Being bitten by insects is a common occurrence in childhood. Most bites and stings require little attention, even on the part of the family. In a few cases, such as venomous snake and spider bites, serious medical complications can quickly ensue, and the prompt recognition and treatment of the effects of the toxin is important to optimize outcome.
Approximately 1,600 venomous bites from domestic snakes were reported to the American Association of Poison Control Centers in 1998.1 Not every bite from a poisonous snake injects venom. Those that do not are referred to as "dry bites." The incidence of these is controversial, with some authors reporting such dry bites among as many as 30% of venomous snake bites.2
Crotalids include rattlesnakes (many species of the genus Crotalus), water moccasins (Agkistrodon piscivorus), and copperheads (Agkistrodon contortrix). These snakes are members of the pit viper family. Designed to immobilize and kill prey, these venoms use enzymes that cause toxic effects through the action of proteolytic enzymes on the cardiovascular and neuromuscular systems. Hematologic toxins damage cells and increase capillary permeability, allowing blood and fluid extravasation through the action of cytokines. This results in local edema that spreads to surrounding tissues. Other toxins lead to necrosis of skeletal muscle, coagulopathies, thrombocytopenia, and defibrination without disseminated intravascular coagulation.3
Although most of these patients present with some history of snake bite, small children may not report the event. When a crying child presents with progressive, significant limb swelling, snake bite should be considered, particularly in the southeastern United States, where venomous snake bites are most prevalent. Puncture wounds (although a single puncture wound may be present when just one fang has penetrated the skin), pain, swelling, and erythema may occur. In more severe cases, paresthesias occur both periorally and in the periphery. Nausea, an unusual taste sensation, diarrhea, light-headedness, and diaphoresis may occur. In the most severe cases, hypotension, shock, bleeding, respiratory insufficiency, fasciculations, altered mental status, and seizures occur.
First aid should be limited because most recommended measures have been of little value, and some are harmful. Elevation of the affected limb to reduce swelling may be of value, but ice should be avoided because of the resulting vasoconstriction. If immediately available, a suction device can be used within the first 10 minutes after a bite. A cellular phone, to activate the emergency medical system, has been advocated by some authorities as the most useful first aid device.
Laboratory evaluation is primarily directed toward assessment of coagulation function. The prothrombin time (PT), partial thromboplastin time (PTT), fibrinogen, fibrin degradation products, and a complete blood count should be obtained initially and repeated in 4 to 6 hours to look for late development of hematologic toxicity. A creatine Phosphokinase level should be obtained for evaluation of rhabdomyolysis, and a urinalysis should be examined for hematuria or hemoglobinuria.
Initial treatment for snake bites is no different from that for any other acutely ill or injured child. Assessment and support of airway and breathing should be accomplished. Early endotracheal intubation should be considered if respiratory muscle weakness occurs, or if the bite is on the face or neck, to secure the airway prior to the development of massive edema. Intravenous access and volume resuscitation with isotonic crystalloid solutions such as normal saline or lactated Ringer's solution should be instituted.
Wound care to maintain a clean, dry wound is important, but tape should be avoided near the bite because it may cause bullae formation. Tetanus prophylaxis is indicated if dictated by the immunization history. Prophylactic antibiotics have not been shown to be beneficial.
Antivenin is available for moderate to severe bites. Copperhead bites usually do not require antivenin therapy, but moccasin bites may and rattlesnake bites generally do require treatment. In mild bites, only local symptoms and perioral paresthesias occur. In moderate bites, local symptoms plus paresthesias, nausea, diarrhea, and weakness occur with changes in the PT, PTT, platelet count, and fibrinogen. When severe envenomation occurs, the symptoms of moderate envenomation are accompanied by shock, ventilatory insufficiency, bleeding, neurologic symptoms such as seizures or altered mentation, and the coagulation alterations previously mentioned. For antivenin therapy, the dose is based on the severity of symptoms, rather than the weight of the child.
For mild envenomations, antivenin is usually not needed unless local injury worsens or systemic symptoms develop. Should this occur, 10 vials should be given. When moderate symptoms occur, 10 to 20 vials should be given, and 20 vials are recommended for severe envenomations. Antivenin is derived from horse serum, so a number of hypersensitivity reactions may occur, including true anaphylaxis and anaphylactoid reactions. Most patients will have a delayed type III reaction (serum sickness).
Antivenin must be carefully reconstituted, as shaking it causes protein denaturation. A test dose using horse serum (supplied with the antivenin) is given intradermally with observation for wheal, flare, erythema, or any signs of systemic toxicity. If no such reaction is seen, the antivenin should be administered, starting at slow infusion rates and increasing every few minutes as tolerated. If a reaction occurs, it may be treated with epinephrine, antihistamines, and corticosteroids. A recent study of adults in Sri Lanka demonstrated the efficacy of low doses of subcutaneous epinephrine in reducing the incidence of severe anaphylaxis and anaphylactoid reactions during antivenin administration.4 If antivenin is deemed essential and anaphylaxis occurs, consultation with a toxicologist is recommended. Concomitant infusions of low doses of epinephrine have been used in this instance.
A newer polyvalent, ovine-derived antivenin is currently undergoing testing.5 Initial human experience has been promising, although the coagulation abnormalities may reoccur because of the short duration of action of the product.6
Local wound care rarely requires surgical intervention. Because most venom deposition is in the subcutaneous tissues and not in deep compartments, compartment syndrome is rare. Fasciotomy should be performed only when high pressures are demonstrated using intracompartmental pressure monitoring.
Coral snakes (several species from the Micrurus and Micruroides genera) are much less common in the United States than are pit viper snakes. Coral snakes have brightly banded colors that resemble those of other, nonvenomous snakes. The colloquial expression "red on yellow, kill a fellow; red on black, venom lack" helps differentiate this snake from other nontoxic snakes. A red band is adjacent to a yellow band on the coral snakes found in the United States. The bites of coral snakes differ from those of crotalids in both the toxicity of the venom and the manner in which they are inflicted. Venom is not injected through fangs; a coral snake must gnaw and hang onto its victim for several seconds for the venom to reach the victim via grooves in its fangs. Because the bite may produce little pain and symptoms may be delayed, the diagnosis can be difficult.
The venom of the coral snake is neurotoxic with little tissue toxicity. The venom binds postsynaptically at the neuromuscular junction, and the symptoms of these bites may be delayed for many hours. Fang marks are present in most victims, but local swelling is minimal. Paresthesias, nausea, vomiting, euphoria, weakness, diaphoresis, diaplopia, dyspnea, and fasciculations have been reported.7 Deaths generally occur from respiratory failure, and may be preceded by bulbar signs such as ptosis, dysarthria, and dysphasia.8 The hematologic toxicity seen with crotalid bites does not occur with coral snake bites.
Attention to the ABCs (airway, breathing, and circulation) of resuscitation may require endotracheal intubation and mechanical ventilation for victims of coral snake bites. An equine antivenin is also available for coral snake bites; this product requires the same skin testing as described for the crotalid antivenin. This antivenin is recommended when a positive identification has been made or signs and symptoms consistent with coral snake envenomation occur. Five to 10 vials are generally recommended. Respiratory failure may persist if it occurred prior to antivenin therapy. A newer ovine-derived antibody fragment is also under development for coral snake bites.9
The bites of only two spiders are clinically important in North America: the brown recluse (Loxosceles reclusa) and the black widow (Latrodectus mactans). Brown recluse bites are much more prevalent. Most of the features of brown recluse bites are related to sphingomyelinase D, a toxin found in the venom. This phospholipase induces dermal necrosis and also causes system effects through its interaction with red blood cells, platelets, and endothelium.
Brawn Recluse Bites
Brown recluse bites often occur when this usually nonaggressive spider is threatened, such as when trapped against the skin by clothing or linens. A mild or sharp stinging sensation may be felt at the time of the bite, and worsening pain and itching occur during the ensuing hours.10 Classically, a central blister is found with surrounding erythema. A purple discoloration may be noted during the next several hours as hemorrhage and vascular thrombosis develop at the site of the bite.11 The bite may grow in size over hours to days. Systemic signs, including fever, nausea, vomiting, and arthralgias, may occur and evidence of hemolysis and thrombocytopenia may be found on laboratory testing.
A wide variety of treatments have been tried, including corticosteroids, antibiotics, dapsone, hyperbaric oxygen therapy, and early excision of the bite. No therapy has been proven effective in human trials, and many of the animal studies are limited by the lack of similarities between human skin and the skin of laboratory animals. Only local wound care is indicated. If extensive dermal necrosis occurs, debridement and even possibly skin grafting may be necessary. A plastic surgeon should be consulted when extensive necrosis is present.
Anemia secondary to hemolysis may occur, and care should be taken to protect renal function when extensive intravascular hemolysis is present. Maintaining high urinary flow rates (2 to 3 mL/kg/h) with alkalinzation of the urine by infusing sodium bicarbonate is the mainstay of therapy. The authors have found that using 5% dextrose in water with 75 mEq/L of sodium bicarbonate infused at 1.5 to 2 times the child's maintenance fluid requirement usually suffices to keep urine pH greater than 7.0. Should the urine pH fall, an additional bolus of 0.5 to 1 mEq/kg of sodium bicarbonate should be infused during 15 to 30 minutes. Some authors also recommend mannitol in the prevention of hemoglobin- or myoglobininduced nephropathy.12 Repeated monitoring of electrolytes and renal function should be performed. If anemia is severe and symptomatic, red blood cell transfusion may be required. Rarely, dialysis is required because of acute tubular necrosis, particularly if there is a delay in seeking or instituting appropriate therapy.
Black Widow Bites
The black widow spider, which includes several species of Latrodectus, is found in most areas of North America. Bites from these creatures, however, are much less common than bites from brown recluse spiders. The venom of the black widow spider lacks a tissue toxin, so there is little (if any) local effect. Instead, this venom affects the presynaptic membrane of the neuromuscular junction. The effect on the membrane results in both the release and the decreased uptake of acetylcholine from the neuromuscular junction. Some victims report an initial "pinprick" sensation, followed by regional lymph node tenderness during the next 30 to 120 minutes.3 A target lesion may develop at the bite site. The hallmark of black widow spider envenomation is muscle cramping, generally involving the abdomen, chest, and back, depending on the location of the bite. Autonomic symptoms may include nausea, vomiting, sweating, hypertension, tachycardia, and even priaprism on rare occasions.
Death from black widow spider bites is rare, although life-threatening hypertension can develop. Analgesia is the mainstay of care for victims of black widow spider bites. Oral narcotics such as codeine, hydrocodone, or oxycodone can be used in milder cases. Intravenous morphine is appropriate for more severe cases, and benzodiazepines such as diazepam, lorazepam, or midazolam can be beneficial for both relief of anxiety and smooth muscle relaxation through centrally mediated responses.
An antivenin is also available for the bite of black widow spiders. It is indicated for only the most severe cases of envenomation that are unresponsive to other measures.13 Life-threatening hypertension and tachycardia are considered indications for this antivenin, which may cause immediate type hypersensitivity reactions resulting in death. One vial of anti venin is generally all that is needed, and treatment promptly relieves symptoms. Up to 5% of victims died in the era prior to the availability of intensive care, but death is now distinctly uncommon.
The Hymenoptera order of insects includes bees, wasps, and ants. Bees can only sting once because their venom sac eviscerates the abdomen after it becomes detached. The bee sting produces only a local reaction, unless anaphylaxis occurs. Anaphylaxis must be treated immediately, and individuals known to be sensitive should carry an automatic epinephrine injector. Death may also occur from a large number of stings (500 to 1,500). Wasp stings primarily cause local reactions, with anaphylaxis less common than with bee stings.
Treatment of a local reaction includes applying an ice pack and administering an oral antihistamine such as diphenhydramine. For severe local reactions, a short course of corticosteroids may be useful. If anaphylaxis occurs, epinephrine (0.01 mg /kg) should immediately be given subcutaneously or intramuscularly, and may need to be repeated multiple times. Antilustamines are generally given to block the effects of further histamine release, but these are a much lower priority than epinephrine. The emergency medical system should be activated. Corticosteroids such as methy !prednisolone (2 mg /kg) or dexamethasone (0.2 to 0.4 mg /kg) are beneficial to block the response that may occur several hours later. If significant bronchospasm occurs, a beta-agonist such as inhaled albuterol should be given. Profound vasodilatation may occur, requiring volume boluses of isotonic crystalloid (normal saline or lactated Ringer's solution, 20 mL/kg).
Fire ants (Solenopsis invida) are an increasing problem in many areas of the southern United States, and multiple bites are the norm for these social creatures. Stings frequently occur on the feet and legs of children. Bites are common. The venom produces severe burning pain (hence the name of this insect) and generally causes only local symptoms. Good local wound care is important, and an ice pack plus an oral antihistamine may be beneficial. Systemic corticosteroids should be considered in severe cases.
Similar to bee and wasp stings, most scorpion stings require little care. Only one species of scorpion is found in the United States that produces serious toxicity. Centruroides exilicauda is found primarily in Arizona, but also in other parts of the southwest. Because it generally resides beneath tree bark, it is commonly referred to as the "bark scorpion." Most stings occur in adults, with only approximately 20% reported in children.
The venom of this scorpion causes an excitatory state in the autonomic nervous system, resulting in tachycardia, agitation, abnormal eye movements, paresthesias, hypersalivation, gastrointestinal symptoms, and hypertension.2 Although tachycardia and hypertension are more frequent, the opposite effects are also possible when the parasympathetic nervous system is predominately activated by the venom. In young children, the diagnosis may be difficult when they present with extreme agitation and roving eye movements.14
Most stings require only home treatment with over-the-counter analgesics.15 In severe cases, parenteral analgesics may be necessary for pain, and agitation is treated by benzodiazepines. Many authorities prefer midazolam, which may be used as a continuous infusion.16 Some patients with primarily muscarinic symptoms such as bronchorrhea may benefit from atropine. Intubation may be required if respiratory failure or airway obstruction occurs. In Arizona, an antidote is available that is approved by the Arizona State Board of Pharmacy; however, because it is not approved by the Food and Drug Administration, this antidote cannot be used in other states. Similar to other antivenin produced in animals, it may cause both immediate and delayed type hypersensitivity reactions. One vial is generally given after a test dose. Improvement is usually within 30 minutes of administration.17
Fortunately, bites and stings are usually just sources of discomfort for children. However, when they are more than that, prompt attention to the basics of resuscitation is paramount. Knowledge of when to treat and when not to treat with antivenin is important to maximize the risk-benefit balance that accompanies any therapy.
1. Litovitz TL, Klein-Schwartz W, Caravati EM, Youniss J, Crouch B, Lee S. 1998 annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System. Am J Emerg Med. 1999;17:435-487.
2. Russell FE. Snake Venom Poisoning, 5th ed. Great Neck, NY: Scholium International; 1983.
3. Walter FG, Bilden EF, Gibly RL. Envenomations. Crit Care Clin. 1999;15:353-386.
4. Premawardhena AP, de Silva CE, Fonseka MM, Gunatilake SB, de Silva HJ. Low dose subcutaneous adrenaline to prevent adverse reactions to antivenom serum in people bitten by snakes: randomised, placebo controlled trial. BMJ. 1999;318:1041-1043.
5. Dart RC, Seifert SA, Carroll L, et al. Affinity-purified, mixed nonspecific crotalid antivenin ovine Fab for the treatment of crotalid venom poisoning. Ann Emerg Med. 1997;30:33-39.
6. Boyer LV, Seifert SA, Clark RF, et al. Recurrent and persistent coagulopathy following pit viper envenomation. Arch Intern Med. 1999;159:706-710.
7. Kitchens CS, Van Mierop LH. Envenomation by the Eastern coral snake (Micrurus fulvius): a study of 39 victims. JAMA. 1987;258:1615-1618.
8. McCollough NC, Gennaro JF. Treatment of venomous snakebite in the United States. Clinical Toxicology. 1970;3:483-500.
9. Rawat S, Lang G, Smith DC, Theakston D, Landon J. A new antivenin to treat Eastern coral snake (Micrurus fulvius) envenoming. Toxicon. 1994;32:185-190.
10. Allen C. Arachnid envenomations. Emerg Med Clin North Am. 1992;10:269-298.
11. Butz WC. Envenomation by brown recluse spider and related species: a public health problem in the United States. Clinical Toxicology. 1971;4:515-524.
12. Jones DP, Chesney RW, Friedman AL. Glomerulotubular dysfunction and acute renal failure. In: Fuhrman BP, Zimmerman JJ, eds. Pediatric Critical Care, 2nd ed. St. Louis, MO: Mosby; 1997:759-760.
13. Bond GR. Snake, spider and scorpion envenomation in North America. Pediatr Rev. 1999;20:147-150.
14. Berg RA, Tarantino MD. Envenomation by the scorpion Centruroides exilicauda (C sculpturatus): severe and unusual manifestations. Pediatrics. 1991;87:930-933.
15. Likes K, Banner W Jr, Chavez M. Centruroides exilicauda envenomation in Arizona. West J Med. 1984;141:634-637.
16. Gibly R, Williams M, Walter FG, McNaIIy J, Conroy C, Berg RA. Continuous intravenous midazolam infusion for Centruroides exilicauda scorpion envenomation. Ann Emerg Med. 1999;34:620-625.
17. Bond GR. Anti venin administration for Centruroides scorpion sting: risks and benefits. Ann Emerg Med. 1992;21: 788-791.