General Management

When faced with an envenomated child, the treating physician should anticipate a dynamic clinical syndrome that may progress with time. A high level of diligence should be maintained so that important, potentially subtle findings are not missed. As with any disease process, treatment of an envenomated child should start with assessing and managing as necessary the airway, breathing, and circulation (ABCs). Most envenomations require little more than local wound care, pain control, reassurance, and possibly observation. The severely envenomated child may need airway and respiratory protection and support (e.g., high-concentration oxygen administration and endotracheal intubation) and adequate IV access in an unaffected extremity if possible. Early hypotension tends to be related to vasodilatation and should be treated with volume expansion using appropriate infusion of physiologic saline solutions (normal saline boluses of 20 mL/kg body weight; repeated as needed up to 3 times). Shock unresponsive to volume repletion may require addition of a vasoactive pharmacologic agent such as epinephrine or dopamine (in addition to antivenom administration as appropriate—see later).

The affected body part should be immobilized in a position of function and any areas of edema should be marked, measured and monitored. If antivenom (AV) is available for the envenomation, efforts should be initiated to locate and secure an adequate amount to treat the patient (at least a starting dose). In the USA, regional poison control centers can facilitate this effort and are especially helpful if the offending species is exotic. Guidance in dosing the appropriate AV can generally be found in the package insert that accompanies the agent, although the advice in inserts for some products from developing countries may contain inaccurate and incorrect recommendations. Physicians who do not regularly treat venomous bites and stings should consult local or regional experts for assistance.

Antivenom Administration

Specific AVs are available for many venomous creatures of the world, particularly snakes, spiders, and scorpions. These products essentially impart passive immunity to the victim and should be given in cases of significant envenomation as early in the process as possible, because AV is capable of neutralizing only circulating, unbound venom components in the blood.

Antivenoms may be either in liquid form or lyophilized (requiring reconstitution prior to administration). Most AVs are given intravenously. There is no benefit to giving any AV locally at the bite site. As soon as the need for AV is established, it should be placed into solution (generally diluted in a quantity of normal saline equivalent to 20 mL/kg body weight, up to 250-1000 mL total).

As heterologous serum products, AVs carry some variable risk of inducing nonallergic or allergic anaphylactic reactions. Therefore, the patient should be closely monitored, and a physician should be present during the infusion, with access to all the appropriate equipment and medications needed to reverse such a reaction. Skin tests, often recommended by AV manufacturers, are unreliable and should be omitted.

Intravenous AV should be started slowly, and the rate gradually increased as tolerated by the patient, with a goal to administer the entire dose in approximately 1 hr.

If the victim experiences a reaction to the product, it should be temporarily stopped. Intramuscular epinephrine and intravenous antihistamines and steroids should be given. Then the AV should be restarted, possibly at a slower rate and in more dilute solution. If the reaction is severe, the decision must be made as to whether the benefits of the AV outweigh the risks of anaphylaxis on the basis of the patient’s clinical condition.

AV can also cause delayed immunoglobulin G and M–mediated serum sickness in some patients. Serum sickness occurs 1-2 weeks after AV administration, manifesting as fever, myalgias, arthralgias, urticaria, and potential renal and neurologic involvement. It is easily treated with oral steroids, antihistamines, and acetaminophen.

General Wound Care

As with all other breaks in the skin, bites and stings require basic wound care, including copious tap water or normal saline irrigation under pressure when possible. Tetanus immunization should be updated as needed. Blisters should be left intact to act as natural bandages and help prevent infection. Exposed tissue should be covered with wet to dry dressings. Necrotic wounds, such as those that might follow some snake and spider bites, should be judiciously debrided, with removal of only clearly necrotic tissue. Reconstructive surgery with skin grafts or muscle/tendon grafts may be necessary. In general, prophylactic antibiotics are not necessary except, perhaps, in cases in which an ill-informed “rescuer” cut into the bite and applied mouth suction. Antibiotics should generally be reserved for signs of established secondary infection.

Venoms and Effects

Snake venoms are complex mixtures of proteins including large enzymes that cause local tissue destruction and low molecular weight polypeptides that have the more lethal systemic effects. The symptoms and severity of an envenomation vary according to the type of snake, the amount of venom injected, and the location of the bite. The fear caused by a snake bite can result in nausea, vomiting, diarrhea, cold/clammy skin, and even syncope regardless of whether or not venom was injected. In general, viper venoms can have deleterious effects on almost any organ system. Most viper bites cause significant local pain, swelling, ecchymosis, and variable necrosis of the bitten extremity (Fig. 706-2). The pain and swelling typically begin quickly after the bite and progress over hours to days. Serious envenomations may result in a consumptive coagulopathy, hypotension, and respiratory distress. In contrast, venoms from the Elapidae tend to be more neurotoxic with little or no local tissue damage. These bites cause variable local pain and the onset of systemic effects can be delayed for hours. Manifestations of neurotoxicity generally begin with cranial nerve palsies such as ptosis, dysarthria, and dysphagia and may progress to respiratory failure and complete paralysis. There are exceptions; some members of the Elapidae family cause little or no neurotoxicity but rather severe tissue necrosis (e.g., African spitting cobras). Some vipers cause significant neurotoxicity (e.g., some populations of the Mohave rattlesnake [Crotalus scutulatus]). Physicians should proactively learn the important species in their regions, including how the species can be identified, the expected effects of their venoms, and proper approaches to management.

Figure 706-2 Southern Pacific rattlesnake bite (Crotalus oreganus helleri) in a 2 yr old boy. Note the fang marks, swelling, and bruising of the tissues (photograph taken 2 hr following the bite).

(Courtesy of Sean Bush, MD.)

Management

Prehospital care should focus on immobilization and rapid transport to the emergency department. Constrictive clothing, jewelry, and watches should be removed, and the injured body part should be immobilized in a position of function at the level of the heart. All proposed field treatments for snake bites, such as tourniquets, ice, electric-shock, incision, and suction, have proven problematic, with most being ineffective and deleterious.