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1358 SECTION 16: Environmental Injuries CLINICAL FEATURES Blister beetles contain a highly potent vesicant (either cantharidin or pederin) that can be exuded or released if the beetle is brushed against, pressed, or crushed on the skin. For this reason, a blister beetle should be removed from the skin by blowing or flicking. Cantharidincontaining preparations are used medicinally for wart removal. Application of these substances in low concentration is without adverse effect. However, higher concentrations or contact with the beetle’s venom may cause local inflammation, leading to bullae formation. Severe conjunctivitis may also occur if cantharidin or pederin contacts the eyes from contaminated hands. Most described cases of blister beetle dermatosis are from seasonal outbreaks due to pederin-containing beetles. 50 At least one outbreak has been described in the United States. Topical exposure to blister beetles can cause a vesiculobullous eruption typical of a vesi cant. Pederin-containing dermal exposures result in a more delayed (up to 36 to 72 hours) but more painful and symptomatic eruption than those from cantharidin-containing beetles. Due to the delay in onset of symptoms and signs, misdiagnosis is common. High concentrations of cantharidin preparations may result in dermal absorption and systemic toxicity. Systemic toxicity is well described following ingestion, either of the whole beetle or of cantharidin-containing preparations. Severe vomiting, hematemesis, abdominal pain, and diarrhea may occur, fol lowed by dysuria, hematuria, oliguria, and renal failure. Although the exact mechanism by which cantharidin produces systemic toxicity is unknown, the vesicant action likely explains most of the findings. Direct cardiac toxicity with large ingestions of cantharidin is possible, and deaths have been reported. Fortunately, most preparations sold as “Spanish fly” for their purported aphrodisiac properties have very low concentrations of cantharidin. The local vascular congestion and ure thral inflammation that occur following ingestion may be interpreted by some as enhanced sexuality. TREATMENT Treatment is supportive. The skin should be irrigated thoroughly after topical exposure to remove any persistent vesicant, followed by local wound care. Patients who are symptomatic after ingestion should be admitted and treated supportively. REFERENCES The complete reference list is available online at www.TintinalliEM.com. Snakebite Richard C. Dart Julian White INTRODUCTION AND EPIDEMIOLOGY Venomous snakes account for an annual estimated 1.5 million to 3 million bites and possibly greater than 100,000 deaths worldwide.1 The American Association of Poison Control Centers reports an annual average of 6000 bites, approximately 2000 of them by venomous snakes. Because of underreporting, the true number of snakebites in the United States is possibly as high as 45,000 per year, with 7000 to 8000 by venomous snakes. 2 The major venomous snakes of the world can be divided into three groups: Viperidae (vipers and pit vipers), Elapidae (includes Hydrophiinae, or sea snakes; see Chapter 213, “Marine Trauma and Envenomation”), and the diverse group of non–front-fanged colubrid snakes (former family Colubridae, now split into several families). In the United States, most snakebites 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%.

n”), and the diverse group of non–front-fanged colubrid snakes (former family Colubridae, now split into several families). In the United States, most snakebites 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 five deaths occur per year. 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). Venomous 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.  CROTALINAE (PIT VIPER) BITES The crotaline snakes are called pit vipers because of bilateral depres sions or pits located midway between and below the level of the eye and the nostril (Figure 212-1). The pit is a heat receptor that guides strikes at warm-blooded prey or predators. Crotaline snakes are also distin guished 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 neu romuscular dysfunction, resulting in a mixture 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 fibrino gen 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 envenomation involve a com plex 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 sever ity of envenomation following a crotaline bite is therefore variable. An CHAPTER Heat-sensing pit NostrilElliptical slit pupil FIGURE 212-1. Pit viper. Tintinalli_Sec16_p1333-1418.indd 1358 8/2/19 8:23 PM

e or bites (location, depth, and number; the amount of venom injected) all affect the clinical evolution. The sever ity of envenomation following a crotaline bite is therefore variable. An CHAPTER Heat-sensing pit NostrilElliptical slit pupil FIGURE 212-1. Pit viper. Tintinalli_Sec16_p1333-1418.indd 1358 8/2/19 8:23 PM CHAPTER 212:  Snakebite      1359 initially minimal bite may evolve into a more serious bite and require large amounts of antivenom. The cardinal manifestations of crotaline envenomation are the pres ence of one or more fang marks, localized pain, and progressive edema extending from the bite site. Other early symptoms and signs are nausea and vomiting, weakness, oral numbness or tingling of the tongue and mouth, dizziness, and muscle fasciculation. Systemic effects include 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 without causing systemic effects. 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; it can be 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 212-1). Take all patients bitten by a pit viper to a healthcare facility. Avoid dangerous first aid treatments such as suction and incision. Do not use kits that contain suction cups; the cups 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 are questioned. 3 Electric shock treatment of the bite site is dangerous and ineffective and can cause electrical injuries. Ice water immersion worsens the venom injury. Do not use tourniquets 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 and applied with enough tension to restrict superficial venous and lymphatic flow while maintaining distal pulses and capillary filling. Apply the band snugly but loose enough to avoid arterial compromise.

is an elastic bandage or Penrose drain, thick rope, or piece of clothing wrapped circumferentially above the bite and applied with enough tension to restrict superficial venous and lymphatic flow while maintaining distal pulses and capillary filling. Apply the band snugly but loose enough to avoid arterial compromise. It should be easy to insert one or two fingers under the band. A constriction band can delay venom absorp tion without causing increased swelling. 4 In distinction to a constric tion band, a pressure immobilization bandage is a compression pad placed over the bite site combined with a snug elastic bandage wrap and extremity immobilization. This technique is recommended for coral snake and other elapid snake bites but is generally discouraged for cro taline bites because it may increase pain at the site.  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. Do not remove tourniquets or constricting bands until anti venom is available, except where there is clear arterial vascular com promise threatening limb viability; in this latter situation, anticipate possible rapid development of systemic envenomation upon removal of first aid. Institute advanced life support measures as indicated. If the patient is hypotensive, rapidly administer IV isotonic fluids. Immobilize the limb in a neutral position during transport to reduce further venom absorp tion. Consult with a physician or poison control center familiar with the management of snake envenomation.  ED MANAGEMENT Antivenom is the mainstay of therapy for venomous snakebites 1,5 (Table 212-2). 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 United States. Crotalidae Immune F(ab’)2 (Equine) (Fab 2AV) is now commercially available. The serum half-life of Fab2AV is longer, and a prospective trial reported that the incidence of recurrent coagulopathy was reduced. The relative effectiveness and safety of each product are unknown. Each antivenom is produced by immunizing sheep or horses with crotaline snake venoms, which vary by the product. The immune serum is harvested from the host animals and then digested with papain (FabAV) or pepsin (Fab 2AV) to produce antibody fragments. In both cases, the more immunogenic Fc portion of the antibody is eliminated during purification. All snakebite patients who develop progressive signs and symptoms should be treated promptly with antivenom. Progression is defined as worsening of local injury (e.g., pain, ecchymosis, swelling), abnormal laboratory results (e.g., worsening platelet count, prolonged coagulation times, decreased fibrinogen level), or systemic manifestations (e.g., unstable vital signs, abnormal mental status) (Table 212-3). Administer antivenom IV to establish “initial control” (Figure 212-2). Initial control is cessation of progression of three clinical evalu ation parameters: local effects, systemic effects, and hematologic TABLE 212-1 Recommended First Aid Measures for Snakebite •   Retreat well beyond striking range. Many victims are bitten again while trying to capture the snake. •   Remain calm. Movement will increase venom absorption. •   Immobilize the extremity in a neutral position below the level of the heart. •   Ensure prompt transport to a medical facility whether or not there are signs of envenomation. •   Constriction bands (see text) can be applied if there is no nearby medical facility.

emain calm. Movement will increase venom absorption. •   Immobilize the extremity in a neutral position below the level of the heart. •   Ensure prompt transport to a medical facility whether or not there are signs of envenomation. •   Constriction bands (see text) can be applied if there is no nearby medical facility. TABLE 212-2 Clinical Features and Treatment of Reptile Envenomation Reptile Clinical Findings Antivenom Crotaline snake (pit viper) Fang marks Local tissue injury Fibrinolysis Thrombocytopenia Systemic effects Crotalidae Polyvalent Immune Fab Crotalidae Immune F(ab’)2 (Equine) Coral snake Neurologic dysfunction Antivenom (Micrurus fulvius) Elapid snake Coagulopathy for some species Systemic effects, primarily neurologic dysfunction Cardiac arrhythmias and dysfunction Local injury for some species Each species has monovalent or polyvalent antivenoms Tintinalli_Sec16_p1333-1418.indd 1359 8/2/19 8:23 PM

ke Neurologic dysfunction Antivenom (Micrurus fulvius) Elapid snake Coagulopathy for some species Systemic effects, primarily neurologic dysfunction Cardiac arrhythmias and dysfunction Local injury for some species Each species has monovalent or polyvalent antivenoms Tintinalli_Sec16_p1333-1418.indd 1359 8/2/19 8:23 PM 1360 SECTION 16: Environmental Injuries abnormalities. It is crucial to document initial control because the most common error in management is insufficient dosing early in treatment. After reconstitution, dilute each dose of antivenom in crystalloid and infuse over 1 hour. After initial control has been established, two-vial maintenance doses are recommended (Figure 212-2) for FabAV . Fab 2AV will be introduced in 2019 6; dosing schedules are different, and the healthcare provider should be careful to use antivenom according to the product label and in consultation with a poison center. In children, the total volume, but not the number of vials, may be reduced. 7 If IV access is unavailable, the IO route may be used. Do not inject antivenom IM or directly into a digit, because venominduced hypovolemia may retard absorption of antivenom. Hospital pharmacies in regions where venomous snakes are prevalent should maintain adequate stocks of antivenom. Unfortunately, many hospitals stock insufficient amounts of antivenom, even in endemic areas. The package insert is useful as a guide for antivenom preparation. Give antivenom in a critical care facility such as an ED or intensive care unit, under direct physician supervision, and with resuscitative drugs (including epinephrine) and equipment immediately available. The incidence of acute reactions to modern antivenoms is low. 9 If an acute allergic reaction occurs, stop the infusion immediately and administer antihistamines (both histamine-1 and histamine-2 receptor blockers). Epinephrine should be readily available and administered for anaphylaxis. Continue to observe for progression of edema and systemic signs of envenomation during and after antivenom infusion. Measure limb circumference at several sites above and below the bite, and outline the advancing border of edema with a pen every 30 minutes. These measures serve as an index of the progression as well as a guide for antivenom administration. Repeat laboratory determinations every 4 hours or after each course of antivenom therapy, whichever is more frequent. Additional doses of antivenom may be warranted if the patient’s condition worsens. The use of crotaline antivenom for copperhead envenomation is controversial, but recent studies indicate effectiveness of FabAV . 10 It should be administered in copperhead bites where progression occurs over time. The value of aggressive support ive care cannot be overemphasized. Administer isotonic fluid resus citation followed by vasopressor agents for hypotension. Antivenom is the best treatment for hematologic abnormalities, but if active bleeding occurs, blood component replacement may be necessary after antivenom has been given. Compartment syndrome is another complication of snakebite. Increased compartment pressure may occur when venom is injected or spreads into a compartment; this is often manifested by severe pain that is localized to a compartment and usually resistant to opiate anal gesia. Table 212-4 presents the suggested treatment of compartment syndrome. 11 The use of fasciotomy is controversial, and there is no firm evidence supporting its use. Clean the bite wound and determine the need for tetanus immuniza tion. 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 are not effective and could be harmful.

the bite wound and determine the need for tetanus immuniza tion. 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 are not effective and could be harmful. Steroids should be reserved for the treatment of allergic reactions or serum sickness. Serum sickness is uncommon after antivenom treatment. The symp toms are fever, rash, and arthralgias. Start prednisone, 1 milligram/kg PO once daily, and taper 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 exclude significant envenomation. Observe patients for at least 6 to 8 hours in the ED before determining disposition. Discharge patients with dry bites who have been observed for 6 to 8 hours with instructions to return if pain, swelling, or bleeding devel ops. Admit patients with severe or life-threatening bites and patients receiving antivenom 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. Patient with indication for FabAV administration Establish initial control of envenomation by administering 4–6 vials of FabAV Initial control* achieved? Yes Infuse additional 2-vial doses at 6, 12, and 18 h after initial control is achieved FIGURE 212-2. General  strategy  for  administration  of  pit  viper  antivenoms  in  the United States. Both antivenoms use the same strategy of establishing initial control followed by additional antivenom as needed. However, the dosage varies; the package insert should be consulted for dosing recommendations. *Initial control is cessation of progression of all components  of  envenomation:  local  effects,  systemic  effects,  and  coagulopathy. FabAV  = Crotalidae Polyvalent Immune Fab (Ovine). TABLE 212-3 Laboratory Evaluation in Crotaline or Elapid Snakebite •   CBC* •   INR or prothrombin time* •   PTT* •   Fibrinogen level* •   Fibrin degradation product levels •   Serum electrolyte levels •   Glucose level •   BUN level •   Platelet count •   Creatine kinase level •   ECG† •   Arterial blood gas analysis‡ *Should be performed as soon as possible and repeated within 12 h. †Suggested for patients >50 y of age and patients with a history of heart disease. ‡Should be performed if any signs or symptoms of respiratory compromise are evident. TABLE 212-4 Management of Compartment Syndrome Caused by Crotalinae Snake Envenomation*† •   Determine intracompartmental pressure. •   If pressure is not elevated, continue standard management. •   If signs of compartment syndrome are present and compartment pressure is >30 mm Hg: •   Elevate limb. •   Administer mannitol, 1–2 grams/kg IV over 30 min. •   Simultaneously administer additional antivenom over 60 min. •   If elevated compartment pressure persists another 60 min, consider fasciotomy. *Elevated compartment pressure is caused by the action of the venom on the tissues, and thus management of compartment syndrome due to snakebite is unique; therefore, the most effective treatment is to neutralize the venom, which may reduce the compartment pressure. †The mannitol and antivenom deliver a high osmotic load, and fluids and electrolyte levels need careful monitoring. The administration of mannitol and antivenom must be completed promptly so that, if ever needed, fasciotomy may be performed as early as possible. Tintinalli_Sec16_p1333-1418.indd 1360 8/2/19 8:23 PM

ure. †The mannitol and antivenom deliver a high osmotic load, and fluids and electrolyte levels need careful monitoring. The administration of mannitol and antivenom must be completed promptly so that, if ever needed, fasciotomy may be performed as early as possible. Tintinalli_Sec16_p1333-1418.indd 1360 8/2/19 8:23 PM CHAPTER 212:  Snakebite      1361 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. Patients should return if symptoms recur or if they develop bruising or other signs of recurrent coagulopathy. Outpatient follow-up is necessary to monitor for infection and serum sickness. The patient should be instructed about serum sickness symptoms and advised to report if such symptoms develop.  ELAPID SNAKEBITE U.S. CORAL SNAKEBITES U.S. coral snakes include the eastern coral snake ( Micrurus fulvius), the Texas coral snake ( Micrurus tener), and the Arizona (Sonoran) coral snake (Micruroides euryxanthus). The eastern coral snake is found pri marily in the southeastern United States. The Texas and Arizona coral snakes are found primarily in their eponymous states. 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 nonvenomous 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 United States. Coral snake venom is primarily composed of neurotoxic components that do not cause marked local injury ( Table 212-2). Admit potential victims of coral snakebite to the hospital for observation, because venom effects may develop hours after a bite and are not easily reversed. Administer three to five vials of antivenom, Anti venin ® ( M. fulvius), IV 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 antive nom 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 (e.g., inspiratory pressure and vital capacity), in addition to intensive care observation, may be useful. Prolonged ventilatory support may be required in severe cases. Observe the patient closely for signs of respiratory muscle weakness and hypoventilation. Bites by the Sonoran coral snake are mild, and antivenom is not usually needed. ELAPID BITES WORLDWIDE Elapids are found throughout the world in warm climates. Elapids occur in Australia, New Guinea, Asia, Africa, and the Americas. All sea snakes are elapids (subfamily Hydrophiinae). Medically significant groups include some venomous snakes of Australia (tiger snakes [Notechis], brown snakes [Pseudonaja], taipans [Oxyuranus], death adders [ Acanthophis], “black” snakes [ Pseudechis], pygmy copperheads [ Austrelaps], rough-scaled snake [Tropidechis carinatus ], broad-headed snakes [Hoplocephalus ]) and, in other areas, cobras (Naja; Asia and Africa), mambas (Dendroaspis; Africa), kraits (Bungarus; Asia), coral snakes (Micrurus; Americas), and a variety of less common genera and species. Elapid bites produce systemic effects, particularly neurologic effects: tremor, salivation, dysarthria, diplopia, bulbar paralysis with ptosis, fixed and constricted pupils, dysphagia, dyspnea, and seizure.

ca), kraits (Bungarus; Asia), coral snakes (Micrurus; Americas), and a variety of less common genera and species. Elapid bites produce systemic effects, particularly neurologic effects: tremor, salivation, dysarthria, diplopia, bulbar paralysis with ptosis, fixed and constricted pupils, dysphagia, dyspnea, and seizure. 14 Some groups (e.g., cobras) also produce pain, local injury, and necrosis, which may be more clinically prominent than systemic effects. 14 The immediate cause of death is usually paralysis of respiratory muscles. Australian elapids produce coagulopathy; some cause rhabdomyolysis, as do some kraits. Signs and symptoms may be delayed 12 or more hours. Some cobras in Africa and Asia (“spitting cobras”) can spit venom several feet. If spit into the eye, this venom can cause venom spit ophthalmia, a very painful acute corneal injury rendering the victim temporarily blind, but systemic envenomation does not occur. In general, a spitting cobra bite causes moderate to severe local effects, including necrosis, with paralytic effects uncommon in most species. PATHOPHYSIOLOGY The Elapidae possess nonretractile small- to medium-sized paired fangs that have grooved, often enclosed venom channels rather than hollow venom ducts. 14 It is thought that the Elapidae exert voluntary control over the injection of venom, hence the frequent occurrence of a dry bite. The venom of the Australian elapids contains several important components. 14,15 Neurotoxins (tiger snake, taipan, death adder, and others) act at the neuromuscular junction and cause descending symmetric flaccid paralysis. Signs usually develop within 2 to 12 hours after the bite and may include ptosis, partial ophthalmoplegia (diplopia), dys arthria, loss of facial expression, loss of airway control, and respiratory paralysis. The procoagulant toxins (seen in brown snake, tiger snake, taipan, and others) act as prothrombin converters, leading to a venominduced consumptive coagulopathy with fibrinogen depletion and variable thrombocytopenia. Intracranial hemorrhage is a recognized complication. Brown snake envenomation can cause rapid collapse and death. 15,16 Renal impairment or failure may also result from snakebite. The mechanisms are poorly understood and may include hypotension, myoglobinuria, coagulopathy, and direct renal toxicity. 14,15 Myolysins (tiger snake, taipan, and mulga snake) are structurally related to the neurotoxins but instead produce rhabdomyolysis, which may result in muscle pain, weakness, myoglobinuria, secondary renal failure, and hyperkalemia. 14,15 Rarely, a venom-induced thrombotic microangi opathy may complicate brown and tiger snake envenomation. 16-18 Local tissue destruction is uncommon with the bite of any Australian species, although mild to moderate ecchymosis and swelling may occur. This likely accounts for the popularity of pressure bandages and immobilization in Australia. CLINICAL FEATURES The severity of elapid envenomation cannot be estimated by the clinical appearance of the bite site or by initial symptoms. 14-17 Even with severe envenomation, patients may initially feel well and manifest few clinical features. Early symptoms include nausea, vomiting, headache, abdomi nal pain, diplopia, dysphonia, progressive muscle weakness, discolored urine, and seizures. 15 Y oung children may not provide a history of snakebite; if a child develops toxicity in a region populated with elapids, envenomation should be suspected. 15 In Australia, the most common cause of snakebite fatality is a prehospital cardiac arrest, inadequately resuscitated, as a result of a brown snake (Pseudonaja spp.) bite. DIAGNOSIS The diagnosis requires correlation of history, clinical features, and laboratory investigations.

pids, envenomation should be suspected. 15 In Australia, the most common cause of snakebite fatality is a prehospital cardiac arrest, inadequately resuscitated, as a result of a brown snake (Pseudonaja spp.) bite. DIAGNOSIS The diagnosis requires correlation of history, clinical features, and laboratory investigations. Laboratory tests often determine if the patient requires antivenom treatment. 14-17 Key tests include prothrombin time (PT), INR, activated PTT, d-dimer, fibrinogen, fibrin degradation products, hemoglobin, platelet count, electrolytes, renal function test, and creatine kinase. These tests should be performed prior to removal of first aid, 1 hour after removal of first aid, and at 6 and 12 hours after bite (earlier if clinical abnormalities develop). 15,19 Look for evidence of procoagulant coagulopathy (prolonged PT and activated PTT, high INR, raised d-dimer/fibrin degradation products, low fibrinogen), anticoagulant coagulopathy (abnormal PT and activated PTT with high INR, but normal fibrinogen and d-dimer/fibrin degradation products), platelet effects, rhabdomyolysis (grossly elevated creatine kinase, myo globinuria), renal damage (abnormal renal function tests, reduced urine output), hyponatremia, and a syndrome similar to hemolytic-uremic syndrome (thrombocytopenia, anemia, intravascular hemolysis). 15 A Snake Venom Detection Kit® (SVDK; bioCSL, Parkville, Victoria, Aus tralia) is available to identify snake venom at the bite site or in the urine, correlated to venom immunotype (which corresponds to “monovalent” antivenom type), for use exclusively with Australian and New Guinea snakes. 15 Positive SVDK identification of venom at the bite site or in the urine assists in selecting a “monovalent” antivenom, but does not Tintinalli_Sec16_p1333-1418.indd 1361 8/2/19 8:23 PM