Dan Quan and Timothy Davie
Spiders of the genus Loxosceles are distributed throughout the world. L. reclusa, the brown recluse spider (BRS) and most important of these species in the United States, is most common in the southern Midwest states. Depending on the temperature, it prefers living outdoors (under rocks, woodpiles, and debris) or in structures (basements, attics, and storage areas). The name reclusa describes its 'margin-bottom:0cm;margin-bottom:.0001pt;text-align: justify;text-indent:12.0pt;line-height:14.4pt'>L. reclusa is fawn to dark brown and has, on its dorsal cephalothorax, a violin- or fiddle-shaped, dark brown marking with the larger end toward the head. The body of a large spider will measure 1 cm in length by 0.5 cm in width. The short-haired abdomen is oval, and the legs are long and slender, measuring 1 to 5 cm. Three pairs of eyes, rather than four, is a distinctive but not unique feature of this genus. Although all Loxosceles species are often called brown, violin, or fiddleback spiders, the recognized common name brown recluse should be reserved only for L. reclusa.
Loxosceles venom contains at least 11 components, mostly enzymes with cytotoxic activity (e.g., protease, S-ribonucleotide phosphohydrolase, hyaluronidase, collagenase, esterase, sphingomyelinase-D), which cause both local and systemic toxicity (2–4). Dermonecrosis is caused by endothelial cell damage by venom and ischemia secondary to thrombosis, inflammation caused by leukocyte infiltration, hemolysis, complement activation, and intravascular coagulation (5).
CLINICAL PRESENTATION
Most bites from the BRS have a benign clinical course. Cutaneous (necrotic arachnidism) and systemic toxicity (visceral loxoscelism) may occur, and the systemic reaction is not necessarily proportional to the local reaction. Systemic symptoms may develop before a necrotic lesion appears. Severity relates to the amount of venom injected, the bite location, and the victim’s immune status. Children and debilitated victims are at greater risk for severe reaction, but the elderly are often asymptomatic, possibly because of immunity that developed from earlier bites in their lives. Children are more susceptible to severe systemic loxoscelism because of venom dose relative to body size. There is no clinical evidence that risk is greater during pregnancy.
Typically, the bite itself feels like a pinprick that, in a few hours, may itch, tingle, swell, become tender, red, or blanch and has a gravitational spreading. Frequently, a blister or purpuric lesion, or both, form. Necrosis with induration and eschar formation may occur within hours or as late as 2 weeks after the bite. The eschar then falls off, leaving an ulceration that may take months to heal. The most severe necrotic lesions occur in fatty areas such as the abdomen, thighs, and buttocks (6). Occasionally, an erythematous or violaceous reaction at the bite site, surrounded by a ring of pallor (“halo,” “target,” or “bull’s eye” lesion), may be seen soon after envenomation. Vast edema may occur at the general bite site, especially on the neck and face. Angioedema of the airway may be life-threatening (7). The inflammatory reaction (pain, redness, induration, swelling, fever, lymphangitis, and leukocytosis) can be severe. A rarely seen immunodermatologic sequela of loxoscelism in adults is pyoderma gangrenosum with recurrent deep ulcerations.
Systemic effects develop within hours after the bite and include fever, chills, headache, malaise, weakness, nausea, vomiting, arthralgia, myalgia, and rash. These signs and symptoms progress for 48 to 72 hours and then resolve over another 24 to 48 hours. Laboratory findings may include anemia, thrombocytopenia, leukocytosis, hemolysis, and consumptive coagulopathy. Hemolysis may directly result in hemoglobinuria, renal failure, jaundice, and shock or indirectly cause congestive heart failure, coma, convulsions, and death (6). There are a variety of rash presentations. The more common scarlatiniform rash may appear within days and persist a few days. This pruritic scarlatiniform-like eruption represents a toxigenic erythroderma reaction to the venom rather than a Streptococcus or Staphylococcus infection. Because the spider does not transport bacteria, early infection is very unlikely. Cellulitis, bacteremia, or sepsis, is secondary to the victim’s own flora (usually staph or strep). Envenomation may cause toxic hepatitis, pancreatitis, hematuria, and cardiac manifestations. Death, although rare, has occurred from multisystem organ failure, especially in young children (7).
DIFFERENTIAL DIAGNOSIS
The differential diagnosis includes bites and stings from several other arthropods and many medical conditions (Table 373.1). “Spider bite” is overdiagnosed. It is controversial whether the other species of spiders in the United States cause necrosis, although there may be specific regional differences (6). Although there are other species of Loxosceles spiders in the United States, especially in the Southwest, their venom is less potent, so the dermal reaction and systemic effects are less severe. Erythema that evolves into a violaceous macule distinguishes a necrotic from a nonnecrotic bite. In addition, as the macule widens, the edge becomes irregular and the center sinks below skin level. In contrast, nonnecrotic lesions remain edematous, raised, and red (5). The diagnosis often becomes clear only in retrospect. There are only a few other natural toxins that cause hemolysis and possibly dermonecrosis (see Table 373.1) (7). Unless an offending spider is positively identified, a more generic diagnosis such as “cutaneous necrosis,” “necrotic arachnidism,” or “necrotic arthropod bite or sting” should be used.
TABLE 373.1
Differential Diagnoses of Loxoscelism
ED EVALUATION
The history should include timing and circumstances of a lesion, description of the spider (seldom known), and progression of signs and symptoms. The skin should be examined closely for typical lesions and a delayed rash in patients with acute hemolysis and/or coagulopathy of unknown etiology. The general examination should focus on vital signs, skin, musculoskeletal, and neurologic function.
All patients with suspicion of BRS envenomation should have a baseline complete blood count and urinalysis. Those with suspected hemolysis or significant systemic reactions should have plasma-free hemoglobin levels, coagulation studies including fibrinogen, and d-dimer measurement. Other helpful tests include liver function studies, renal function studies (electrolytes), lactase dehydrogenase (LDH), and serum amylase/lipase and rarely serum haptoglobin level/haptoglobin–binding capacity, biopsy, culture, or Gram stain. Inflammatory markers are almost always elevated. Hemolysis may be intravascular and/or extravascular. Extravascular hemolysis is not detected by finding hemoglobin in blood or urine and should be considered in any patient with a falling hemoglobin/hematocrit and elevated LDH or reticulocyte count. Several immunoassay tests have been developed to identify Loxoscelesvenom but are currently only research tools (6,8,9).
KEY TESTING
• Tests for hemolysis and coagulopathy include CBC, UA, plasma-free hemoglobin levels, fibrinogen, LDH, and blood type and cross
• Tests for supportive care as needed include liver and renal function, and amylase
ED MANAGEMENT
Treatment of necrotic arachnidism should be the same, regardless of the specific species of spider. A “benign neglect” approach nearly always results in an excellent dermal outcome. It is impossible to make an early prediction about which bite will result in a disfiguring lesion. General wound care usually suffices and includes tetanus prophylaxis, cleansing, and topical antibiotics. Corticosteroids injected locally or systemically and vasodilators have not proven helpful in preventing or decreasing dermonecrosis (5). Routine antibiotics are not needed initially but may be indicated for secondary bacterial infection. Antipruritic or antianxiety drugs and cool compresses are often comforting (avoid heat, because it may stimulate a toxin-produced cascade of inflammatory reactants) (7). The bite site should be protected from further trauma, but immobilization is not necessary.
Analgesics can be given for pain, but drugs that affect platelet functioning are contraindicated because of possible bleeding problems. Early wide excision is ineffective, unnecessary, and expensive; produces complications, potentially allows venom to penetrate deeper into tissues and may cause disability or worsen scarring. Trimming rapidly enlarging bullae seems to stop their progression but does not necessarily reduce the risk of necrosis within the blister borders (7). Corrective surgery should be delayed for 4 to 8 weeks or longer, until necrosis is clearly demarcated (6). Necrotizing fasciitis or abscess warrants surgical intervention.
The treatment of systemic arachnidism consists mainly of aggressive symptomatic and supportive care. Corticosteroids (methylprednisolone, or equivalent, 1 to 2 mg/kg IV loading dose followed by 0.5 to 1 mg/kg IV every 6 hours) for 3 to 7 days ameliorate hemolysis, and a tapering dosage schedule can be used as necessary. Aggressive hydration can prevent acute renal tubular necrosis due to hemoglobinuria. Anemia and thrombocytopenia should be treated with component therapy (e.g., packed red cells, platelets), as needed. Complement in cryoprecipitate and fresh-frozen plasma reacts with venom components and contributes to further red blood cell destruction, so these products are not recommended (4,10). Blood type and screen/cross-match may be difficult because of interfering antibodies. In severe cases, newer coagulopathy therapies such as antithrombin III or recombinant factor VIIa may be useful.
Though early literature suggested that a polymorphonuclear leukocyte inhibitor such as dapsone may prevent ulceration if started early, there is no evidence supporting dapsone’s effectiveness in preventing dermonecrosis. Dapsone has potentially adverse effects in patients with glucose-6-phosphate dehydrogenase deficiency hemolysis, methemoglobinemia, super infection, leukopenia, rash, toxic epidermal necrolysis and is especially dangerous for children.
Other treatments such as hyperbaric oxygen, colchicine, and triamcinolone have not been shown to be beneficial or effective. In animal studies, there is some evidence that tetracycline may be effective in the treatment of cutaneous loxoscelism by inhibiting matrix metalloproteinases (11). Although experimental antivenoms have been produced, they are not commercially available in the United States (12).
CRITICAL INTERVENTIONS
• Perform standard wound care for necrotic skin lesions.
• Perform serial clinical and laboratory assessments to rule out systemic toxicity.
• Treat hemolysis with high-dose parenteral corticosteroids, hydration, urine alkalinization, and packed red blood cell transfusion as needed.
• Avoid dapsone.
DISPOSITION
Patients who present immediately after a suspected spider bite should be followed as outpatients every 24 to 48 hours with at least a complete blood count and urine dipstick for 4 to 5 days after the bite. Patients who present with or develop large dermonecrosis or ulceration should be referred to a wound care surgeon for follow-up. Patients with significant systemic symptoms or hematologic abnormalities should be admitted for treatment and monitoring progression. Physicians unfamiliar with arachnidism should consult a regional poison control center or toxicologist for advice. Those hospitalized and having a benign course with stable physical and laboratory evaluations for 4 to 5 days can be discharged with follow-up in 2 to 3 days. Liberal admission for observation may be prudent in very young or debilitated patients and in those judged to be unreliable regarding follow-up.
Common Pitfalls
• Diagnosing “BRS bite” rather than “necrotic arthropod bite/sting” or “necrotic skin lesion” when positive identification of the offending creature has not been made and alternative diagnoses have not been fully considered.
• Failure to appreciate that hemolysis secondary to L. reclusa envenomation may be rapid or insidious in onset and be intravascular and/or extravascular.
• Failure to perform laboratory evaluations on patients with signs and symptoms, especially skin lesions, highly suspicious for loxoscelism.
• Failure to discuss to warn patients about potential but unpredictable complications such as hemolysis, coagulopathies, secondary infections, and delayed wound healing and to arrange for follow-up.
• Overly aggressive early debridement of skin lesions.
ACKNOWLEDGMENT
The author thanks Gary S. Wasserman, MD for his contribution to previous editions of this chapter.
REFERENCES
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