Chapter 206. Reptile Bites

An estimated 3 million bites and 150,000 deaths occur each year from venomous snakes in the world.1 The American Association of Poison Control Centers reports an average of 6000 bites each year, approximately 2000 of them by venomous snakes. Because of underreporting, the true number of snakebites is possibly as high as 45,000 per year in the U.S., with 7000 to 8000 by venomous snakes.2 The major venomous snakes of the world can be divided into three groups: Viperidae (vipers), Elapidae, and Hydrophiinae (sea snakes, see Chapter 207, Trauma and Envenomations from Marine Fauna).

Approximately 20 of the 120 snake species indigenous to North America are venomous. Most bites occur in the warm summer months, when snakes and victims are most active. In the past, it was estimated that mortality from venomous snakebite approached 25%. Because of the availability of antivenom and advances in emergency and critical care, mortality rates today are <0.5%; approximately 5 to 10 deaths occur per year.3

Except for bites by imported species, North American venomous snakebites involve the pit vipers (Crotalinae subfamily of Viperidae) or coral snakes (Elapidae family). The crotaline snakes are represented by the rattlesnakes (Crotalus species), pygmy rattlesnakes, and massasauga (Sistrurus species), as well as the copperheads and water moccasins (Agkistrodon species). Poisonous snakebites from imported exotic species are infrequent but may occur in zoo personnel as well as in amateur herpetologists. A regional poison control center can provide information on snake identification, expected toxicity, and location of antivenom.

The crotaline snakes are called pit vipers because of bilateral depressions or pits located midway between and below the level of the eye and the nostril (Figure 206-1). The pit is a heat receptor that guides strikes at warm-blooded prey or predators. Crotaline snakes are also distinguished by the presence of two fangs that fold against the roof of the mouth, in contrast to the coral snakes, which have shorter, fixed, erect fangs. Within the pit viper group, the rattle distinguishes the rattlesnake from other crotaline snakes. The mistaken belief that rattlesnakes always rattle before striking has persisted for centuries. In truth, many strikes occur without a warning rattle.

Pathophysiology

Crotaline venom is a complex enzyme mixture that causes local tissue injury, systemic vascular damage, hemolysis, fibrinolysis, and neuromuscular dysfunction, resulting in a combination of local and systemic effects. Crotaline venom quickly alters blood vessel permeability; this leads to loss of plasma and blood into the surrounding tissue, which causes hypovolemia. Crotaline venom activates and consumes fibrinogen and platelets, causing a coagulopathy. In some species, specific venom fractions block neuromuscular transmission, which leads to cranial nerve weakness (e.g., ptosis), respiratory failure, and altered sensorium.

Clinical Features

Up to 25% of crotaline snakebites are dry bites: venom effects do not develop. The manifestations of crotaline venom poisoning involve a complex interaction of the venom and the victim. The species and size of the snake, the age and size of the victim, the time elapsed since the bite, and characteristics of the bite or bites (location, depth, and number, the amount of venom injected) all affect the clinical evolution. The severity of poisoning following a crotaline bite is therefore variable. An initially minimal bite may evolve into a more serious bite and require large amounts of antivenom.

The cardinal manifestations of crotaline venom poisoning are the presence of one or more fang marks, localized pain, and progressive edema extending from the bite site.2 Other early symptoms and signs of envenomation are nausea and vomiting, weakness, oral numbness or tingling of the tongue and mouth, dizziness, and muscle fasciculation. Envenomation may produce systemic effects with tachypnea, tachycardia, hypotension, and altered level of consciousness. In general, local swelling at the bite site becomes apparent within 15 to 30 minutes, but in some cases, swelling may not start for several hours. In severe cases, edema can involve an entire limb within an hour. In less severe cases, edema may progress over 1 to 2 days. Edema near an airway or in a muscle compartment may threaten life or limb even when no systemic effects are present. Rapid onset of angioedema may occur.

Progressive ecchymosis may also develop because of leakage of blood into subcutaneous tissue. Ecchymoses may appear within minutes or hours, and hemorrhagic blebs may be seen within several hours. Hemoconcentration often develops as a result of fluid extravasation into subcutaneous tissue, followed by a decrease in hemoglobin level over several days as intravascular volume is restored.

Diagnosis

The diagnosis of snakebite is based on the presence of fang marks and a history consistent with exposure to a snake (e.g., walking through a field). Snake envenomation involves the presence of a snakebite plus evidence of tissue injury. Clinically, the injury may be manifest in three ways: local injury (swelling, pain, ecchymosis), hematologic abnormality (thrombocytopenia, elevated prothrombin time, hypofibrinogenemia), or systemic effects (e.g., oral swelling or paresthesias, metallic or rubbery taste in the mouth, hypotension, tachycardia). Abnormalities in any one of these areas indicate that venom effect is developing. The absence of any of these manifestations for a period of 8 to 12 hours following the bite indicates a dry bite.

Treatment

First Aid

First aid measures should never substitute for definitive medical care or delay the administration of antivenom (Table 206-1). All patients bitten by a pit viper should be taken to a health care facility. First aid treatments such as suction and incision are dangerous and should not be done. Snake Bite Kit and similar products should not be used because they contain cups that produce little suction and seal poorly on digits. The blade in the kit, or any method of incision, can injure digital nerves, arteries, and tendons. The Sawyer Extractor (Sawyer Products, Inc., Safety Harbor, FL) suction pump is said to remove venom without incision, but safety and efficacy of the product have been questioned.4 Electric shock treatment of the bite site is dangerous and ineffective, and can cause electric injuries. Ice water immersion worsens the venom injury.

Use of tourniquets is contraindicated because they obstruct arterial flow and cause ischemia. Constriction bands may be useful, especially when immediate medical care is not available. A constriction band is an elastic bandage or Penrose drain, thick rope, or piece of clothing wrapped circumferentially above the bite, applied with enough tension to restrict superficial venous and lymphatic flow while maintaining distal pulses and capillary filling. The band should be snug but loose enough that a finger can slide comfortably underneath. A constriction band can delay venom absorption without causing increased swelling.5

Prehospital Management

In the prehospital phase, immobilize the limb, establish IV access in another limb, administer oxygen, and transport the victim to a medical facility. IV access should be established before tourniquets or constricting bands are removed.

Institute ALS measures as indicated. If the patient is hypotensive, rapidly administer IV isotonic fluids. Continue to immobilize the limb in a neutral position during transport to reduce further venom absorption. Consultation with a physician or poison control center familiar with the management of snake envenomation is recommended for most cases.

ED Management

Antivenom is the mainstay of therapy for poisonous snakebites2 (Table 206-2). Antivenom is composed of heterologous antibodies derived from the serum of animals immunized with the appropriate snake venoms. The antibodies bind and neutralize the venom molecules.

Crotalidae Polyvalent Immune Fab (Ovine) (FabAV) is used in the U.S.; equine-derived products [Antivenin (Crotalidae) Polyvalent; see below] are no longer available. The new antivenom is produced by immunizing herds of sheep with one of four crotaline snake venoms: eastern diamondback (C. adamanteus), western diamondback (C. atrox), Mojave (C. scutulatus), or cottonmouth (A. piscivorus). The immune serum is harvested from each group and then digested with papain to produce antibody fragments (Fab and Fc). The more immunogenic Fc portion of the antibody is eliminated during purification. The four individual monospecific Fab preparations are combined to form the final antivenom product.

All patients with bites that show evidence of progressive signs and symptoms should receive antivenom promptly. Progression is defined as worsening of local injury (e.g., pain, ecchymosis, or swelling), abnormal results on laboratory tests (e.g., worsening platelet count, prolonged coagulation times, decreased fibrinogen level), or systemic manifestations (e.g., unstable vital signs or abnormal mental status) (Table 206-3).

FabAV is effective and has a better safety profile than Antivenin (Crotalidae) Polyvalent [Wyeth], the equine-derived product.6–8 FabAV also dissolves into solution quickly, and skin testing is not required.

FabAV is administered as a larger “initial control” dose followed by three smaller maintenance doses (Figure 206-2). Initial control is defined as cessation of progression of three clinical evaluation parameters: local effects, systemic effects, and hematologic abnormalities. The initial dose is four to six vials, which may be repeated to establish initial control of the envenomation. After initial control has been established, two-vial maintenance doses are recommended (Figure 206-2).

Antivenom should not be injected directly into a digit. IM injection also is not recommended, because venom-induced hypovolemia may retard absorption of antivenom. Hospital pharmacies in those regions of the U.S. where poisonous snakes are prevalent should maintain adequate stocks of antivenom. Unfortunately, many hospitals stock insufficient amounts of antivenom, even in endemic areas.9

The package insert is useful as a guide for antivenom preparation. Antivenom should be initiated in a critical-care facility such as an ED or intensive care unit, under direct physician supervision, and with resuscitative drugs and equipment immediately available. After reconstitution, each dose of FabAV is diluted in 250 mL of crystalloid and is infused over 1 hour. The total volume, but not the number of vials, may be reduced in small children.10

The incidence of acute reactions to FabAV is <10%.6–8 If an acute allergic reaction occurs, the infusion should be stopped immediately and antihistamines administered (both histamine-1 and histamine-2 receptor blockers). Epinephrine should be readily available and should be used, depending on the severity of the reaction.

It is extremely important that observation for progression of edema and systemic signs of envenomation be continued during and after antivenom infusion. Limb circumference should be measured at several sites above and below the bite, and the advancing border of edema should be outlined with a pen every 30 minutes. This serves as an index of the progression as well as a guide for antivenom administration. Laboratory determinations are repeated every 4 hours or after each course of antivenom therapy, whichever is more frequent. Additional doses of FabAV may be warranted if the patient’s condition worsens. FabAV has been formally tested only in the treatment of rattlesnake bites. Initial case reports support its efficacy in treatment of copperhead snakebites.11

The value of aggressive supportive care cannot be overemphasized. Isotonic fluid resuscitation followed by administration of vasopressor agents is appropriate for hypotension. Antivenom is the best treatment for hematologic abnormalities, but if active bleeding occurs, blood component replacement may be necessary. Another complication of snakebite is compartment syndrome. Increased compartment pressure may occur when venom is injected or spreads into a compartment. This is often manifested by severe pain, localized to a compartment and usually resistant to opiate analgesia. Treatment of compartment syndrome is difficult (Table 206-4). The use of fasciotomy is controversial, and there is no firm evidence supporting its use.

The wound area should be cleaned and the need for tetanus immunization determined. Obtain wound specimens for culture and administer antibiotics if signs of infection are present. Although antibiotic prophylaxis is recommended by some authors, the data available do not support its use.12 Steroids do not appear to be effective and could be harmful. Steroids should be reserved for the treatment of allergic reactions or serum sickness.

Serum sickness develops in about 5% of patients after FabAV treatment. The symptoms are fever, rash, and arthralgias. Oral prednisone, 1 milligram/kg/d, should be started and tapered over 1 to 2 weeks.

Disposition and Follow-Up

It cannot be overemphasized that one can easily be deceived by a bite that initially appears innocuous. Unremarkable physical examination and laboratory test results at presentation do not reliably indicate an insignificant envenomation. We recommend that physicians observe patients for at least 8 hours in the ED before determining patient disposition.

Patients with dry bites who have been observed for at least 8 hours may be discharged. They should return if pain, swelling, or bleeding develops. Patients with severe or life-threatening bites and patients receiving antivenom should be admitted to an intensive care unit. The general ward is appropriate for patients with mild or moderate envenomations who have completed or do not require further antivenom therapy.

Patients are ready for discharge from the hospital when swelling begins to resolve, coagulopathy has been reversed, and the patient is ambulatory. Physical therapy for the bitten part (particularly the hand) is recommended after swelling has lessened and coagulopathy has resolved. Outpatient follow-up is necessary to monitor for infection and serum sickness.

Coral Snake Bites

North American coral snakes include the eastern coral snake (Micrurus fulvius fulvius), the Texas coral snake (M. fulvius tenere), and the Arizona (Sonoran) coral snake (Micruroides euryxanthus). The eastern coral snake is found primarily in the southeastern U.S. The Texas and Arizona coral snakes are found primarily in the states that bear their names. Coral snakes account for 20 to 25 bites a year.

All coral snakes are brightly colored with black, red, and yellow rings. The red and yellow rings touch in coral snakes, but they are separated by black rings in nonpoisonous snakes, which led to the well-known rhyme, “Red on yellow, kill a fellow; red on black, venom lack.” This rule is not always true outside of the U.S.

Coral snake venom is primarily composed of neurotoxic components that do not cause marked local injury (Table 206-2). A potential victim of coral snake bite should be admitted to the hospital for observation. Coral snake venom effects may develop hours after a bite, and effects are not easily reversed. Three to five vials of Antivenin (Micrurus fulvius) should be administered to patients who have definitely been bitten, because it may not be possible to prevent further effects or reverse effects once they develop.13 Additional doses of coral snake antivenom are reserved for cases in which symptoms or signs of coral snake envenomation appear. Because respiratory failure may result from clinical effects of the neurotoxin, baseline and serial measurement of pulmonary function parameters (such as inspiratory pressure and vital capacity), in addition to intensive care observation, may be useful. Prolonged ventilatory support may be required in severe cases. The patient must be observed closely for signs of respiratory muscle weakness and hypoventilation. Bites by the Sonoran coral snake are mild, and antivenom is not usually needed.

Australian Elapid Bites

Elapids are found throughout the world in tropical and warm climates. Medically significant groups include most venomous snakes of Australia [tiger snakes (Notechis), brown snakes (Pseudonaja), costal taipan (Oxyuranus), death adder (Acanthophis), red-bellied black snake (Pseudechis)] and cobras (Naja), mambas (Dendroaspis), and kraits (Bungarus) found in Africa and southern Asia.

Elapid bites produce primarily neurologic effects: tremors, salivation, dysarthria, diplopia, bulbar paralysis with ptosis, fixed and constricted pupils, dysphagia, dyspnea, and seizures. The immediate cause of death is paralysis of respiratory muscles. Signs and symptoms may be delayed up to 12 hours (Table 206-2).

Pathophysiology

The Elapidae possess nonretractile small- to medium-sized paired fangs that have grooved venom channels rather than hollow venom ducts. It is thought that the Elapidae exert voluntary control over the injection of venom, hence the occurrence of a dry bite without envenomation.

The venom of the Australian elapids contains several important components.14 Neurotoxins (tiger snake, taipan, and death adder) act at the neuromuscular junction and cause descending symmetric flaccid paralysis. Signs usually become apparent within 2 to 12 hours after the bite and may include ptosis, partial ophthalmoplegia (diplopia), dysarthria, loss of facial expression, and loss of airway control, as well as respiratory paralysis in severe cases. The procoagulant toxins (brown snake, tiger snake, taipan) act as prothrombin converters, leading to a venom-induced consumptive coagulopathy with fibrinogen depletion and variable thrombocytopenia. Intracranial hemorrhage is a recognized complication.

The brown snake can cause rapid collapse and death.15 Renal impairment or failure may also result from snakebite. The mechanisms are poorly understood and may include hypotension, myoglobinuria, coagulopathy, and direct renal toxicity. Myolysins (tiger snake, taipan, mulga snake) are structurally related to the neurotoxins but instead produce rhabdomyolysis, which may result in muscle pain, weakness, myoglobinuria, renal failure, and hyperkalemia. Rarely, a venom-induced thrombotic microangiopathy may complicate brown and tiger envenomation.16 Local tissue destruction is uncommon with the bite of any Australian species, although mild to moderate ecchymosis and swelling may occur.

Clinical Features

The severity of elapid envenomation cannot be estimated by the clinical appearance of the bite site or initial symptoms.17 Even with severe envenomation patients may initially feel well and manifest few untoward clinical features. Initial symptoms include nausea, vomiting, headache, abdominal pain, diplopia, dysphonia, progressive muscle weakness, discolored urine, and seizures. Young children may not provide a history of snakebite, so a high index of suspicion for elapid snakebite is needed if a child develops toxicity in a geographic area populated with elapids.

Diagnosis

Diagnosis of envenomation by Australian Elapidae requires the correlation of history of potential snakebite, clinical features of envenomation, and laboratory investigations. Commonwealth Serum Laboratories (CSL Ltd., Melbourne, Australia) developed a Snake Venom Detection Kit (SVDK) to classify snake venom identified at the bite site or in the urine. Positive SVDK identification of venom at the bite site or in the urine assists in selecting a monovalent antivenom, but does not represent an indication for antivenom therapy without other evidence of systemic venom effects. SVDK testing of blood is not recommended, because false positive and false negative results have been described.15

Treatment

First Aid

The aim of first aid is to delay absorption of venom from the bite site until the patient is in a facility that can administer antivenom if required. In Australia, pressure immobilization of the involved limb is used. The principle is to contain the venom within lymphatic vessels and prevent systemic absorption. This is done by wrapping a snug elastic bandage over the bite site and then extending it to cover the entire limb. The limb is then splinted to prevent motion. Examination of lymphatic flow rates with simulated venom has demonstrated that, even if the upper or lower limb is appropriately bandaged and immobilized, walking will hasten systemic envenoming.18 Use of tourniquets is contraindicated. In the rare circumstance that a bite is inflicted on the trunk, apply firm pressure to the affected area without restricting breathing.

ED Management

Any history suggestive of an elapid bite should prompt the initiation of first aid and transport to a medical facility with appropriate medical expertise, laboratory facilities, and antivenom supplies. The constriction band should be maintained until envenomation is excluded and an IV line is established, or until the patient can receive antivenom. Once the patient is in the hospital, if there are no signs of envenomation and results of laboratory studies are normal, the constriction band should be removed. If the patient’s condition deteriorates immediately after constriction band removal, reapply the band and give antivenom. Once antivenom is infusing, the constriction band should be removed so that venom is available for interaction with circulating antivenom. There is no evidence that venom is inactivated by being trapped at the bite site.15

Antivenom should be given only in cases in which there is clear clinical or laboratory evidence of systemic venom effect (Table 206-2). Clinical indications for immediate antivenom therapy include repeated vomiting and severe headache; neurotoxic effects such as ptosis, cranial nerve involvement, progressive muscle weakness, or diaphragmatic involvement; or evidence of coagulopathy. Pertinent investigations include complete blood count, coagulation studies (including levels of fibrinogen and fibrin degradation products), serum electrolyte levels, renal function tests, creatine kinase level, and urine testing for hematuria or myoglobinuria.14 Abnormal coagulation study results frequently provide laboratory evidence of systemic venom effects before neurotoxic effects are apparent. In the absence of clinical or laboratory evidence of venom effect, the constriction band should be removed and the patient observed for at least 12 hours. Coagulation studies should be repeated 2 hours after band removal and at intervals thereafter, depending on the patient’s condition.

Six antivenom products, derived from equine immunoglobulin G, are available to treat envenomation by the five groups of venomous terrestrial Australian snakes plus the sea snakes. These six products are monovalent antivenoms.14 A polyvalent antivenom, also equine immunoglobulin G, neutralizes the venom of all five major groups of dangerous Australian terrestrial snakes (Table 206-5).

If indicated, monovalent or polyvalent antivenom should be given immediately in sufficient doses to improve coagulation values. A child should receive the same dose of antivenom as an adult.14 Pregnancy is not a contraindication to antivenom therapy. Skin testing before antivenom administration is not recommended,14 and epinephrine and supplies for intubation should be at the bedside to treat anaphylaxis. If the type of snake involved cannot be identified, usually two appropriate monovalent antivenoms may be selected by correlating the clinical presentation with knowledge of snakes found in the geographic area. Until recently, recommended doses of monovalent antivenom and laboratory end points for treatment had been based on clinical evidence and expert consensus. More rigorous research now suggests that lower doses of antivenom may be appropriate.19 Again, expert advice is recommended. The role of polyvalent antivenom therapy is currently ill-defined. Hypersensitivity is usually an uncommon complication of antivenom therapy in Australia, but caution is required.20–22 A 5-day course of prednisolone may be prescribed in an attempt to reduce the incidence of serum sickness in those patients who receive large doses of antivenom, but clear clinical trial data supporting this practice are lacking.15

Cobras are large snakes, typically 1.0 to 1.5 m in length, and indigenous to most of Africa and southern Asia.23 Cobras adapt readily to different habitats and can be found around villages and inhabited areas. The bold defensive posture cobras adopt by elevating the head and spreading the neck is not unique to this group of snakes. Not all cobra bites result in envenomation, and as many as 45% are dry bites. Some species of cobras have the ability to spit jets of venom toward a victim, often hitting the eyes. The incidence of cobra bite and subsequent mortality is difficult to determine because of the lack of accurate reporting systems in most of Africa and southern Asia. In rural Congo, an annual incidence of 430 cobra bites per 100,000 population has been described. In Burma and India, an annual mortality rate of between 3 and 10 per 100,000 has been reported.

Pathophysiology

Cobra venom contains a mixture of toxins. In most cobras, neurotoxins in the venom pose the greatest threat to the victim. Neurotoxins bind to postsynaptic acetylcholine receptors and produce depolarizing neuromuscular blockade. Cell membrane toxins produce arrhythmias and decrease ventricular contractility. Another group of toxins contains enzymes that break down protein and connective tissue. These necrosis-producing toxins are typical of the venom from the spitting cobras (Naja species) of Africa, China, and Sumatra.

Clinical Features

Immediate pain at the bite site is almost always present. Other symptoms and signs are variable and can include local and progressive soft tissue swelling, cranial nerve dysfunction (ptosis, diplopia, dysphagia), generalized muscle weakness followed by flaccid paralysis, and parasympathetic stimulation (salivation, bronchorrhea, nausea, vomiting). Victims who were sprayed in the eye by a spitting cobra describe pain, tearing, and blurred vision.

Signs include altered mental status, sleepiness, respiratory distress, hypotension, ptosis, ophthalmoplegia, and generalized weakness or paralysis. Reaction around the bite site may develop over 48 hours with local hemorrhage, bullae, and necrosis. Venom spit into the eye will produce inflammation, edema, and discharge, but no systemic symptoms or signs. Coagulopathy is rare following a cobra bite, with the exception of a bite from a spitting cobra (Table 206-2).

Diagnosis

Because of venom potency and the size of the snake, a bite resulting in envenomation usually produces obvious symptoms. The difficulty is distinguishing cobra envenomation from bites by other snakes that possess neurotoxic venom. When possible, the snake should be killed and brought in for identification. A variety of snake venom detection assays have been developed that can identify the offending snake with reasonable accuracy from wound aspirate or urine. The availability of these kits is unfortunately poor in most of Africa and Asia. If local or systemic signs of envenomation are present, standard laboratory studies should be performed: complete blood count, serum electrolyte levels, creatinine level, and coagulation tests.

Treatment

First Aid

Most common first aid measures either have no proven efficacy or increase toxicity. The pressure immobilization or constriction band technique used for Australian elapid bites has not proven beneficial for cobra bites. The proximal lymphatic- and vein-constricting elastic band approach used for North American crotaline bites is probably more reasonable, although its efficacy is unproven. Incisions, vacuum extractors, cooling, and ice are not beneficial. The one first aid measure that is beneficial is prompt and copious eye irrigation if the eyes are exposed to venom.

ED Management

There is no correlation between local tissue damage and systemic toxicity, so grading systems based on bite site appearance should not be used. The only proven and specific therapy for cobra envenomation is antivenom.24 Laboratories in Africa, Asia, and Europe have developed cobra antivenom. Some products are monovalent, specific for a single species, but most are polyvalent, containing antibodies against several important or common cobra species in that country or region. The animal of origin varies, as does potency and purity. A high incidence of allergic reactions should be anticipated.

If the patient has evidence of systemic toxicity on arrival to the hospital, antivenom should be started before the constricting band is loosened. For patients without signs of systemic toxicity, the constricting band should be loosened only after antivenom is available. Antivenom is effective in reducing systemic toxicity but does not reduce local tissue damage and necrosis.

For patients with significant muscle weakness or paralysis, a cholinesterase-inhibiting drug, such as edrophonium or neostigmine, should be given until antivenom is available.25 Respiratory failure should be treated with endotracheal intubation and ventilation.26 Hypotension is treated with IV fluids initially, followed by vasopressors if there is an inadequate response. Tetanus immunization should be provided as appropriate.

Disposition and Follow-Up

Patients without signs of envenomation should still be admitted for observation for 24 hours. Death from cobra envenomation typically occurs 2 to 6 hours after the bite. Survival is possible without antivenom treatment provided there is good respiratory and cardiovascular supportive care.23,26 With prompt and appropriate antivenom therapy and supportive pulmonary care, recovery from neurotoxicity is expected, but may take up to 6 days.

Gila monsters are slow-moving lizards that inhabit the desert in the southwestern U.S. They possess venom as potent as rattlesnake venom but lack the apparatus to inject it effectively. Instead of fangs, they have short, grooved teeth down which their venom flows. Therefore, envenomation requires a prolonged bite. Gila monsters bite tenaciously and may be difficult to remove from the bitten extremity, so fractures and deep injury should be suspected.

There are few if any documented deaths from Gila monster bite. Most bites result in local pain and swelling only, which worsens over several hours and then subsides over several more hours. Dislodged teeth often contaminate the wound. Occasionally, a more severe syndrome of systemic toxicity develops, including weakness, light-headedness, paresthesia, and diaphoresis. Severe hypertension may occur, which also resolves over several hours.

First aid involves removal of the reptile from the bite site without sustaining another bite. This may require force. It helps to place the animal on a solid surface, because it often loosens its grip when it is no longer suspended in midair. Once the animal is removed, standard local wound care is sufficient, with care taken to remove any teeth in the wound. Radiographs should be considered if bony injury is possible. Antibiotics should be given if infection develops, and tetanus status should be updated as appropriate.

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