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Essentials of diagnosis are as follows:
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Potential for limb-threatening local reactions20,21,22,23
Coagulopathy, bleeding
Compartment syndrome
Rhabdomyolysis
Capillary leak with intravascular volume depletion and shock
Metallic taste, nerve paralysis and respiratory failure
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Minor local reactions
Neurotoxicity
Respiratory depression
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In North America, venomous snakes include:
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Crotalidae (pit viper): Crotalus (rattlesnakes), Agkistrodon (copperheads), and cottonmouths. Crotalidae are present in most states of the US and are the cause of most snakebites.
Elapidae (coral snakes). Elapidae are present in Gulf Coast states.
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Clinical Features: Crotalidae (pit vipers)
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Pit viper venom contains numerous proteins with complex and variable effects. Digestive enzymes, myotoxins, metalloproteinases, fibrinolytic and thrombin-like molecules, amongst others, induce extensive local tissue damage, edema, and rhabdomyolysis with a cascade of events that may incorporate acute kidney injury, compartment syndrome, coagulopathy, thrombocytopenia, hemorrhage, diffuse capillary leak, and shock. The rattlesnake may deliver an anticholinergic neurotoxin imparting weakness, cranial nerve palsies, and in some cases respiratory failure. The severity of pit viper envenomation can range from very minimal local reactions with no systemic reactions, to very severe limb-threatening local reactions and vital organ failure-inducing systemic reactions. Generally rattlesnakes cause more systemic symptoms, sometimes associated with minimal local reactions, while the other Crotalid snakes cause more local reactions.
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Treatment in the in-hospital setting and ICU consists of administration of polyvalent Crotalide antivenom for more serious reactions, and additional supportive care and management of the usual complications (hypovolemia, shock, bleeding, compartment syndromes, respiratory failure, acute kidney injury, and others). Initiation and dosing of antivenom is dependent on the severity of reaction observed and should be made with expert toxicologic consultation through the toxicology center network at 1-800-222-1222. Antivenom administration can be associated with immediate life-threatening anaphylaxis and delayed hypersensitivity reactions; preparations should be made for the possibility of severe immediate systemic reactions as the antivenom is prepared for administration. Anaphylaxis and other severe immune reactions associated with antivenom administration are treated in the standard fashion, and may preclude repeat administration of such treatment. Close communications with expert toxicology support is essential for determining the optimal course of action in the individual patient. Some of the above complications of Crotalide envenomation, such as severe local reactions, hemorrhages and compartment syndrome, will require surgical consultation and subsequent management.
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Clinical Feature of Elapidae (coral snakes)
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The venom of these snakes contains phospholipase and a neurotoxin, respectively causing local wound reactions and neurotoxic effects. Systemic reactions can occur in the absence of local reactions and be delayed in onset up to 12 hours. Envenomation from the Eastern coral snake results in predominant systemic reactions consisting of nausea, vomiting, headache, paresthesias or numbness, and may progress to paralysis with respiratory failure. The Texas coral snake causes mostly minor local reactions resulting in local pain, swelling, erythema and paresthesia, requiring mostly management of local pain. Given the delayed systemic reaction that could be associated with respiratory failure and significant paralysis following Elapidae envenomation, close observation in a monitored setting is indicated for the first 12 to 24 hours. Treatment of patients is complicated by limited availability of the antivenom whose production has ceased in 2006. If residual stock of FDA-approved antivenom is available, it should be administered in the presence of any systemic signs of envenomation and this should be done with expert consultative support from the poison control center (1-800-222-1222). The serum used in this antivenom is derived from horse serum and can cause similar hypersensitivity reactions as the Crotalide antivenom; similar degrees of precaution are advised before its use.
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SPIDER BITES AND SCORPION STINGS
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Essentials of Lactrodecism (Black Widow Spider Bite) are as follows:23,24,25,26,27,28,29
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Throughout United States
Intense pain
Muscle spasms
Hyperadrenergic response
Neuromuscular manifestations (fasciculations, ptosis, facial spasm)
Abdominal pain may mimic surgical abdomen
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Essentials of Loxoscelism are as follows:
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Southeastern United States
Intense local pain and reaction that may result in necrotic eschar formation
Systemic manifestations (hemolysis, acute kidney injury, rhabdomyolysis)
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Essentials of Scorpion Stings are as follows:
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Southern United States
Intense pain
Neuromuscular manifestations (muscle jerking, opsoclonus, tongue fasciculations, paralysis, and respiratory failure)
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General Considerations
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In North America, the clinically important insults incurred by spider bites are Lacrodectism (bite from Black Widow Spider—Lacrodectus species) and Loxoscelism (bite from the Loxosceles species).
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Clinical Features—Lactrodecism (Black Widow Spider Bite)
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Present throughout the US, this spider resides mostly in dark places, such as woodpiles or garages. The venom contains a toxin that causes catecholamine and acetylcholine release from presynaptic terminals. The ensuing muscle spasms and severe pain are generally accompanied by a hyperadrenergic response. The resulting presentation may suggest an acute abdomen, a primary cardiovascular condition such as an acute coronary syndrome, as well as rabies or tetanus. Treatment of severe reactions requiring admission to an ICU includes management of symptoms with opiates for pain and benzodiazepines for muscle spasms. Expert toxicology consultation via the regional poison control center (1-800-222-1222) should be sought before administration of the available black widow spider antivenom for severe reactions. As in all animal-derived serums, this antivenom can cause serious immediate and delayed hypersensitivity reactions that have resulted in patient fatalities.
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Clinical Features—Loxoscelism (Recluse or Brown Spider Bite)
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Loxoscelism is the term used to describe the syndrome caused by the Loxosceles species (the recluse or brown spider) that is present in the Southeastern US. Envenomation is most likely to be incurred by the female upon unintended provocation; sphingomyelinase D and hyaluronidase are the active enzymatic components of the venom. As the initial bites are often painless, the victim will often be unaware of the insult and thus unable to identify the spider. Cutaneous insult is manifested as pain and erythema (within 12-24 hours). Painful edema, irregular areas of ecchymosis and hemorrhagic blisters may form. Within 72 hours, there is a possibility of ulcer and necrosis formation. This may eventually culminate in dry necrotic eschar formation within 5 to 7 days. This progression of events, if it is to occur, will culminate in a fairly well defined ulcer with granulation formation in 2 to 3 weeks. In about 50% of cases, the cutaneous form will be accompanied by nonspecific symptoms such as headache, nausea, and vomiting. The systemic variant of loxoscelism may occur in approximately 10%, and includes renal failure, rhabdomyolysis, and intravascular hemolysis. Systemic loxoscelism occurs 24 to 72 hours after the bite, and this presentation may require ICU admission.
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Management of the rare systemic loxoscelism is supportive, and may include mechanical ventilation and hemodialysis. In other cases, expertise from a wound specialist should be sought. Loxosceles antivenom is not available in the United States, but is used in South America.
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Scorpion Envenomation
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Scorpions, located in the Southern USA, are nocturnal and favor dry environments. Accidental transport of scorpions as stowaways may result in envenomation outside of their endemic area. Only the Centruroides sculpturatus (also known as Centruroides exilcauda or the “bark scorpion”) causes clinically relevant presentations in the USA. The intent of the scorpion venom, which acts as a neurotoxin via its action on sodium channels, is to immobilize the victim. Envenomation may result in vomiting, adrenergic effects (tachycardia, hypertension), localized pain, paresthesias, muscle jerking, opsoclonus, tongue fasciculations, rhabdomyolysis, and respiratory failure (loss of airway muscle tone in combination with increased salivation resulting in the inability to handle secretions). In the absence of antivenom administration, 24% may end up requiring mechanical ventilation. Symptom onset will begin 15 minutes after envenomation. Severity of envenomation ranges from self-limited local discomfort and paresthesia, to a more generalized pain with associated skeletal and cranial nerve paralysis, and autonomic nervous dysfunction. Supportive management will include analgesia (opioid analgesia is indicated), benzodiazepines, and intravenous fluid administration. Severe systemic symptoms warrant the administration of the antivenom, immune F(ab')2 (equine) injection, with readministration at 30 minute serial evaluations if symptoms persist. This equine preparation has been successfully demonstrated to resolve Centruroides scorpion envenomation mediated neurotoxicity in children if administered within 4 hours of insult. Expedient administration in the emergency room may altogether obviate the need for ICU admission. For patients admitted to the intensive care unit with persistent symptoms or significant organ dysfunction expert consultation with toxicology specialists at a regional poison control center (1-800-222-1222) is advised.
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Marine Life Envenomations
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Essentials of diagnosis are as follows:
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Stingrays (Class Chondrichthyes)
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Stingrays are found worldwide, and account for around 2000 emergency room visits per year in the United States. The insult inflicted on the human will be the result of an unintended encounter, as opposed to an attack. The stingray is often buried in the sand; the victim may unknowingly step on it, causing the stingray to unleash its tail (decorated with up to 6 barbs) on the extremity. The laceration induced by this may cause hemorrhage if an artery is struck. The embedded spines then release their venom. The venom of the Stingray consists of amino acids, serotonin, 5'-nucleotidase, and phosphodiesterase. The net effect of the venom is potent vasoconstriction and wound necrosis, with the victim experiencing considerable pain and edema. Clinical examination reveals swelling, erythema, and cyanosis. The symptoms peak at 30 to 90 minutes, and last up to 48 hours. The embedded spines, if not removed, remain an active source of venom. The affliction of the heart or secondary trauma accounts for mortality. Systemic symptoms may include excessive salivation, muscle cramps, nausea, and vomiting.
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The hallmarks of therapy include hemostasis, hot-water immersion, analgesia, and wound-exploration. Hemostasis should the first priority. The treatment of hot water immersion (43.3°C-45.6°C) takes advantage of the heat-labile nature of the venom. Imaging and exploration should be directed at removing embedded spines.
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The Scorpaenidae Family (spiny fish) consists of Stonefish and Lionfish. In the United States, the afflicted victims will usually be aquarium owners. The affected extremity will be edematous and painful, with the possibility of wound necrosis development. Systemic effects, though rare, may include myotoxicity, neurotoxicity, and cardiotoxicity. It is suggested that the systemic effects of nausea and syncope may actually be due to the pain inflicted by envenomation from the embedded spines.
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As with the envenomation induced by the Stingray, the hallmarks of therapy include hemostasis, hot-water immersion (45°C), analgesia, and wound exploration. In the case of the Stonefish, antivenom may be administered intramuscularly. All spines must be removed (and confirmation should be sought with plain radiographs). The affected extremity must be elevated and washed with water. The wounds may take months to heal, and expert consultation from a Wound specialist should be sought.
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Portuguese-man-of-war (Physalia physalis)
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The Portuguese-man-of-war is found in the Atlantic Ocean, in shallow water and along the shore. Its nematocysts may remain active for months. The victim experiences pain upon exposure; the erythematous skin irritation that accompanies it may eventually progress to wound necrosis. Some may develop a delayed hypersensitivity reaction. Systemic reactions in the form of nausea, vomiting, dyspnea, headache, abdominal pain, and cardiovascular compromise are infrequent but have resulted in death.
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The victim should be removed from the water to prevent further envenomation. The tentacles can be removed manually (preferably with forceps or the gloved hand) or by pouring salt water over the affected area. Hot-water immersion will serve to inactivate the heat-labile venom. As of yet, there is no definitive antivenom targeting Physalia physalis.