
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Dog bite |
Pasteurella canis, Streptococci, Staphylococci |
As below, when indicated* |
|
Cat bite |
Pasteurella multocida, Streptococcus, Staphylococcus |
As below |
|
Human bite* (including closed fist injuries) |
Eikenella, Viridans streptococcus, Staphylococcus, Corynebacterium |
PO regimen: Amoxicillin-clavulanate 40-45 mg/kg daily divided into BID or TID dosing for 3-5 days IV regimen: ampicillin-sulbactam 100-150 mg/kg daily divided into QID dosing for 10-14 days** |
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*Article elaborates on which bites necessitate antibiotics. **In case of penicillin allergy, clindamycin plus trimethoprim-sulfamethoxazole can be substituted. BID refers to twice daily dosing. TID refers to dosing three times per day. QID refers to dosing four times per day |
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Vaccination. Like all wounds, bites carry a risk of infection from Clostridium tetani, bacteria that commonly live in the soil. If the wound is clean with only a small injury noted, tetanus vaccination within the last 10 years is sufficient; however, if the wound is dirty, tetanus vaccination within 5 years is recommended (DTaP < 7 years old, Tdap ≥ 7 years old). In the setting of a high-risk wound, the administration of tetanus immune globulin is indicated if the patient has had fewer than three (usually < 6 months of age) or an unknown number of tetanus vaccinations.5,11
Rabies is a neurotropic virus that results in progressive central nervous system deterioration and almost invariably leads to death. Symptoms may begin anywhere from weeks to months, and possibly years, after exposure, depending on the inoculum of virus and the distance the wound is from the central nervous system. Symptoms may include anxiety, dysesthesias, hydrophobia, paralysis, and dysautonomia.11 Rabies virus is transmitted in the saliva of an infected animal. More than 85% of reported rabies cases are caused by wild animals, with raccoons, skunks, foxes, and bats being the main reservoirs of the virus in North America.11 Rabies is rarely transmitted as a result of dog, cat, or human bites in the United States. However, if a patient presents with an unprovoked bite from an unknown cat or dog, it is recommended that the wound surface be washed with copious amounts of a virucidal solution, such as 1% povidone-iodine, and then irrigated with a clean solution.11,23 If there is a concern about an animal having rabies, contact Animal Control so that the animal in question can be evaluated. If the animal can be observed for 10 days, then no further treatment is needed on the initial evaluation. If the animal is healthy at the end of the 10-day period, it does not have rabies. If rabies is confirmed or if the animal cannot be obtained for observation in a situation with high potential for rabies exposure, then the rabies vaccine should be given in the standard post-exposure prophylaxis four-dose regimen per CDC guidelines on days 0, 3, 7, and 14.24-26 Unvaccinated patients who are at high risk for rabies exposure (e.g., high-risk animal based on species, animal behavior [i.e., unprovoked attack], or geographic setting) should receive human rabies immune globulin (HRIG), which is administered via local infiltration of the wound with HRIG 20 IU/kg body weight, in addition to the rabies vaccine (see Table 2).26 The first dose of the vaccine and HRIG should not be administered in the same extremity, but subsequent vaccines in the series can be.27 Although rabies is considered invariably fatal, there has been a recent article of interest that may dispute this accepted fact.28 A small community in Peru was recently found to have six individuals with rabies-neutralizing antibodies present in their serum who had not before been vaccinated or received treatment for rabies, calling into question the commonly held belief that rabies is invariably fatal.28 If there is any question as to whether to begin post-exposure prophylaxis, the medical provider should consult the local health department.
Table 2. Rabies Post-exposure Prophylaxis |
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Rabies Vaccination and Human Rabies Immune Globulin (HRIG) – Dosing and Administration Route11,26 |
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Rabies vaccine 1 mL, intramuscular injection into deltoid muscle on days 0, 3, 7, 14*
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HRIG Local infiltration of wound with 20 IU/kg body weight |
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*If the patient has previously been vaccinated, thoroughly clean the wound and give the patient two booster vaccines on days 0 and 3. HRIG is not indicated in patients with adequate pre-exposure rabies immunization. |
Snakebites
Epidemiology. Venomous snakebites, while infrequent, require special consideration in children because of the potentially large venom load received per unit body weight. In the United States, an estimated 7000-8000 people are bitten by venomous snakes each year, with approximately six deaths annually.29-31 In North America, two groups of venomous snakes are medically important — the pit vipers (Family Viperidae, subfamily Crotalinae) and the coral snakes (family Elapidae). North American pit vipers include rattlesnakes, cottonmouth/water moccasins, and copperheads. Their venom causes tissue damage and hematologic toxicity, resulting in the potential for significant tissue edema, necrosis, and coagulopathy.32,33 Pit vipers are found throughout most of North America and account for the majority of snake envenomations within this region, with rattlesnakes causing the greatest morbidity and mortality.32,34
Coral snakes are found in the southwestern and southeastern United States and much of Mexico.33 Coral snake venom is largely neurotoxic, and can cause paralysis and respiratory failure. Coral snakes have much smaller fangs than do pit vipers, making it harder for them to envenomate humans. Consequently, coral snake bites rarely cause a fatal injury.34,35 Coral snakes are the snakes referenced in the childhood saying “red on yellow, kill a fellow; red on black, venom lack,” which is used to remind people of the subtly different appearance of coral snakes and harmless king snakes and milksnakes (see Figure 1).33 This color pattern, however, is unreliable in Latin America.36
Figure 1. Rattlesnake, Coral Snake, and King Snake |
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Micrurus fulvius — Eastern coral snake "Red on yellow, kill a fellow; red on black, venom lack.
Lampropeltis triangulum campbelli — Pueblan milksnake
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Crotalus oreganus — Northern Pacific rattlesnake
Photos courtesy of Michael Cardwell |
Pit Vipers
Pathophysiology. Approximately 75% of pit viper bites result in envenomation, with the remainder being “dry bites.”31 There are numerous variables that can explain why a snake may deliver a dry bite, but those will not be covered in this article. The bite pattern on the skin is unreliable in identifying a pit viper bite, as there may be one or multiple puncture wounds from the snake’s fangs and accessory teeth.34 Pit viper venoms are complex and contain a number of constituents, including metalloproteinases that damage basement membranes of capillary endothelial cells at the site of the bite and more remotely. As a result, there is considerable damage to the capillaries, resulting in tissue edema. Resulting platelet aggregation can occlude damaged capillaries. Pit viper venoms can also directly activate the coagulation cascade via thrombin-like enzymes that stimulate formation of abnormal, unstable fibrin clots that are rapidly lysed. This results in a venom-induced consumptive coagulopathy (VICC) with associated thrombocytopenia and hypofibrinogenemia, making hematologic laboratory values useful in directing management.34,37 Although laboratory values may resemble those seen in disseminated intravascular coagulation (DIC), VICC tends to have a quicker onset and resolution than DIC, and typically does not directly result in end-organ damage.38,39
Clinical Presentation. Most pit viper envenomations present with early local pain and swelling. Systemic findings may include an odd (possibly metallic) taste in the mouth, nausea, vomiting, muscle fasciculations (myokymia), tachycardia, and hypotension. Progressive edema and lymphadenopathy can result in severe pain and the affected limb may become tense, raising the concern for compartment syndrome.34, 37, 40 Most of the edema is subcutaneous, however, and elevated compartment pressures are rare (discussed below). In pediatric patients, the onset of clinical findings, including edema, can be delayed, so monitor up to 24 hours.34 Despite laboratory values commonly consistent with VICC, clinically significant hemorrhage is rare.34
Diagnostic Testing. Initial laboratory studies should include a complete blood count, prothrombin time, D-dimer, and fibrinogen level. These values will help evaluate for thrombocytopenia, coagulopathy, and hemoconcentration, as third-spacing ensues as a result of the cytotoxic mechanism of action of the venom.38 Platelet and fibrinogen levels are especially important, as they help guide initiation of antivenom therapy.41 A metabolic panel may be helpful in guiding volume resuscitation, and a creatine phosphokinase (CPK) level may detect evidence of rhabomyolysis in pit viper bites. A sample for blood typing and screening should be sent to the laboratory early for use in the rare case where blood products become necessary. For patients with signs of systemic toxicity or progressive findings on exam, baseline and interval platelet counts and fibrinogen levels should be monitored.
Treatment and Management. The only first aid measure truly helpful following a pit viper bite is expeditious delivery of the patient to a hospital capable of administering antivenom. Tourniquets, wraps, incision, suction, cooling, electric shocks, and the like should all be avoided. Any jewelry that might become constrictive should be removed, and the extremity should be elevated and immobilized for comfort as the patient is transported to a hospital setting.37,42 It is not necessary or advisable to kill or capture the snake.
Initial priorities on hospital arrival are stabilizing the patient’s airway, breathing, and circulation as needed. Swelling at the bite site should be assessed for progression every 15 minutes by either marking the leading edge of tissue edema or marking and measuring limb circumferences. If there are no signs of progressive local findings or systemic toxicity on examination or laboratory markers, no antivenom needs to be administered during initial treatment; but adult patients should be observed for a minimum of 8 hours and pediatric patients for at least 24 hours to rule out delayed onset of envenomation.34,37
The current recommended antivenom for use in the United States and Canada is Crotalidae Polyvalent Immune Fab (Ovine) (CroFab; BTG International, Inc.) (FabAV). A separate polyvalent antivenom (Antivipmyn; Instituto Bioclon) is used in Mexico, and a second, novel antivenom (Anavip) produced by the same company has been found to be effective in the United States, but will not be further discussed here.43 Indications for giving FabAV to a North American pit viper bite victim are:
- Progressive local tissue effects (e.g., worsening soft tissue swelling, edema extending beyond the area of demarcation — with special attention to swelling that crosses a joint line) OR
- Any evidence of systemic toxicity (systemic signs or symptoms including hemodynamic instability) OR
- Laboratory abnormalities (e.g., thrombocytopenia, coagulopathy)34,37,44,45
Relative contraindications to FabAV are hypersensitivity to the product, papaya, or papain. However, the benefits of administration should be weighed against the risk of not treating the envenomation.32
FabAV is packaged in lyophilized form and must be reconstituted carefully prior to administration. Each vial should be reconstituted by slowly injecting 18 mL of normal saline into the vial and then gently agitating (not shaking) until the proteins are fully reconstituted. It is critical that the mixture not be allowed to foam, as this reduces the amount of Fab solubilized for administration. This reconstitution process can take several minutes, but the ED provider may be the only person aware of this necessary precaution in the patient’s care.32,46 All vials to be given in the initial dose should be placed in a 250 mL bag of normal saline. The volume of normal saline can be reduced based on the provider’s judgment if the total volume is thought to be excessive based on the weight of the child.46 The intravenous tubing can be primed with normal saline.
The starting dose for FabAV is 4-6 vials given over 1 hour (see Table 3). If the patient is hemodynamically unstable, increase the initial dose to 8-12 vials.34,37 Antivenom is dosed based on the potential venom load received by the victim, not on the victim’s size. Thus, there is no adjustment in dose based on the patient’s age or weight.32 Start the infusion slowly, with the physician at the bedside to intervene if a reaction occurs (discussed below). If no reaction occurs, increase the rate of infusion so that it is completed in 1 hour. If an acute reaction occurs, stop the infusion and treat the reaction with epinephrine, antihistamines, and steroids. Then, restart and complete the infusion while closely monitoring the patient. It may help to further dilute the dose and to administer at a slightly slower rate. If the reaction was severe, then assess the merits of attempting to proceed with administration considering the severity of envenomation.47
Table 3. Crotalidae Polyvalent Immune Fab |
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Crotalidae Polyvalent Immune Fab Preparation and Dosing34,37 |
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Reconstitution – Swirl, Don’t Shake!
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Dosing
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Recommended Source for Assistance: Regional Poison Control Center (800) 222-1222 |
After administering FabAV, reassess the patient over the next hour and repeat laboratory studies. If the patient has not stabilized (e.g., continued progression of swelling or lack of improvement in repeated labs), repeat the starting dose and continue this pattern until achieving stability. It may take a few hours for coagulation studies to return to normal, even after administering adequate antivenom, as it takes time for the liver to replace consumed coagulation proteins. Once stable, dose the patient with two vials of FabAV every 6 hours for three more doses to prevent recurrence of toxicity.46 Although some centers have opted to withhold maintenance dosing, choosing instead to monitor and treat recurrence if and when it occurs, this decision should be made in consultation with a Poison Control Center at (800) 222-1222. Contact a Poison Control Center early for treatment recommendations and also to help locate a supply of antivenom.32,34
Since FabAV is a heterologous serum product, it carries a risk of inducing anaphylactoid reactions, thus the admonition of the physician being at the bedside while initiating the infusion. All medications and equipment necessary to intervene in the event of an acute adverse reaction should be immediately available (epinephrine, airway equipment, etc.). The incidence of anaphylactoid reactions to FabAV is approximately 8% with most cases being mild.48 There is also a risk of delayed serum sickness that occurs in approximately 13% of patients, but serum sickness is easily treated with steroids and antihistamines.48
The safety of FabAV in children has now been documented in several studies.32,49,50 Researchers at Arkansas Children’s Hospital looked at 204 snakebite admissions to their hospital, 82 of which received FabAV. Among those 82 pediatric patients, six (7.3%) experienced an adverse reaction characterized as mild, allergic symptoms.49
Pain control for victims of pit viper envenomation should be through the use of acetaminophen or opioids rather than nonsteroidal anti-inflammatory drugs due to their antiplatelet effects. In terms of wound care, the bite site should be cleaned and splinted. After administering antivenom, elevate the extremity to reduce swelling. Update tetanus immunization as indicated. Keep intact any vesticles that develop. If they rupture, debride and treat with wet-to-dry dressings. .45 There is no role for prophylactic antibiotics unless the bite site was contaminated with an ill-advised pre-hospital incision or mouth suction.51,52 Excision of clearly necrotic tissue should await full reversal of coagulopathy. Early physical therapy can help speed functional recovery.47
Following a serious pit viper bite, the involved extremity can become severely swollen and very painful, often raising concern for a possible compartment syndrome. Again, the majority of swelling in these cases is subcutaneous, and raised intracompartmental pressures are relatively rare.34,37,41,44 If there is concern for compartment syndrome, continue antivenom administration, place the limb at approximately heart level, and, in consultation with a surgeon, check compartmental pressures. If the pressures are elevated above 30-40 mmHg, attempt a trial of intravenous mannitol (1 gm/kg), although evidence of its benefit, as well as use of hyperbaric oxygen therapy, in snakebite-related compartment syndrome is anecdotal.53, 54
If the compartmental pressures remain elevated after 1 hour, then consider proceeding with fasciotomy following informed consent. While there is evidence that fasciotomy might increase muscle necrosis, it may still be necessary to salvage neurologic function.55,56 Bites to the digits may also require surgical release (digital dermotomy) if swelling becomes extreme.57
As mentioned, clinically significant bleeding is uncommon following pit viper envenomation, despite the fact that many such patients have laboratory confirmed VICC. The treatment for VICC is expeditious, adequate antivenom. Rarely are blood products, such as packed red blood cells, platelets, cryoprecipitate, and fresh frozen plasma, required, and these are indicated only when antivenom has not been sufficient. If blood products are deemed necessary, continue antivenom treatment as well to avoid further fueling of the VICC.58
At discharge, warn families about the possibility of delayed serum sickness and instruct them to return if symptoms arise. Schedule a follow-up for wound checks and repeat laboratory testing at 48-72 hours after the last dose of FabAV and again at 5 to 7 days to rule out delayed onset or recurrent VICC. If coagulation studies are found to be significantly abnormal on follow-up, obtain assistance from a Poison Control Center, as further FabAV may be needed.37
Given the complexity in managing pit viper envenomation, it is always reasonable to seek guidance from an envenomation expert or a regional Poison Control Center.
Coral Snakes
Pathophysiology. The neurotoxins of coral snake venoms have pre-synaptic and post-synaptic effects, limiting the release of acetylcholine at the synapse and its ability to bind to its receptors.59 This can manifest as ptosis, difficulty swallowing, skeletal muscle weakness, fasciculations, respiratory distress, and respiratory failure.34
Clinical Presentation. Bites from coral snakes do not result in significant local tissue effects other than mild swelling and discomfort. Onset of neurotoxicity can be delayed for many hours, and, therefore, it is prudent to admit any child with a potential coral snake bite for at least 24 hours of observation. The initial evidence of neurotoxicity may be a slight alteration in level of consciousness, mild ptosis, or some difficulty swallowing.34 Once findings occur, the progression to potentially fatal respiratory failure can be rapid.
Diagnostic Testing. There are no laboratory tests of diagnostic value in coral snake bites. Coral snake venoms do not cause coagulopathy or necrosis. Any comorbidities should guide laboratory testing.47
Treatment and Management. Currently, production of coral snake antivenom in the United States has ceased, with a small stockpiled supply still available. If a patient presents after having been bitten by a coral snake, contact a regional Poison Control Center early to evaluate logistics for obtaining 3 to 5 vials of the remaining stock for use if the patient develops any neurologic abnormalities.34 The dose does not change based on weight, as the dose of venom does not vary based on patient’s size. While there is a likely effective coral snake antivenom produced in Mexico, it is not commercially available in the United States; the future of antivenom therapy for coral snake bites in this country is unclear. There is no benefit to using pit viper antivenom for coral snake bites. It may be that management of serious coral snake bites will have to rely entirely on sound supportive care, especially aggressive airway management and respiratory support. Prolonged (up to a week) intubation and ventilator support may be necessary.60 In a review of coral snake bites from 1983-2009, there were no fatalities among 1337 envenomations.10 Nevertheless, don't discount a potential fatal outcome. Admit all patients bitten by a possible coral snake, regardless of presence or absence of symptoms, for monitoring for at least 24 hours.35 Antibiotics are not routinely recommended in treatment of coral snake bites.51,52
Spider Bites
Epidemiology. It is not uncommon for patients to present to the ED with lesions (blisters, bullae, or eschars) that they have “self-diagnosed” as spider bites. In most cases these lesions are unrelated to spiders, but rather are the result of bites by other arthropods or simple skin abscesses or cellulitis and should be treated accordingly.34,61 Although it may be difficult, obtaining a good history of the patient’s presentation is key to diagnosis of an actual spider bite. Young patients may be unable to relate the history of a bite, so a careful history from the parent about exposure risk coupled with appropriate clinical suspicion is often necessary to make this diagnosis.
In North America, there are only two spiders that have the ability to cause significant harm to humans — widow spiders (Latrodectus spp) and recluse spiders (Loxosceles spp). Most other spiders either have venom that produces nothing more than mild pain and local irritation, or they are incapable of biting through human skin. In the United States, black widow spiders (L. mactans, L. hesperus, or L. variolus) are found in every state except Alaska. The female black widow has a characteristic red hourglass on her ventral side, and only the female is large enough to cause human envenomation.34,62 Widow spiders tend to live under stones, shrubs, and logs when in the natural environment. In human habitats, they have commonly been found in outdoor toilets, but can be seen in cabins and homes as well.62 Recluse spiders, such as the brown recluse (L. reclusa), may be somewhat more difficult to definitively identify (see Figure 2), can be various shades of brown, and range from 1-2 cm in size. Almost all of the recluse spiders have a violin-shaped dark marking on their back, thus the common name “fiddle-back spider.”33 Since they primarily live in hidden places, often under rocks or household objects, curious children can understandably be the unsuspecting victims of their bites. In the United States, recluse spiders are mainly found in the southwestern and southeastern states.34,62
Figure 2. Black Widow and Brown Recluse Spiders |
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Female Black Widow Spider Ventral abdomen — note red hourglass pattern
Courtesy of Dr. M. Amieva Brown Recluse Spider Note violin-shaped marking on dorsal cephalothorax (where legs join body)
Courtesy of Dr. M. Amieva |
Widow Spiders
Pathophysiology. Widow spiders mediate their effects through a neurotoxin (alpha-latrotoxin) that works on pre-synaptic membranes causing dramatic release of acetylcholine, epinephrine, and norepinephrine, resulting in significant muscle contractions, and adrenergic and cholinergic clinical features.33
Clinical Presentation. In the case of a widow spider bite, the patient may feel immediate sharp pain at the bite site, and commonly presents with an erythematous lesion with an area of central pallor. Of patients with these lesions, approximately 25% will progress to latrodectism, characterized by severe muscle pain and spasms, including potential for a rigid abdomen, which can be misdiagnosed as a surgical abdomen (though rebound is absent).34,44,62-65 As a result of epinephrine and norepinephrine release, autonomic manifestations may be seen, including tachycardia, hypertension, and diaphoresis (particularly facial diaphoresis). Less common findings include priapism, fever, and paresthesias.44,62
Diagnostic Testing. Laboratory testing is rarely indicated but when systemic manifestations are present, consider the following: complete blood count, basic metabolic panel, CPK, and an electrocardiogram due to adrenergic surge.10,66
Treatment and Management. The tenet of therapy in suspected widow spider bites is aggressive supportive care. This includes the titration of benzodiazepines and opioids for pain control and muscle spasms, wound care, and tetanus immunization update as indicated.33,34 Pediatric patients may be unable to fully explain the context of their injuries or communicate that they were bitten by a spider, which can lead to misdiagnosis. There are reports of black widow spider bites mistakenly being diagnosed as appendicitis in the past with fatalities that have been reported in such cases.33 In a review of black widow spider bites from 1983-2009, there were no fatalities.10
Symptoms related to widow spider envenomation usually largely resolve within 24-96 hours with supportive care alone. If pain cannot be controlled or if the patient becomes hemodynamically unstable, antivenom should be considered.33 Black widow spider antivenom is effective for all Latrodectus species, but has the potential for significant side effects. It is equine-derived and carries the risk of acute reactions and serum sickness — two deaths have been reported secondary to anaphylactoid reactions caused by the antivenom.33,34,64,67 When considering using this antivenom, it is recommended that the provider consult with a Poison Control Center.34 Although intravenous calcium gluconate previously was recommended as part of treatment for widow spider bites, there are data demonstrating its lack of efficacy and it is no longer recommended.34,68 Most cases of widow spider envenomation require admission for observation.
Recluse Spiders
Pathophysiology. Recluse spider venom contains hyaluronidase and sphingomyelinase D — enzymes that lyse cell walls and can produce dermonecrotic lesions and potentially hemolysis, which can progress to DIC.33,44,69,70
Clinical Presentation. The actual bite of a recluse spider is generally painless and, therefore, most patients present in a delayed fashion, never having seen the offending spider.70 Presenting symptoms fall on a spectrum, ranging from minimal discomfort and erythema to significant skin necrosis and systemic effects (e.g., fevers, gastrointestinal symptoms, and arthralgias), which may take up to 72 hours to develop.34,62 The wound may progress from a necrotic base that may develop with an area of ischemia, appearing as a whitish halo, and with surrounding erythema — forming the commonly described “red, white, and blue” or “bullseye” wound.71 Systemic manifestations are rare but are seen more commonly in pediatric patients.34,69
Diagnostic Testing. When systemic manifestations occur, initiate laboratory testing for DIC, hemolysis, rhabdomyolysis, and renal injury and include serial hemoglobins, hemolysis labs, lactate, D-dimer, coagulation studies (prothrombin time, partial thromboplastin time, fibrinogen), type and screen, basic metabolic panel, and CPK. Hemolysis labs to consider include haptoglobin, lactate dehydrogenase, indirect bilirubin, and reticulocyte count.34,69
Treatment and Management. The mainstay of treatment is again supportive care and wound management. There is no antivenom available for these spiders in North America.33 Clean the wound and update the tetanus immunization as needed. Given that differentiating these wounds from skin infections can be challenging, maintain a low threshold for starting antibiotics (including coverage for methicillin-resistant Staphylococcus aureus). Since spider venoms tend to have temperature-dependent activity, there may be value in having the patient locally cool the wound several times per day for 72 hours (with precautions not to induce cold injury). The majority of recluse spider bite wounds heal well with standard conservative therapy. Analgesia should involve opioids rather than nonsteroidal anti-inflammatory drugs due to potential for coagulopathy. Check wounds on a daily basis until they are clearly improving. Any debridement of necrotic tissue should be done judiciously. If a wound is deemed to require skin grafting, delay for several weeks to allow venom effects to fully resolve lest the applied graft is lost.72 In the past, hyperbaric oxygen, dapsone, cyproheptadine, and nitroglycerin paste have all been proposed therapies, but none of these have sufficient evidence to support recommendation of their use.33,73 In the rare cases of suspected recluse spider bites with systemic involvement, admit and monitor patients until clearly clinically stable. Management of systemic toxicity relies on sound supportive care and fluid and electrolyte management. While there is no role for steroids (by any route) for managing the bite wound itself, there may be a role for systemic corticosteroids for patients with evidence of systemic hemolysis — to stabilize red cell membranes.74 If DIC does develop, transfusion of blood products may become necessary, and laboratory results can help guide management.
Disposition. In each of the bites and envenomations described, there is potential for significant morbidity and in some cases, mortality. Carefully follow up all wounds to assess for infection and wound healing. In all but the most trivial of envenomations, children should be admitted.
Conclusion
Children frequently present to the ED with bite wounds and occasionally envenomations. A thorough history, physical examination, and scrupulous wound care will serve these children well. Attention to immunization status, provision of analgesia, consideration of antibiotics, and consultation with a Poison Control Center when antivenom may be indicated will help the ED provider properly address the patient’s bite wound needs.
Case Discussion
The young girl is up to date with her tetanus. You arrange for intranasal midazolam and repair the laceration with absorbable sutures.
The police inform you that the dog has been taken to the local Animal Control center for behavior observation. You notify the mother and describe how this will affect whether her daughter will have to be immunized for rabies, although you think it will be unlikely given the statistics regarding rabies in dogs in the United States. The patient tolerates the laceration repair well, her mother is given a prescription for amoxicillin-clavulanate for 5 days, and she will follow up with her physician in 24 hours.
REFERENCES
- Ward MA. Bite wound infections. Clin Pediatr Emerg Med 2013;14:88-94.
- Sacks JJ, Kresnow M, Houston B. Dog bites: How big a problem? Inj Prev 1996;2:52-54.
- Langley RL. Human fatalities resulting from dog attacks in the United States, 1979-2005. Wilderness Environ Med 2009;20:19-25.
- Centers for Disease Control and Prevention. Non fatal dog bite-related injuries treated in hospital emergency departments — United States, 2001. MMWR Morb Mortal Wkly Rep 2003;52:605-610.
- Rempe B, Aloi M, Iskyan K. Evidence-based management of mammalian bite wounds. Pediatr Emerg Med Pract 2009;6:1-18.
- Steele M, Ma OJ, Nakase J, et al. Epidemiology of animal exposure presenting to emergency departments. Acad Emerg Med 2007;14:398-403.
- Kannikeswaran N, Kamat D. Mammalian bites. Clin Pediat 2009;48: 145-148.
- Kellogg N; American Academy of Pediatrics Committee on Child Abuse and Neglect. Oral and dental aspects of child abuse and neglect. Pediatrics 2005;116:1565-1568.
- Thomas N, Brook I. Animal bite-associated infections: Microbiology and treatment. Expert Rev Anti Infect Ther 2011;9:215-226.
- Marx JA, Hockberger RS, Walls RM. Rosen’s Emergency Medicine — Concepts and Clinical Practice. 8th ed. Philadelphia, PA: Elsevier Saunders; 2014.
- Committee on Infectious Diseases, et al. Red Book: 2012 Report of the Committee on Infectious Diseases. 29th ed. Elk Grove Village, IL: American Academy of Pediatrics; 2012.
- Gabriel A. Wound Irrigation. Medscape 2015 August 2, 2013. Available at: http://emedicine.medscape.com/article/1895071-overview. Accessed April 6, 2015.
- Moran GJ, Talan DA, Abrahamian FM. Antimicrobial prophylaxis for wounds and procedures in the emergency department. Infect Dis Clin North Am 2008;22:117-143.
- Chen E, Hornig S, Shepherd SM, Hollander JE. Primary closure of mammalian bites. Acad Emerg Med 2000;7:157-161.
- Nakamura Y, Daya M. Use of appropriate antimicrobials in wound management. Emerg Med Clin North Am 2007;25:159-176.
- Medeiros I, Saconato H. Antibiotic prophylaxis for mammalian bites. Cochrane Database Syst Rev 2001;2:CD001738.
- Talan DA, Abrahamian FM, Moran GJ, et al. Clinical presentation and bacteriologic analysis of infected human bites in patients presenting to emergency departments. Clin Infect Dis 2003;37:1481-1489.
- Merriam CV, Fernandez HT, Citron DM, et al. Bacteriology of human bite wound infections. Anaerobe 2003;9:83-86.
- Paschos NK, Makris EA, Gantsos A, Georgoulis AD. Primary closure versus non-closure of dog bite wounds. A randomised controlled trial. Injury 2014;45:237-240.
- Perron AD, Miller MD, Brady WJ. Orthopedic pitfalls in the ED: Fight bite. Am J Emerg Med 2002;20:114-117.
- Zubowicz VN, Gravier M. Management of early human bites of the hand: A prospective randomized study. Plast Reconstr Surg 1991;88:111-114.
- Patil P, Panchabhai T, Galwankar S. Managing human bites. J Emerg Trauma Shock 2009;2:186-190.
- Manning SE, Rupprecht CE, Fishbein D, et al. Human rabies prevention — United States, 2008: Recommendations of the Advisory Committee on Immunization Practices. MMWR Recomm Rep 2008;57:1-28.
- Centers for Disease Control and Prevention. Use of a reduced (4-dose) vaccine schedule for postexposure prophylaxis to prevent human rabies-recommendations of the Advisory Committee on Immunization Practice. Ann Emerg Med 2010;56:64-67.
- Rupprecht CE, Gibbons RV. Clinical practice: Prophylaxis against rabies. N Engl J Med 2004;351:2626-2635.
- Mittal MK. Revised 4-dose vaccine schedule as part of post-exposure prophylaxis to prevent human rabies. Pediatr Emerg Care 2012;29:1119-1121.
- Center for Disease Control and Prevention. Human Rabies Immune Globulin. Rabies — Medical Care. April 22, 2011. Available at: http://www.cdc.gov/rabies/medical_care/hrig.html. Accessed June 15, 2015.
- Friedrich MJ. Human rabies resistance. JAMA 2012;308:1081.
- Langley RL. Animal-related fatalities in the United States — an update. Wilderness Environ Med 2005;16:67-74.
- Parrish HM. Incidence of treated snakebites in the United States. Public Health Rep 1966;81:269-276.
- Russell FE. Clinical aspects of snake venom poisoning in North America. Toxicon 1969;7:33-37.
- Goto CS, Feng SY. Crotalidae polyvalent immune fab for the treatment of pediatric crotaline envenomation. Pediatr Emerg Care 2009;25:273-279.
- Holve S. Venomous spiders, snakes, and scorpions in the United States. Pediatr Ann 2009;38:210-217.
- Levine M. Pediatric envenomations: Don’t get bitten by an unclear plan of care. Pediatr Emerg Med Pract 2014;11:1-12.
- Norris RL, Pfalzgraf RR, Laing G. Death following coral snake bite in the United States — first documented case (with ELISA confirmation of envenomation) in over 40 years. Toxicon 2009;53:693-697.
- Minton SA. Snake Venoms and Envenomation. New York: Marcel Dekker, Inc.; 1971.
- Lavonas EJ, Ruha AM, Banner W, et al. Unified treatment algorithm for the management of crotaline snakebite in the United States: Results of an evidence-informed consensus workshop. BMC Emerg Med 2011;11:2. doi: 10.1186/1471-227X-11-2.
- Berling I, Isbister GK. Hematologic effects and complications of snake envenoming. Transfus Med Rev 2015;29:82-89.
- Isbister GK. Snakebite doesn’t cause disseminated intravascular coagulation: Coagulopathy and thrombotic microangiopathy in snake envenoming. Semin Thromb Hemost 2010;36:444-451.
- Tanen DA, Ruha AM, Graeme KA, et al. Rattlesnake envenomations: Unusual case presentations. Arch Int Med 2001;161:474-479.
- Swadron S, Nordt S. Rattle Snake Bites, in EM:RAP. June 2011. Podcast. Available at: https://www.emrap.org/episode/2011/june/rattlesnake. Accessed Nov. 12, 2014.
- Alberts MB, Shalit M, LoGalbo F. Suction for venomous snakebite: A study of “mock venom” extraction in a human model. Ann Emerg Med 2004;43:181-186.
- Bush SP, Ruha AM, Seifert SA, et al. Comparison of F(ab’)2 versus Fab antivenom for pit viper envenomation: A prospective, blinded, multicenter, randomized clinical trial. Clin Toxicol (Phila) 2015;53:37-45.
- Levine M, Ruha AM, Graeme K, et al. Toxicology in the ICU: Part 3: Natural toxins. Chest 2011;140:1357-1370.
- Norris RL. Venomous bites and stings. In: A Practical Guide to Pediatric Emergency Medicine. Amieva-Wang NE, ed. New York: Cambridge University Press; 2011: 242-247.
- CroFab full prescribing information. BTG International Inc. West Conshohocken, PA. 2014. Available at: http://www.crofab.com/. Accessed Feb. 23, 2015.
- Norris RL, Bush SP, Smith J. Bites by venomous reptiles in Canada, the U.S. and Mexico. In: Wilderness Medicine. 6th ed. Auerbach PS, ed. Philadelphia: Elsevier Mosby; 2012.
- Schaeffer TH, Khatri V, Reifler LM, Lavonas EJ. Incidence of immediate hypersensitivity reaction and serum sickness following administration of Crotalidae polyvalent immune Fab antivenom: A meta-analysis. Acad Emerg Med 2012;19:121-131.
- Farrar HC, Grayham T, Bolden B, et al. The use and tolerability of Crotalidae Polyvalent Immune FAB (Ovine) in pediatric envenomations. Clin Pediatr 2012;51:945-949.
- Pizon AF, Riley BD, LoVecchio F, Gill R. Safety and efficacy of Crotalidae Polyvalent Immune Fab in pediatric crotaline envenomations. Acad Emerg Med 2007;14:373-376.
- Campbell BT, Corsi JM, Boneti C, et al. Pediatric snakebites: Lessons learned from 114 cases. J Pediatr Surg 2008;43:1338-1341.
- Correa JA, Fallon SC, Cruz AT, et al. Management of pediatric snake bites: Are we doing too much? J Pediatr Surg 2014;49:1009-1015.
- Gomez HF, Dart RC. Clinical toxicology of snakebite in North America. In: Handbook of Clinical Toxicology of Animal Venoms and Poisons. Meier J, White J, eds. Boca Raton, FL: CRC Press; 1995: 619-644.
- Gold BS, Barish RA, Dart RC, et al. Resolution of compartment syndrome after rattlesnake envenomation utilizing non-invasive measures. J Emerg Med 2003;24:285-288.
- Tanen DA, Danish DC, Grice GA, et al. Fasciotomy worsens the amount of myonecrosis in a porcine model of crotaline envenomation. Ann Emerg Med 2004;44:99-104.
- Hardy DL Sr, Zamudio KR. Compartment syndrome, fasciotomy, and neuropathy after a rattlesnake envenomation: Aspects of monitoring and diagnosis. Wilderness Environ Med 2006;17:36-40.
- Toschlog EA, Bauer CR, Hall EL, et al. Surgical considerations in the management of pit viper snake envenomation. J Am Coll Surg 2013;217:726-735.
- Burgess JL, Dart RC. Snake venom coagulopathy: Use and abuse of blood products in the treatment of pit viper envenomation. Ann Emerg Med 1991;20:795-801.
- Vital Brazil O. Coral snake venoms: Mode of action and pathophysiology of experimental envenomation (1). Rev Inst Med Trop Sao Paolo 1987;29:119-126.
- Kitchens CS, Mierop LHV. Envenomation by the eastern coral snake (Micrurus fulvius fulvius). A study of 39 victims. JAMA 1987;258:1615-1618.
- Furbee RB, Kao LW, Ibrahim D. Brown recluse spider envenomation. Clin Lab Med 2006;26:211-226.
- Vetter RS, Isbister GK. Medical aspects of spider bites. Annu Rev Entomol 2008;53:409-429.
- Levine M, Canning J, Chase R, Ruha AM. Cardiomyopathy following latrodectus envenomation. West J Emerg Med 2010;11:521-523.
- Murphy CM, Hong JJ, Beuhler MC. Anaphylaxis with Latrodectus antivenin resulting in cardiac arrest. J Med Toxicol 2011;7:317-321.
- Norris RL, Auerbach PS, Nelson EE. Bites and stings. In: Sabiston Textbook of Surgery, 18th ed. Townsend CM, ed. Philadelphia: W.B. Saunders; 2008: 586-601.
- Isbister GK, Fan HW. Spider bite. Lancet 2011;10:2039-2047.
- Hoyte CO, Cushing TA, Heard KJ. Anaphylaxis to black widow spider antivenom. Am J Emerg Med 2012;30:836.e1-e2.
- Clark RF, Wethern-Kestner S, Vance MV, Gerkin R. Clinical presentation and treatment of black widow spider envenomation: A review of 163 cases. Ann Emerg Med 1992;21:782-787.
- Hogan CJ, Barbaro KC, Winkel K. Loxoscelism: Old obstacles, new directions. Ann Emerg Med 2004;44:608-624.
- Tambourgi DV, Gonçalves-de-Andrade RM, van den Berg CW. Loxoscelism: From basic research to the proposal of new therapies. Toxicon 2010;56:1113-1119.
- Bhatti AZ, Adeniran A, Salam S, et al. Brown recluse spider bite to the leg. Injury Extra 2006;37:45-48.
- Wasserman GS. Wound care of spider and snake envenomations. Ann Emerg Med 1988;17:1331-1335.
- Andersen RJ, Campoli J, Johar SK, et al. Suspected brown recluse envenomation: A case report and review of different treatment modalities. J Emerg Med 2011;41:e31-37.
- Stoecker WV, Wasserman GS, Calcara DA, et al. Systemic loxoscelism confirmation by bite-site skin surface: ELISA. Mo Med 2009;106:425-427, 431.
As a consequence of their playful and curious nature, children not uncommonly present to the ED with bite injuries; in fact, more than half of bite victims in the ED are children. Although envenomations are infrequent, the relatively high dose of venom per body weight in a young child can lead to significant effects. This article will discuss the key clinical features and management of bites from dogs, cats, and humans, as well as envenomations from snakes and spiders. Although not exhaustive, this review will provide a framework for the care of children who have sustained a bite or possible envenomation.
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