Occupational setting

Gardeners, orchard workers, farmers and agricultural workers, florists and workers in the flower industry, forestry workers, and sanitation workers are potentially at risk.

Exposure (route)

Exposure occurs through physical trauma to the skin and occasionally the oral mucosa as a result of a bite or sting.

Pathobiology

Bees have a barbed stinger that becomes attached to the human skin after a sting, when it deposits its venom. In honeybee stings, the stinger apparatus becomes disengaged from the bee with its venom sac intact. Wasps also have a stinging apparatus but it does not contain barbs; therefore, they are able to withdraw the stinger and sting again. Ants have powerful jaws that grasp the skin and cause the release of venom locally; they are capable of inflicting multiple bites.

The Hymenoptera venom of the bee (Apoidea) consists of histamine, dopamine, enzymes (phospholipase A₁ and hyaluronidase), and peptides, including neurotoxins and hemolysins.¹ The Vespoidea venom is very similar to the bee venom, except that both wasp venom and hornet venom contain serotonin, and the venom of the hornet also contains acetylcholine.¹ The Formicoidea venom contains alkaloids and a small amount of proteins. Histamine is released when these alkaloids come in contact with the mast cells, causing a local reaction. The hypersensitivity-type reaction appears to be caused by the low-molecular-weight proteins found in the venom.^2,3 Hymenoptera stings most often cause pain characterized as sharp stabbing or burning; they are accompanied by a local reaction consisting of mild erythema, edema, and pruritus.

Stings can cause severe local reactions, systemic or anaphylactic reactions, as well as delayed and unusual reactions. Severe local reactions consist of increased swelling (edema) around the sting site. The severity depends on the sting location. Stings in the mouth, upper airway, or esophagus may cause obstruction of the airway or dysphagia.⁴ Stings that occur on the eye structures or around the eye may cause local complications, including cataract formation and glaucoma. Severe local reactions on an extremity may include swelling of one or more joints without systemic toxicity.

Systemic or anaphylactic reactions may consist of mild symptoms and signs, including malaise, urticaria, pruritus, and anxiety. A moderate response may present with tightness in the throat or chest, generalized angioedema, nausea, vomiting, and abdominal discomfort. A severe reaction consists of cyanosis, hypotension, loss of consciousness, and other signs of shock, as well as dyspnea, hoarseness, increased malaise, and incontinence. A systemic or anaphylactic reaction may occur from single or multiple stings; its severity may increase rapidly within minutes to cardiovascular collapse and death.

Delayed hypersensitivity reactions may occur within the first 2 weeks after an envenomation. Symptoms often include fever, urticaria, arthralgias, malaise, headache, lymphadenopathy, and myalgias. Unusual reactions include neurologic complications of encephalopathy, neuritis, Guillain–Barré-type reaction, myasthenia gravis, multiple sclerosis exacerbations, extrapyramidal disorders,^5–7 hemolytic anemia,⁸ and the nephrotic syndrome.⁹

Diagnosis

The specific identification of the organism causing the sting is difficult and is usually dependent on history. The history should include the geographic location where the sting took place, and the location of any nests should be carefully noted. Wasps usually make nests under eaves, hornets choose bushes or tree limbs, and yellow jackets usually make nests in the ground. Pictures or photographs of the various Hymenoptera species often help the patient to identify the insect.

The site of the sting is usually not helpful, except in the stings of the honeybee and the fire ant. The honeybee almost always leaves its stinger at the site of the sting with its venom sac attached. The fire ant usually inflicts a distinctive pattern of multiple bites, which subsequently produce pustules. Laboratory tests are not usually helpful in the diagnosis of Hymenoptera envenomations, except in the few unusual cases of hemolytic anemia subsequent to a wasp bite.

Treatment

Most local reactions can be treated with local wound care. If a stinger is in place at the envenomation site, it should be removed immediately by gently scraping or teasing the affected area, thereby minimizing the spread of venom into the wound. All sites should be washed thoroughly with an antiseptic, and the tetanus status of the patient should be assessed. All potentially constrictive jewelry should be removed. Ice packs at the sting site decrease venom absorption and edema. Oral analgesics and antihistamines (e.g., diphenhydramine) usually relieve the pain and subsequent pruritus associated with a mild reaction. Elevation and rest are indicated if there is increased edema of a limb. Antibiotics are indicated only if a secondary infection occurs.

Anaphylactic reactions are medical emergencies. Initial mild systemic symptoms may progress very rapidly to respiratory obstruction, cardiovascular compromise, and death. Any patient who displays signs of a systemic reaction should immediately be placed on a cardiac monitor, an intravenous line should be started, and epinephrine should be administered. In patients who are not in shock, 0.3–0.5 mL for an adult, or 0.01 mL/kg (~0.3 mL) for a child, of 1 : 1000 epinephrine hydrochloride should be administered subcutaneously and the site of administration massaged. A second injection of epinephrine may be needed in 10–15 minutes if symptoms do not improve or have become more severe. For severe anaphylactic reactions, epinephrine should be given slowly intravenously in a 1 : 10 000 solution and the patient observed and monitored closely. A repeat dose may be needed in 20–30 minutes.

Antihistamines such as diphenhydramine may be given intramuscularly or intravenously, depending on the severity of the anaphylactic reaction. Corticosteroids may also be helpful; but, as with antihistamines, their effect may be delayed and they should be used only as adjuncts to epinephrine therapy. Bronchospasm usually responds well to intravenous aminophylline after a loading dose (5–6 mg/kg over 20 minutes). The use of nebulized β-agonists may also be considered for patients with significant bronchospasm. Vasopressors are indicated in situations where hypotension is unresponsive to intravenous fluids and epinephrine.

Individuals who have moderate to severe systemic reactions to Hymenoptera venom with positive skin reactions should undergo desensitization with venom immunotherapy.^10,11 Immunotherapy usually consists of extracts containing purified insect venom rather than whole-body extracts, which appears to limit substantially the number of systemic reactions to the therapy.^12,13

Prevention

Preventive measures, especially in allergic individuals, include the avoidance of bright or flowered clothing and the avoidance of scented deodorants, perfumes, and shampoos. Individuals should avoid going outdoors barefoot. Nests around the home or frequented dwellings should be destroyed, preferably with professional assistance. Sensitized individuals should carry commercial epinephrine kits for self-administration; they should be available for use in their home and car and carried along with other personal belongings, such as golf bags). Sensitized patients should wear a medical alert bracelet or tag. Potential victims should stand still or retreat slowly when a Hymenoptera species is encountered. They should be instructed to brush the insect off their skin but avoid swatting or moving quickly. Sensitized individuals should avoid gardening. They should use caution when visiting places with open garbage cans, such as picnic areas, or other locations where insects are likely to be found.

Occupational setting

Farmers, gardeners, and forestry, construction, and sanitation workers are at risk for exposure.

Exposure (route)

Exposure occurs through physical trauma (bite) to the human skin with injection of venom.

Pathobiology

The female black widow spider is almost twice the size of its male counterpart. Although both are considered venomous, only the female spider is able to bite and envenomate humans. During the summer months, the female black widow spider is the most venomous. The body of the female can range from 8 to 15 mm long, with a leg span of 5 cm. The spider undergoes multiple moltings throughout the year and often changes color. The female is most often shiny black in color and has a rounded abdomen with a red distinctive hourglass on its ventral surface. Occasionally, two red spots may be seen instead of the hourglass configuration.

The five species in the United States are Latrodectus mactans, Latrodectus hesperus, Latrodectus variolus, Latrodectus bishopi, and Latrodectus geometricus. Although variations occur between species, most Latrodectus venoms contain multiple proteins and a potent neurotoxin. The proteins include hyaluronidase, phosphodiesterase, GABA, and 5-hydroxytryptamine. This neurotoxin is one of the most potent human neurotoxins. Neurotransmitters (GABA, acetylcholine, and norepinephrine) appear to be released secondary to the Latrodectus venom.^1,2 The clinical presentation usually begins with a pinprick sensation, followed by the appearance of mild swelling and erythema around the bite wound. It is not unusual for the patient to be unaware of the bite until a local reaction has occurred. Close evaluation of the site may reveal two erythematous fang marks. In the first hour after the bite, pain often increases around the area of the bite and spreads to the entire body. Symptoms peak at 3–4 hours. Upper extremity bites often lead to spasm of the upper trunk muscles; bites of the lower extremity often lead to abdominal spasms. These muscle spasms can become very intense and painful and have been misdiagnosed as an acute surgical abdomen. However, cases of abdominal spasms secondary to the black widow bite do not present with associated fever or a leukocytosis.

Other common symptoms include paresthesias and hyperesthesia, especially of the lower extremities and feet. Increased deep tendon reflexes, headache, anxiety, nausea, vomiting, diaphoresis, tremor, restlessness, and seizures may also be seen. Symptoms usually resolve within 24–48 hours. Pregnancy,³ infancy, increased age, and chronic debilitating illness appear to increase the risk of complications.

Diagnosis

Laboratory studies are usually not helpful in diagnosis. A description of the spider’s appearance, identification of the geographic area where the bite took place, and the clinical presentation and evaluation are the most helpful factors in diagnosing a black widow spider bite. The bite area usually consists of two closely approximated erythematous fang marks. In L. hesperus bites, there may be a target or halo lesion.⁴ Severe chest and back spasms must be carefully distinguished from myocardial infarction or an acute surgical abdomen.

Treatment

In general, treatment is supportive and includes local wound care, tetanus prophylaxis, and pain control (i.e., salicylates, opioids). All victims should be monitored for 6–8 hours for progression of symptoms. Airways, breathing, and circulation should be closely monitored and assisted, if necessary. The pain of severe generalized spasm may be treated with intravenous morphine. Intravenous calcium gluconate (10 mL of 10% solution) can be used to decrease cramping and spasm in select individuals. Methocarbamol and diazepam have also been used as muscle relaxants and for their anxiolytic effect. The use of intravenous dantrolene sodium for muscle relaxation is controversial and needs further study.^5,6

Most cases can be appropriately managed without the equine-derived antivenom. However, in cases where there is severe hypertension, or in the case of a pregnant woman at risk for premature labor or spontaneous abortion because of severe muscle spasms, the lyophilized antivenom may be indicated. Other indications for antivenom include respiratory distress, protracted symptoms despite treatment, cardiovascular symptoms, and symptomatic patients younger than 16 years and older than 65 years.^2,7–9 The Latrodectus antivenom is effective for all species. Unfortunately, it has the potential to cause immediate hypersensitivity, including anaphylaxis, as well as delayed onset serum sickness within 2 weeks. One vial of antivenom is usually necessary for envenomations. All patients should be skin tested for horse serum sensitivity prior to administration.

Prevention

Prevention measures should focus on the use of personal protective equipment such as gloves, heavy garments that are fully buttoned, and protective footwear when working in endemic areas. These spiders generally inhabit places that are dark and protected, such as woodpiles, barns, stables, garages, homes, outdoor sanitation facilities, and walls made of rock. Areas suspected of harboring black widows should be subjected to professional pest control.

Occupational setting

Gardening, housekeeping, forestry, farming, and agricultural workers are at risk of exposure.

Exposure (route)

Exposure occurs through physical trauma (bite) to the human skin with injection of venom.

Pathobiology

The brown recluse spider is ~1 cm in body length, with a leg span of up to 2.5 cm. The color of these spiders is usually tan to brown. In the United States, there are 13 species of Loxosceles, but Loxosceles reclusa is the most commonly found. The female is more dangerous than the male. These spiders contain a very distinctive violin-shaped, dark brown to yellow marking on the dorsal cephalothorax.

The Loxosceles venom contains a number of enzymes, including sphingomyelinase D, the agent believed to be responsible for skin necrosis and hemolysis by its direct effect on the cell plasma membrane as well as sulfated nucleosides.^1–3 The venom also contains hyaluronidase, which does not appear to cause skin necrosis. Loxosceles envenomation is initially painless for most victims. Within the first few hours, pain and erythema occur at the bite site. A central bleb or vesicle forms. It is surrounded by a blanched, whitish ring of ecchymosis and ischemia. The appearance resembles a bull’s-eye and it is most often 1–5 cm in diameter. Over the next few days, the central vesicle ulcerates, necroses, spreads in diameter, and involves the skin and subcutaneous fat. In ~1 week, an eschar develops that eventually sloughs and can require many months to heal.

Systemic reactions to Loxosceles envenomation, while uncommon, can occur. Systemic symptoms and signs usually occur within the first 2 days after envenomation; they include fever, chills, generalized rash, nausea, vomiting, and hemolysis with possible renal failure. Disseminated intravascular coagulation and thrombocytopenia are rare but have been reported.⁴ The size of the necrotic ulcer does not seem to correlate with the frequency or severity of the systemic symptoms.⁵

Diagnosis

Laboratory studies are not usually helpful in diagnosing a Loxosceles envenomation. A description of the spider’s appearance, identification of the geographic area where the bite took place, and the clinical presentation and evaluation are the most helpful factors in diagnosing a brown recluse spider envenomation. Moreover, it should be noted that there are other species that may reproduce the symptoms of the brown recluse spider.⁶

Treatment

In general, treatment should begin with local wound care, tetanus prophylaxis, immobilization, elevation, observation, and antipruritic agents, as needed. Local wound care has been controversial. Some authorities advocate early surgical excision of the wound; others recommend allowing complete delineation of the necrotic area before surgical intervention.⁷ The use of dapsone in Loxosceles envenomations is controversial and may cause methemoglobinemia in some cases.⁸ The use of hyperbaric oxygen to decrease the extent of the necrosis has been successful in a number of cases.⁹

All patients with systemic symptoms must be hospitalized and followed closely for hemolysis, coagulopathy, and renal failure. Treatment for systemic symptoms is supportive. There is no commercially available antivenom.

Prevention

Prevention measures should focus on the use of personal protective equipment like gloves, fully buttoned heavy garments, and protective footwear when working in endemic areas. The spider is usually not aggressive. Its habitat includes woodpiles, barns, the underside of rocks, closets, attics, clothing, carpets, linen, and other dry, dark places. Areas suspected of harboring these spiders should undergo professional pest control.

Occupational setting

Persons employed in farming, agriculture, construction, forestry, and other outdoor occupations in the southwestern part of the United States are at risk of exposure.

Exposure (route)

Exposure occurs through physical trauma (sting) to the human skin with injection of the venom.

Pathobiology

The scorpion consists of anterior pincers, a pseudoabdomen, and a tail that ends in a bulbous structure called the telson. Within the telson is the stinger and venom. The scorpion usually grasps the victim using its pincers, then arches its body and strikes the victim with the stinger located in its tail, injecting the venom. It ranges in size from 1 to 7 cm. A nocturnal creature, it prefers to take shelter during the day under rocks, debris, or objects outside the house. It generally climbs rather than burrows and therefore is often found among trees.

The venom consists of enzymes (hyaluronidase, acetylcholinesterase, and phospholipase), proteins, serotonin, and neurotoxins, which appear to affect the sodium channel.¹ It results in increased stimulation at the neuromuscular junction and increased axonal discharges.²

The clinical presentation usually consists of immediate, severe burning pain at the site of the sting. Paresthesias around the area of the sting may occur. There may be some local inflammation around the site, but most often there is no erythema, swelling, or evidence of ecchymosis.

Severe systemic symptoms may occur in some victims, with a greater incidence in victims under the age of 10 years. Systemic symptoms may occur within minutes or hours after the envenomation. Symptoms result from excitation of the sympathetic and parasympathetic nervous systems, as well as the neuromuscular junction. Symptoms include hyperexcitability, diplopia, nystagmus, restlessness, diaphoresis, muscle fasciculations, tachycardia, hypertension, opisthotonus, and convulsions. Cardiovascular collapse, respiratory arrest, disseminated intravascular coagulation, renal failure, and death are rare.

A clinical grading system for Centruroides sculpturatus envenomation uses the following 4-point scale: I (local pain), II (pain or paresthesia remote from sting site), III (either cranial nerve or somatic skeletal neuromuscular dysfunction), and IV (both cranial nerve and somatic skeletal neuromuscular dysfunction).³ There is a case report of a scorpion sting that appeared to relieve the symptoms of multiple sclerosis.⁴

Diagnosis

Laboratory studies are usually not helpful in diagnosis. Description of the scorpion’s appearance, identification of the geographic area where the sting took place, and the clinical presentation are the most helpful factors in making the diagnosis. In Centruroides stings, tapping or pressure on the site of the wound (“tap test”) usually produces severe discomfort.

Treatment

Most Centruroides stings can be managed with local wound care, tetanus prophylaxis, and the application of ice to the affected area. Systemic reactions should be treated as necessary, with advanced life support and supportive measures, and should be monitored very closely in the hospital. Antivenom has been used successfully in many severe cases.^5,6 Complications of the use of antivenom include immediate hypersensitivity (anaphylaxis) and delayed hypersensitivity (serum sickness) reactions.

Prevention

Prevention measures should focus on the use of personal protective equipment like gloves, heavy garments that are fully buttoned, and protective footwear when working in areas that the scorpion inhabits. Areas suspected of harboring scorpions should undergo professional pest control.

Occupational setting

Occupations with potential exposure include commercial fishing, diving, seafaring, and fish handling.

Exposure (route)

Exposure occurs through physical trauma (sting) to the skin with release of venom.

Pathobiology

The catfish has dorsal and pectoral fins with venom-containing spines. The most common affected sites are the hands of fishermen and fish handlers.^2–5 The venom contains agents that can cause skin necrosis and vasoconstriction, as well as other heat-labile agents.

The clinical presentation includes burning and throbbing at the envenomation site that usually resolves within a few hours but can last for days.⁴ The wound site may contain fragmented spines and is often edematous or may appear ischemic. Gangrene is possible secondary to severe envenomation.

Diagnosis

There are no known laboratory tests that are helpful in diagnosing these envenomations. Positive identification of the offending organism is helpful. Barring positive identification, the clinical presentation and geographic location of the envenomation are used to determine the appropriate treatment modality. Since most catfish spines are radiopaque, a radiograph of the affected area may be useful in identifying retained spines.

Treatment

Local wound care, including careful removal of the spines and tetanus prophylaxis, is extremely important. Immediate immersion in hot water (110–115°F) gives adequate pain relief.^2–5 Analgesics are a helpful adjunct in pain relief. Close observation of the wound site for infection is indicated.

Prevention

Preventive measures include wearing gloves and long-sleeved garments when handling organisms or specimens, avoiding any contact with reefs, and never contacting or touching an unknown organism. Persons at risk should always dive with a skilled diver (never alone) in unknown waters. Before working in unknown waters, they should become familiar with the potential marine envenomations and the local medical facilities in case treatment is needed.

Occupational setting

Workers with potential exposure include sailors, divers, fishermen, and seafood producers.

Exposure (route)

Exposure occurs through physical trauma (sting) to the skin caused by nematocysts that release venom.

Pathobiology

Sea anemones contain stinging structures, called nematocysts, which contain venom. They are abundant, flower-like structures that are usually sessile and have the ability to envenomate with their tentacles but rarely do so.¹ The soft and true corals do not contain nematocysts and therefore cannot envenomate. The venom of coelenterates is not well characterized, but serotonin (5-hydroxytryptamine (5-HT)) appears to be a major component.^{2, 3} It produces pain, vasoconstriction, and histamine release.

The clinical presentation of sea anemone envenomation is stinging, pain, and a burning rash. Systemic reactions are rare and the envenomations are infrequent. The coral usually causes injury secondary to trauma sustained when the victim brushes against the extremely sharp, calcified exoskeleton, suffering lacerations.

Diagnosis

There are no known laboratory tests that are helpful in diagnosing these envenomations. Positive identification of the offending organism is helpful. Barring positive identification, the clinical presentation and geographic location of the envenomation are very useful in determining the appropriate treatment modality.

Treatment

Treatment for the sea anemone envenomation includes inactivating the nematocysts by applying alcohol (i.e., isopropyl) or salt water. Alternatively, dilute vinegar, papain, or baking soda can be used. Fresh water should be avoided because it can cause increased venom release from the nematocysts. Immobilization of the affected area is also useful. Baking soda and abrasion of the area with a sharp knife can help to remove any remaining tentacles. Soaking the affected area in hot water (110–115°F) will alleviate severe pain.⁴ Narcotics, such as codeine, may also be given for pain control. Tetanus prophylaxis and local wound care should be administered. Oral antihistamines are often given routinely and can be especially effective with symptoms of pruritus. Tissue trauma caused by the corals should be treated with appropriate wound care and tetanus prophylaxis.

Prevention

Preventive measures include wearing gloves and long-sleeved garments when handling organisms or specimens, avoiding contact with reefs, and never contacting or touching an unknown organism. At-risk workers should always dive with a skilled diver (never alone) in unknown waters. Before working in unknown waters, they should become familiar with the potential marine envenomations and the local medical facilities, in case treatment is needed.

Occupational setting

Sailors, divers, fishermen, and seafood producers are at risk for exposure.

Exposure (route)

Exposure results from physical trauma (sting) to the skin inflicted by a stinging structure (nematocyst) containing the venom.

Pathobiology

All members capable of inflicting stings possess stinging structures, called nematocysts, which contain venom. The Portuguese man-of-war consists of a body and tentacles. On these tentacles, there are millions of nematocysts that can release venom upon contact. The tentacles of the Physalia can be up to 10 ft long. This creature can be found in all oceans. The hydroids and fire coral, also members of the Coelenterata, possess calcareous growths and inhabit coral reefs in tropical oceans. They also have venom-containing nematocysts.

The venom of coelenterates is not well characterized, but serotonin (5-hydroxytryptamine) appears to be a major component.^1,2 It produces pain, vasoconstriction, and histamine release. In particular, the venom of the Portuguese man-of-war contains a neurotoxin that produces severe pain and possible systemic symptoms.³

The clinical presentation of the Portuguese man-of-war envenomation is severe pain with multiple, linear, erythematous macules and papules, which may progress to vesicular lesions. Systemic reaction to envenomation may cause nausea, vomiting, chills, myalgias, and respiratory and cardiovascular depression. The clinical presentation of the envenomation caused by the fire coral and hydroids consists of erythema, pruritus, and edema of the affected skin area. Vesicular lesions and ulcer formation can occur. Systemic reactions of fever, chills, fatigue, myalgias, and abdominal discomfort occur infrequently.⁴

Diagnosis

There are no known laboratory tests that are helpful in diagnosing these envenomations. Positive identification of the offending organism is useful. Barring positive identification, the clinical presentation and geographic location of the envenomation are very helpful in determining the appropriate treatment modality.

Treatment

Treatment includes inactivating the nematocysts by applying alcohol (i.e., isopropyl) or salt water. Alternatively, dilute vinegar, papain, or baking soda can be used. Vinegar appears to be especially effective in Portuguese man-of-war envenomations.^5,6 Fresh water should be avoided because it can cause increased venom release from the nematocysts. Immobilization of the affected area is also helpful. Baking soda and abrasion of the area with a sharp knife can help to remove any remaining tentacles. Soaking the affected area in hot water (110–115°F) will alleviate severe pain. Narcotics, such as codeine, can be given for pain control. Tetanus prophylaxis and local wound care should be administered. Oral antihistamines are often given routinely and can be especially helpful with symptoms of pruritus.

Prevention

Preventive measures include wearing gloves and long-sleeved garments when handling organisms or specimens, avoiding contact with reefs, and never contacting or touching an unknown organism. Persons at risk should always dive with a skilled diver (never alone) in unknown waters. Before working in unknown waters, they should become familiar with the potential marine envenomations and the local medical facilities, in case treatment is needed.

Occupational setting

Sailors, divers, fishermen, and seafood producers are at risk for exposure.

Exposure (route)

Exposure occurs through physical trauma (sting) to the skin inflicted by a stinging structure (nematocyst) containing venom.

Pathobiology

All members contain stinging structures called nematocysts that contain venom. Jellyfish are found in many shapes, sizes, and colors. They can ride the waves or swim freely on their own. Their tentacles contain numerous nematocysts. Sea wasps are found in Australian waters; the sea nettle is a type of jellyfish found in waters off the Middle Atlantic States.

The venom of coelenterates is not well characterized, but serotonin (5-hydroxytryptamine) appears to be a major component.¹ It produces pain, vasoconstriction, and histamine release.

Jellyfish envenomations usually cause erythematous papular lesions followed by vesicles within the first day. The victim experiences pain, regional lymphadenopathy, and burning. Anaphylactic reactions can occur in some envenomations. The sea wasp, which is found only in Australian waters, causes the most poisonous of all marine envenomations. It can result in death within minutes.² Envenomation by this creature can cause pain, nausea, vomiting, erythematous lesions, headache, chills, and occasionally immediate cardiovascular collapse.

Diagnosis

There are no laboratory tests that are helpful in diagnosing these envenomations. Positive identification of the offending organism is helpful. Without positive identification, the clinical presentation and geographic location of the envenomation are very helpful in determining the appropriate treatment.

Treatment

Treatment includes inactivating the nematocysts by applying alcohol (i.e., isopropyl) or salt water. Alternatively, dilute vinegar, papain, or baking soda can be used. Fresh water should be avoided because it can cause increased venom release from the nematocysts. Immobilization of the affected area is also helpful. Baking soda and abrasion of the affected area can be effective in removing any remaining tentacles. Soaking the affected area in hot water (110–115°F) will alleviate severe pain. Narcotics, such as codeine, may be given for pain control. Tetanus prophylaxis and local wound care should be administered. Oral antihistamines are given routinely and can be especially helpful with symptoms of pruritus.

An antivenom is available for sea wasp envenomations. It should be given immediately after skin testing in all severe envenomations. Cardiovascular support (e.g., fluids, vasopressors) may also be needed.^{3, 4}

Prevention

Preventive measures include wearing gloves and long-sleeved garments when handling organisms or specimens, avoiding contact with reefs, and never contacting or touching an unknown organism. Persons at risk should always dive with a skilled diver (never alone) in unknown waters. Before working in unknown waters, they should become familiar with the potential marine envenomations and the local medical facilities, in case treatment is needed.

Occupational setting

Commercial fishermen, divers, and sailors are at risk of exposure.

Exposure (route)

Exposure occurs through physical trauma to the skin with the release of venom.

Pathobiology

The stingray is a bottom dweller that usually envenomates by raising its barbed, stinger-like tail in a defensive posture after it has been touched or stepped on. The tail apparatus penetrates the skin, usually fracturing the creature’s spine in the wound, and envenomates the victim. The laceration and wound are usually deep and irregular.¹ The venom appears to contain cardiotoxins, convulsants, and respiratory depressants.¹

The stingray envenomation is followed by almost immediate severe pain. The pain’s intensity is grossly out of proportion to the degree of trauma visualized; thus, it is helpful in making the diagnosis when the organism was not seen. Edema, erythema, and cyanosis often appear around the wound site. The fragmented spine is also often seen. Systemic symptoms include nausea, vomiting, muscle cramps, syncope, tachycardia, abdominal pain, cardiac arrhythmias, convulsions, hypotension, and (rarely) death.²

Diagnosis

There are no known laboratory tests that are helpful in diagnosing these envenomations. Positive identification of the offending organism is useful. Barring positive identification, the clinical presentation and geographic location of the envenomation are very helpful in determining the appropriate treatment.

Treatment

Initial treatment includes local wound care, including removal of any of the fragmented spines, tetanus prophylaxis, and immersion in hot water (110–115°F) for 1 hour.^3,4 Analgesics may be an important adjunct for pain control. Prophylactic antibiotics are not indicated, but these wounds must be observed closely for evidence of infection. Systemic symptoms should receive prompt supportive care and close observation in a hospital setting.

Prevention

Preventive measures include wearing gloves and long-sleeved garments when handling organisms or specimens, avoiding contact with reefs, and never contacting or touching an unknown organism. Persons at risk should always dive with a skilled diver (never alone) in unknown waters. Before working in unknown waters, they should become familiar with the potential marine envenomations and the local medical facilities, in case treatment is needed.

Occupational setting

Sailors, divers, fishermen, and seafood producers are at risk from exposure.

Exposure (route)

Exposure occurs through physical trauma to the skin with the release of venom.

Pathobiology

Sea urchins are bottom-dwelling organisms that have calcareous exoskeletons. They are covered with spines that become embedded in the victim’s skin upon contact. Some species contain venom in their spines. The venom contains steroid glycosides, acetylcholine-like substances, and serotonin.¹

The clinical manifestation of sea urchin envenomation includes both an immediate and a delayed reaction. The immediate reaction consists of severe pain and localized edema and erythema. Dye within the sea urchin spine (usually black or purple) may stain the surrounding skin. Paresthesias around the untreated wound site are common. Occasionally, systemic symptoms of nausea, myalgias, fatigue, syncope, and respiratory difficulties occur.^2,3 The delayed reaction consists of diffuse inflammation or local granuloma formation a few months after the initial injury.² Bone destruction is a rare occurrence. Sea urchins can also cause direct injury to joints, nerves, and soft tissue secondary to their sharp spines.²

Starfish have sharp spines and secrete a slimy venom. Envenomation can cause nausea, vomiting, paresthesias, and muscle paralysis.⁴ Sea cucumbers are sausage-shaped organisms that produce a venom called holothurin, which is a cardiac glycoside. The venom causes a macular and papular rash. Contact with the eyes can cause severe conjunctivitis, opacities, and blindness. The sea cucumber also ingests nematocysts from other species and can secrete them later in intact form as a self-defense measure, causing symptoms of coelenterate envenomation.

Diagnosis

There are no laboratory tests that are helpful in diagnosing these envenomations. Positive identification of the offending organism is useful. Barring positive identification, the clinical presentation and geographic location of the envenomation are very helpful in determining the appropriate treatment.

Treatment

Treatment should begin with local wound care and tetanus prophylaxis. Immersion in hot water (110–115°F) should be done and analgesics should be administered. Spines should be removed carefully in order to avoid fragmentation. Granulomas secondary to delayed reaction may need specific surgical or dermatologic procedures. Steroids, ammonia, antibiotics, and acetone have all been used with limited success.⁵

Prevention

Preventive measures include wearing gloves and long-sleeved garments when handling organisms or specimens, avoiding contact with reefs, and never contacting or touching an unknown organism. Persons at risk should always dive with a skilled diver (never alone) in unknown waters. Before working in unknown waters, they should become familiar with the potential marine envenomations and the local medical facilities, in case treatment is needed.

Occupational setting

Sailors, divers, fishermen, and seafood producers are at risk from exposure.

Exposure (route)

Exposure occurs through physical trauma to the skin with injection of venom.

Pathobiology

Conidae, which are found mainly in tropical waters, are cone-shaped, univalve organisms surrounded by a shell. They contain a radula tooth apparatus that envenomates its victims. The blue-ringed octopus is found mainly in Australian waters. It injects its venom through a beak-like apparatus. The venom appears to contain a number of neurotoxins.

The initial symptoms of envenomation include pain, stinging, burning, numbness, and paresthesias around the wound site. In severe envenomations, local ischemia and cyanosis can occur. Systemic reactions include fatigue, dysphagia, diplopia, paresthesias, dyspnea, coma, and cardiovascular collapse.¹ Systemic reactions to severe envenomations include paresthesias, slurred speech, weakness, dysphagia, and respiratory depression. Allergic reactions to the envenomation have been reported.^2,3

Diagnosis

There are no known laboratory tests that are helpful in diagnosing these envenomations. Positive identification of the offending organism is useful. Barring positive identification, the clinical presentation and geographic location of the envenomation are very helpful in determining the appropriate treatment.

Treatment

Conidae envenomations respond to hot water immersion (110–115°F) as well as analgesics. All patients should be observed for 6 hours for systemic reactions. Blue-ringed octopus envenomations do not respond to hot water immersion. These victims also need to be observed for systemic symptoms.

Prevention

Preventive measures include wearing gloves and long-sleeved garments when handling organisms or specimens, avoiding contact with reefs, and never contacting or touching an unknown organism. At-risk persons should always dive with a skilled diver (never alone) in unknown waters. Before working in unknown waters, they should become familiar with the potential marine envenomations and the local medical facilities, in case treatment is needed.

Occupational setting

Sailors, divers, fishermen, and seafood producers are at risk from exposure.

Exposure (route)

Exposure occurs through physical and chemical irritation of the skin.

Pathobiology

Sponges contain calcareous spines that can cause direct trauma to the skin. The components of the sponge’s venom are unknown, but it does cause symptoms similar to those of Rhus dermatitis.^1,2 Initially, there is pruritus and erythema in the area of contact, followed by progressive swelling and vesicle formation within a few hours. Lymphadenopathy can also occur. Anaphylactoid reactions and erythema multiforme have been reported.³

Diagnosis

There are no laboratory tests that are helpful in diagnosing these envenomations. Positive identification of the offending organism is useful. Barring positive identification, the clinical presentation and geographic location of the envenomation are very helpful in determining the appropriate treatment.

Treatment

Local wound care and tetanus prophylaxis should be administered. Topical steroids and antihistamines may be helpful. Tape can be used to remove spines. Dilute vinegar (30 mL in 1 L) or 5% acetic acid applications may be helpful with the acute dermatitis.

Prevention

Preventive measures include wearing gloves and long-sleeved garments when handling organisms or specimens, avoiding contact with reefs, and never contacting or touching an unknown organism. Persons at risk should always dive with a skilled diver (never alone) in unknown waters. Before working in unknown waters, they should become familiar with the potential marine envenomations and the local medical facilities, in case treatment is needed.

Occupational setting

Workers with potential exposure include commercial fishermen, divers, sailors, aquarists, and fish handlers.

Exposure (route)

Exposure occurs through physical trauma (sting) to the skin, with the potential release of venom.

Pathobiology

The Scorpaenidae are usually bottom dwellers with fins that are supported by venomous spines. They live in shallow waters around coral reefs and rocky formations. Envenomation can occur when the fish is stepped on or touched by the hand. A fragmented spine is often left in the wound site. The venom is a heat-labile mixture that can cause hypotension, weakness, vasodilation, and respiratory depression.^1,2

The clinical presentation of envenomation includes local effects such as edema, erythema, and ecchymosis at the wound site with intense, severe pain that can last up to 2 days if not treated. Paresthesias of the affected extremity are common. Neuropathy is rarely seen. Severe envenomation can cause hypotension, cardiac arrhythmias, syncope, nausea, vomiting, diaphoresis, convulsions, and paralysis. These systemic symptoms can develop very quickly.

Diagnosis

There are no known laboratory tests that are helpful in diagnosing these envenomations. Positive identification of the offending organism is useful. Barring positive identification, the clinical presentation and geographic location of the envenomation are very helpful in determining the appropriate treatment. Laboratory studies such as complete blood count (CBC), electrolytes, glucose, blood urea nitrogen (BUN), creatine phosphokinase, creatinine, ECG, chest radiograph, and urinalysis will not be diagnostic, but they are helpful adjuncts to care of the patient.

Treatment

The local wound site should be examined, and local wound care and tetanus prophylaxis should be given. The extremity should be immediately immersed in hot water at 110–115°F for at least 1 hours. This treatment usually decreases the severe pain of the sting.^3,4 Analgesics can also be used as an adjunct. The wound site should be examined carefully for any fragmented spines, which should be removed with care. Radiograph of the affected site may be helpful in revealing these fragmented spines; however, a negative radiograph does not rule out the presence of spines, because not all spines are radiopaque.

In severe envenomations, Scorpaenidae antivenom may be indicated. Assistance can be obtained from the local/regional poison control center. Immediate supportive care is needed for patients with severe envenomations who present with hypotension, arrhythmias, convulsions, or paralysis.

Prevention

Preventive measures include wearing gloves and long-sleeved garments when handling organisms or specimens, avoiding contact with reefs, and never contacting or touching an unknown organism. At-risk persons should always dive with a skilled diver (never alone) in unknown waters. Before working in unknown waters, they should become familiar with the potential marine envenomations and the local medical facilities, in case treatment is needed.

Occupational setting

Farming and agricultural workers, gardeners and orchard workers, forestry workers, construction workers, veterinary office workers, pet store workers, and zoo personnel are at risk of exposure.

Exposure (route)

Exposure occurs through physical trauma (bite) to the human skin, with injection of venom.

Pathobiology

There are 1400 species in the Colubridae family. The majority contains teeth and no venom-injecting apparatus and is therefore nonpoisonous. However, a small percentage of colubrids, like the hognose snake, have rear fangs with a venom-injecting apparatus.¹ Because of its small size and the posterior location of its fangs, these snakes do not usually envenomate their victims, but they are capable of doing so, given the right circumstances. All colubrids, whether rear-fanged or not, contain saliva that has been shown to be toxic.²

The colubrid bite usually presents as a minor abrasion or an imprint of teeth on the skin surface. Occasionally, there is evidence of a puncture wound inflicted by rear-fanged colubrids, but this would take prolonged skin contact time and can usually be elicited with the history. Occasionally, erythema, pruritus, and swelling are seen around the bite site; however, most bites cause only minor discomfort for the victim secondary to the abrasion.

Rare envenomations usually produce low-grade, mild symptoms. Fibrinolysis was reported secondary to a bite of a red-necked keelback snake that was purchased in a pet store.³ Fibrinolysis has also been reported with other colubrid bites.^1,4,5 In a number of reports, a garter snake produced local hemorrhage, pain, and swelling of an upper extremity as well as neurologic complications without systemic symptoms.^6,7

Diagnosis

The identification of the snake that inflicted the bite is extremely helpful in the management of all snakebites. The actual snake should be brought to the treating physician for identification, if possible, or the snake should be identified using well-defined photographs of different varieties of snakes. A herpetologist or regional poison control center may need to be consulted. Envenomation can occur hours after a snake’s death; therefore, these snakes should be handled carefully.

The victim should be evaluated carefully for fang marks, swelling, erythema, pain, local reaction (i.e., blebs, vesicles, petechiae), and any systemic reactions. Most colubrid bites present with minor abrasions or the imprint of teeth on the skin surface. Any deviation from this minor abrasion, without positive identification of the offending snake, should make the treating physician suspicious of a more venomous species. Laboratory data are usually not helpful in making the diagnosis. Coagulation abnormalities suggest a severe envenomation.

Treatment

Treatment usually consists of local wound care and tetanus prophylaxis. Antibiotics may be indicated if there is any suspicion of infection. After an uncomplicated colubrid bite, observation for at least 4 hours is indicated to rule out systemic symptoms. If fang marks are present and the snake has been identified as a colubrid, then at least 6 hours of observation is prudent to rule out systemic symptoms and a significant envenomation. Fibrinolysis and hemorrhage should be treated with conventional therapy. There is no approved antivenom currently available. The vast majority of bites need only local wound care. Any systemic symptoms respond well to supportive measures.

Prevention

Whether dead or alive, snakes should always be handled carefully, especially when the treating personnel are attempting to identify the snake. Snakes can still envenomate hours after their death. Snakes are ubiquitous in all outdoor areas. Areas like rock crevices, caves, and unusual terrain should be avoided. Trousers, gloves, boots, and long-sleeved shirts should be worn in areas where snakes may be present. Pest control professionals should be consulted when work must be performed in high-risk areas. One should never awaken or try to molest a snake. Venomous snakes should not be sold or kept as pets.

Occupational setting

Farming and agricultural workers, gardeners and orchard workers, construction workers, veterinary and ancillary staff workers, pet store personnel, and zoo workers are at risk of exposure.

Exposure (route)

Exposure occurs through physical trauma (bite) to the human skin, with injection of venom.

Pathobiology

All pit vipers (Crotalidae) have a vertical, elliptical pupil; facial pits located between the nostril and the eye, which are used to sense heat and vibration; a triangular head; and a single row of subcaudal plates (in contrast to the double row found in nonvenomous snakes). Most true rattlesnakes also contain a terminal segment called a rattle, but not all species contain this rattle. In some cases, trauma or congenital anomaly can also contribute to the lack of the rattle apparatus. Cottonmouths (Agkistrodon piscivorus) have a white buccal mucosa and usually a dark green to black appearance; they are often found in swampy marshes, lakes, or other aquatic environments. Copperheads have a head that is copper to brown in color and a distinctive band-like appearance on their bodies. Copperheads can be found in any outdoor area. Neither copperheads nor cottonmouths have rattles.

Pit vipers have anterior fangs on the roof of their mouths that can be up to 20 mm in length, allowing for easy envenomation and injection of venom. The venom contains numerous components, with a predominance of enzymes and neurotoxins that are used to immobilize and kill the animal prey.¹ The potency and amount of venom injected varies within the individual species. In general, the potency of the venom of the true rattlesnake is greater than that of the cottonmouth, which is, in turn, greater than that of the copperhead.

After a Crotalidae bite, there are typically two or more fang or puncture marks on the victim’s skin. In minutes, the victim experiences pain, edema, and erythema around the site of envenomation. Over the next few hours, the edema progresses proximally, the erythema increases, and there is evidence of hemorrhagic blebs or vesicles and ecchymosis. An affected extremity can become quite large, secondary to edema. Hypovolemic shock may occur in some cases. If progressive swelling has not occurred in the first few hours, then envenomation probably has not occurred.² The exception is the Mojave rattlesnake (Crotalus scutulatus scutulatus), whose envenomation produces little or no local symptoms but may cause the delayed systemic symptoms of muscle fatigue, ptosis, and respiratory depression.

Systemic effects of Crotalidae envenomation include fatigue, muscle fasciculations, light-headedness, minty or metallic taste, nausea, vomiting, and paresthesias (both perioral and peripheral). Thrombocytopenia and coagulopathy can occur.^3,4 Hypotension, pulmonary edema, and renal failure may also be seen.⁵

Diagnosis

The identification of the snake that inflicted the bite is critical in the management of all snakebites. The snake should be brought to the treating physician for identification, if possible, or it should be identified using well-defined photographs of different varieties of snakes. A herpetologist located at a local zoo, park, or aquarium may be consulted. The regional poison control center or the Antivenom Index of the Arizona Poison Control Center may be helpful. Snakes should be handled carefully even when dead, since envenomation can occur hours after a snake’s death.

The victim should be evaluated for fang marks, swelling, erythema, pain, local reactions (i.e., blebs, vesicles, petechiae), and any systemic reactions. The classic symptoms and signs of Crotalidae envenomation include puncture or fang wounds, pain, erythema, and edema around the bite site. The evaluation of the site may reveal one or more puncture wounds, which could represent the number of fangs the snake had or the number of strikes that occurred.⁶

There is no specific assay or laboratory test that can reliably identify and thereby assist in the diagnosis of Crotalidae envenomation. However, cell blood count, coagulation studies, disseminated intravascular coagulopathy (DIC) panel, blood type and screen, platelet count, creatine phosphokinase, and urine for myoglobin can be helpful.

Treatment

In the field, prior to definitive care by medical personnel, the affected bite area should be immobilized in a dependent position. Ice should not be applied. Tourniquets as well as incision and suction are controversial and can be deleterious.⁷

Medical personnel should monitor all Crotalidae envenomation for at least 4 hours for local and systemic effects. In the case of the Mojave rattlesnake, observation should be for 12–24 hours because of the delayed effects of the venom in this species. The affected limb should be closely monitored for local swelling, ecchymosis, and circulatory compromise. Tetanus prophylaxis and local wound care should be administered. Any complication regarding the wound, especially a compartment syndrome, should be referred to an experienced surgeon.

Systemic effects should be monitored closely and treated immediately. Respiratory depression requires immediate airway maintenance and assisted ventilation. Coagulopathy, hypotension, and rhabdomyolysis also require immediate treatment.

If documented envenomation has occurred, antivenom should be administered. Most local and systemic symptoms improve with the antivenom. The Crotalidae antivenom is equine based and is therefore contraindicated in individuals with known hypersensitivity to the antivenom or horse serum. Antivenom may need to be given cautiously in severe envenomations despite a positive allergic history. All patients should be initially skin tested. Both immediate hypersensitivity (anaphylaxis) and delayed hypersensitivity (serum sickness) can occur.

The amount of antivenom to administer is determined by the degree of envenomation.^8,9 It is wise to consult the regional poison control center prior to its use. For bites that produce very minor local symptoms and no systemic symptoms after 6 hours, no antivenom is recommended. In moderate envenomations where there is progression of local symptoms beyond the bite site and minor systemic symptoms such as nausea, anxiety, or paresthesias, fewer vials of Crotalidae antivenom can be administered, depending on the severity of the symptoms. In severe envenomations, where there is progressive local pathology and severe systemic symptoms, more vials may be needed. All patients receiving antivenom should be closely observed and monitored in a hospital setting.

Prevention

Whether dead or alive, snakes should be handled carefully, especially when the treating personnel are attempting to identify the snake. Dead snakes can still envenomate hours after their death. Snakes are ubiquitous in all outdoor areas. Areas like rock crevices, caves, and unusual terrain should be avoided. Trousers, gloves, boots, and long-sleeved shirts should be worn in areas where snakes may be present. Pest control professionals should be consulted when work must be performed in high-risk areas. One should never awaken or try to molest a snake. Venomous snakes should not be sold or kept as pets.

Occupational setting

Farming and agricultural workers, gardeners and orchard workers, forestry workers, construction workers, veterinary and ancillary staff workers, pet store personnel, zoo workers, and research personnel are at risk from exposure.

Exposure (route)

Exposure occurs through physical trauma (bite) to the human skin with injection of venom.

Pathobiology

Coral snakes, the only members of the Elapidae family native to the United States, are found in the southeastern and south central states. They include the Sonoran or Arizona coral snake (Micruroides euryxanthus), the Eastern coral snake (Micrurus fulvius fulvius), and the Texas coral snake (Micrurus fulvius tenere). The eyes are round and the mouth is small, with a row of teeth and rear fangs. This anatomy forces the coral snake to hold on and “chew” its victim in order to get its rear fangs into the skin and cause envenomation. Because of its anatomy, the coral snake is unable to envenomate its victim in most circumstances. The venom is a complex mixture of many components, including a neurotoxin.¹ Coral snake venom causes very little local destruction, but it can cause systemic reactions that are primarily neurologic.

Coral snakes have a distinct pattern of red and black bands that are interspaced with narrower yellow bands. This is often remembered as: “Red on yellow, kill a fellow”—coral snake; “Red on black, venom lack”—nonvenomous snake.

There are usually very mild (if any) swelling, erythema, and pain around the bite site. Occasionally, paresthesias occur around the site. A few hours after envenomation, the victim experiences nausea, vomiting, confusion, euphoria, or drowsiness. The systemic effects, which are predominantly neurologic, can progress to diplopia, fasciculations, slurred speech, dysphagia, paralysis, and respiratory depression. It is important to realize that the systemic symptoms of a coral snake envenomation may be delayed for up to 10 hours.² The Arizona coral snake appears to cause greater neurologic symptomatology than the Texas or Eastern coral snakes.³

Diagnosis

The identification of the snake that inflicted the bite is critical in the management of all snakebites. The actual snake should be brought to the treating physician for identification, or the snake should be identified using well-defined photographs of different varieties of snakes. A herpetologist located at a local zoo, park, or aquarium may need to be consulted. The regional poison control center or the Antivenom Index of the Arizona Poison Control Center may be helpful. Because envenomation can occur even hours after a snake’s death, snakes should be carefully handled even when dead.

The victim should be evaluated for fang marks, swelling, erythema, pain, local reaction (i.e., blebs, vesicles, petechiae), and any systemic reaction. Most victims of coral snake bites present with minor abrasion or the imprint of teeth on the skin surface. Fang or puncture marks reveal possible severe envenomation. The victim should be observed for up to 12 hours for systemic symptoms, which are predominantly neurologic and would be consistent with a coral snake envenomation.

Treatment

Most coral snake envenomations can be treated with local wound care and tetanus prophylaxis. The presence of fang or puncture marks is a sign of a potentially serious envenomation and necessitates observation for at least 12–24 hours. The affected area should be immobilized in a dependent position to decrease the spread of the venom. Cryotherapy should not be used, and incision and suction are usually not warranted.

In severe envenomations, consultation with a regional poison center and local herpetologist is recommended before using the Micrurus fulvius antivenom. In general, any victim with severe envenomation from an Eastern coral snake or Texas coral snake, which causes systemic neurologic symptomatology or coagulopathy, should receive the antivenom.⁴ It is not effective for envenomation by the Arizona or Sonoran coral snake. Hypersensitivity to horse serum or the antivenom is a relative contraindication, but it may be given with extreme caution in severe envenomations. All victims should be skin tested with the antivenom prior to administration. Adverse effects include immediate hypersensitivity and possible anaphylaxis as well as delayed hypersensitivity (serum sickness).

Prevention

Whether dead or alive, snakes should be handled carefully, especially when the treating personnel are attempting to identify the snake. Dead snakes can still envenomate hours after their death.

Snakes are ubiquitous in all outdoor areas. Areas like rock crevices, caves, and unusual terrain should be avoided. Trousers, gloves, boots, and long-sleeved shirts should be worn in areas where snakes may be present. Pest control professionals should be consulted when work must be performed in high-risk areas. One should never awaken or try to molest a snake. Any snake that has the potential of envenomation should not be sold or kept as a pet.

Occupational setting

Fishermen and diving personnel, especially those in the Pacific and Indian oceans, are at risk from exposure. There do not appear to be any sea snakes in the Atlantic Ocean or the Caribbean.

Exposure (route)

Exposure occurs through physical trauma (bite) to the human skin, with potential envenomation.

Pathobiology

Sea snakes have a compressed, fin-like tail that allows them to propel themselves in the water. They have two to four fangs, which are attached to venomous glands, but the fangs are short; therefore, most bites result in no envenomation. There are at least 52 species and all are venomous. Enhydrina schistosa is the most dangerous. The venom is a potent neurotoxin^{1, 2} that contains myotoxins, such as phospholipase A, which can cause striated muscle necrosis.³ Many other substances are present in this complex venom.

Most often, the initial bite is painless and the victim asymptomatic. If envenomation did occur, symptoms can develop within 10 minutes and will usually be present within an 8-hour period. In actual envenomations, there are puncture wounds on the victim’s skin. The classic envenomation results in muscle pain, difficulty with muscle movement, and myoglobinuria.¹ Ophthalmoplegia, trismus, ptosis, paralysis (flaccid or spastic) of the lower extremities, and respiratory failure can occur.²

Diagnosis

The identification of the snake that inflicted the bite is critical in the management of all snakebites. The snake should be brought to the treating physician for identification, if possible, or it should be identified using well-defined photographs of different varieties of snakes. Specifically, with sea snakes, the bite must have been inflicted in the Pacific or Indian Ocean. The evaluation of the bite site should reveal two or more puncture wounds secondary to the fang marks. The clinical presentation of a painless bite followed by trismus, ptosis, myalgias, difficulty with muscle movement, or lower extremity paralysis should make the treating personnel suspicious of a sea snake envenomation.

Treatment

Treatment consists of immobilizing the victim with the affected site in a dependent position to decrease the spread of the venom. Cryotherapy is not indicated nor is incision and drainage of the affected site in most cases. Most victims can be treated with supportive care.

For severe envenomations, there is antivenom available from Australia, as well as a polyvalent tiger snake antivenom.^3,4 As with all antivenom, sensitivity testing should be performed prior to administration and the victim observed for signs of anaphylaxis and serum sickness. In all systemic reactions to the sea snake bite, the victim should be closely monitored in a hospital setting, since respiratory failure is possible.

Prevention

Trousers, gloves, boots, and long-sleeved shirts should be worn in areas where the snakes may be present. Sea snakes are often found in fishing nets. Fishermen should be extremely careful when removing entangled sea snakes from these nets. Whether dead or alive, sea snakes should be handled carefully. Dead snakes can still envenomate hours after their death.