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Brown Recluse Spider Bites: A Complex Problem Wound. A Brief Review and Case Study

Case Report

Brown Recluse Spider Bites: A Complex Problem Wound. A Brief Review and Case Study

Index: Ostomy Wound Manage. 2005;51(3):59-66.

    Arthropods comprise the majority (75%) of the world’s animal species. An estimated 170,000 species of spiders exist; 34,000 have been described.1 Although most spiders have little interaction with humans, a few cause significant medical problems.2 The most important group of venomous arthropods are the arachnids, which includes spiders and scorpions.

Both are capable of injecting venom into their victims. The spider injects its venom via hollow modified mouth parts called chelicerae that deliver the venom from modified salivary glands. At the end of their tails, scorpions have a hollow stinger connected to a poison gland that delivers venom when it pierces its victim with a very rapid forward thrust. According to Vetter and Visscher,2 mechanisms located near the mouth (such as chelicerae) are primarily for food gathering — defense is a secondary function; mechanisms located in the rear of the animal (stingers) are considered primarily for defense but also are used in food gathering. Print and television media horror stories have led to a marked exaggeration of the dangers and fear of spiders (arachnophobia) that exaggerate the real threat.3 Nearly all spider fangs or chelicerae are too small to produce any wound.4

    The chelicerae of two types of spiders are large enough to penetrate skin and, although very rare, have resulted in deaths in infants and the elderly. The black widow spider (Latrodectus mactans) produces a neurotoxin that causes systemic symptoms but no necrotic wound.4 Spiders of the genus Loxosceles are found worldwide.5 Of the 18 known species, 13 are found in the US; four of the 13 Loxosceles species, as well as other spiders that produce necrotic wounds, are discussed elsewhere.6

Brown Recluse Spider

    The brown recluse spider is most prevalent and has the most potent venom.7 The venom contains a powerful necrotizing agent with the potential to cause severe cutaneous necrosis; thus, the term necrotic arachnidism. This spider is found predominantly in the South-Central US and is almost never seen in New England, the far Northwest, or California.8 Reports of brown recluse spider bites from these areas are questionable unless the spider has been identified. In South America, a lesion called “gangrenous spot” has been known since 1872 and was described more than 50 years ago. The lesion caused by the brown recluse spider follows a similar pattern as that caused by a Chilean brown spider (Loxosceles laeta) bite.9 The Chilean brown spider has been identified in the US but no injuries have yet been conclusively determined to be caused by L. laeta; however, this spider is larger than the L. reclusa and its venom is thought to be more potent.

    The brown recluse spider, including the legs, is about the size of a US quarter (see Figure 1). The body is approximately 10 mm long and brownish, varying from a dull yellow to a tawny dark brown.4 In most species, a dark brown violin pattern appears on the dorsum of the cephalothorax — this is the basis for the common name of “fiddle-back spider.” However, the violin markings may vary considerably.2

    The L. reclusa is a nocturnal spider that prefers hot, dry, abandoned, or otherwise quiet environments such as woodpiles, vacant buildings, under beds, and in closets. These spiders hibernate during the fall, winter, and early spring and become active in late March or early April.2 The highest incidence of bites occurs between April and October. The bites usually occur because clothing that has been hanging up or stored is donned without first shaking it out. Reaching into dark recesses is also a common source of injuries.5

    The venom of the brown recluse spider is a complex substance. Various purification techniques have identified subcomponents, including proteases, alkaline phosphatase activity, lipase activity, sphingomyelinase-D, hyaluronidase activity, and others.10 Sphingomyelinase-D has been identified as the primary toxin affecting the endothelial cells, red blood cells, and platelets. The pathological sequence includes the aggregation of platelets, endothelial swelling, and destruction; these events plug capillaries with white cells, which, in turn, causes ischemia and necrosis. Therefore, the most convincing subcomponent of the brown recluse Spider’s venom associated with necrosis of the fat and skin appears to be sphingomyelinase-D.11

    Diagnosing the brown recluse spider bite. Diagnosing a spider bite can be difficult. It may be days or weeks after the event before the patient is seen by a physician, usually without the spider. In a study evaluating 600 suspected spider bites, 80% were caused by other arthropods and 10% by other diseases such as Lyme’s disease, poison ivy, poison oak, chronic herpes simplex, squamous cell carcinoma, and bites from the kissing bug.12

    The clinical manifestations of the L. reclusa bite vary depending on the venom load, age, and general health of the patient. Bites of minimal envenomation result in wounds with lesser symptoms: slight erythema, localized urticaria, and discomfort that disappears in 3 to 5 days and requires little or no care.4,13

    Slightly more venom increases the cutaneous reaction, although the bite might not be felt immediately. A dull discomfort in the area may begin 4 to 6 hours after the bite. The area may be pale with a small blister in the center. Discomfort can be controlled with acetaminophen or ibuprofen. These wounds usually heal within 1 to 2 weeks with local wound care such as cleaning, topical applications, and a band aid.5

    A more significant wound may initially be perceived as a tiny pinprick or not at all. Six to 12 hours later the victim begins to develop pain. Two tiny puncture marks are visible and the area becomes erythematous. Within a few hours, a “bull’s eye” appears —the center a bluish, cyanotic color in a blanched ring surrounded by an erythematous ring. The center then forms a hemorrhagic bleb that grows to several centimeters depending on the host and the volume of venom.13 During this time, the patient may experience a generalized fine punctate rash, nausea, vomiting, and malaise and in most cases seeks medical care. The area under the bleb becomes necrotic, gradually expanding to 3 cm to 10 cm in diameter. In some fatty areas, the wound may be larger. As the inflammatory advance slows, the gangrenous area desiccates and becomes an eschar. As the eschar matures, the body gradually sloughs the necrotic tissue and a granulation bed forms. Cicatrization and epithelialization take place and the wound may require 6 weeks to 4 months to heal.2,5

    Treatment. “Significant” L. reclusa wounds should be treated according to the demands of the wound itself. Frank devitalized tissue may be cautiously debrided. No marginal tissue or tissue of questionable viability should be removed. If a bioload is suspected, non-cytotoxic topical antimicrobials may be applied. Routine principles for management of exudate and moist wound healing should be followed.

    The most severe envenomation results in a systemic reaction. Speculation is that this might be due to a direct intracapillary injection of the venom at the time of the bite. Patients experiencing this type of reaction usually become very ill within 2 to 3 days. The venom is a powerful hemolytic agent and can rapidly lyse red blood cells. Patients develop chills, joint pain, malaise, nausea, vomiting, punctate rash, and hemoglobinurea along with low-grade fever. One of the worst complications is disseminated intravascular coagulation. Generally, bites with severe systemic symptoms usually have fewer local wound problems.4,14 With no spider for identification, a careful history and examination of the wound is the best way to determine the cause.

    Patients with significant wounds and/or systemic symptoms require an extensive workup. The wound should be cleaned and dressed; an ice pack should be applied.13,14 As with any insect bite, tetanus toxoid should be given, along with analgesics. A CBC and chemistry panel, glucose-6-phosphate dehydrogenase (G6PD), and urinalysis should be done. An IV should be started along with fluids by mouth to flush the kidneys in case of hemolysis. If a violaceous hue is noted, Dapsone (50 mg to 200 mg/24 h) should be considered.7 Erythromycin or a cephalosporin should be started to prevent secondary infection. Testing to determine a G6PD deficiency is necessary before prescribing Dapsone because the drug may cause hemolysis in these patients. Dapsone is dose-dependent and should be given with caution to patients with infections or diabetic ketosis capable of producing hemolysis.15

    Patients with severe wounds should be admitted to the hospital; patients with systemic symptoms should be treated as an emergency. In addition to the treatment mentioned, patients should be blood-typed and have a Foley catheter for hourly checks on urine output. Because of the usual significant hemolysis, adequate urine output must be maintained to prevent renal shutdown. Hemoglobin levels and platelet counts should be assessed every 4 hours for 24 hours.

    Efforts to provide serological confirmation of brown recluse envenomations and an antivenin against sphingomyelinase-D have been underway for more than 10 years.16 Because the patient generally presents without the spider, a specific Loxosceles species venom assay is extremely helpful. A recent study determined that venom specificity with an Enzyme-linked Immunosorbent Assay (ELISA) is possible and may eventually be available for clinical application in areas native to the Loxosceles species.17

    A passive hemagglutination test has been developed to aid in the diagnosis of brown recluse envenomation. This test is able to identify envenomation up to 2 weeks after the incident; however, results are not available for 6 to 24 hours, past the time to initiate treatment. Additional concerns arise from the number of false-negative reports when the specimen contains bloody exudate.7

    Specific therapies. A number of different forms of therapy have been used over the years since the first case of the brown recluse spider bite was described in 1958.18 Steroids have been tried, both systemically and injected into and under the wound. Neither of these techniques has been helpful except in cases of excessive hemolysis. In this instance, steroids should be administered systemically.8 Heat application was tried but abandoned quickly when it became apparent that it immediately worsened the wound. Cold packs seem to slow the activity of sphyngomyelinase-D.13,14 Various surgical procedures have been tried, including immediate excision, all of which have been abandoned because of increased morbidity.19

    Dapsone. Dapsone (Alvosulfon, Jacobus Pharmaceuticals, Inc., Princeton, NJ) was originally developed for and is still used in the treatment of leprosy.20 In spider bites, it has an antineutrophil effect, resulting in inflammatory suppression that limits the size of the lesions.21 The drug is not benign, but is relatively safe. Dapsone has two absolute contraindications: a documented hypersensitivity reaction to the drug and the previously mentioned G6PD deficiency.22 Both can cause an almost certain fatal reaction. The patient should not be on Probenecid or Trimethoprim and the dose should not exceed 200 mg/day for more than 10 days.

    The primary risks are methemaglobinemia, agranulocytosis, and hypersensitivity reactions, although fatal reactions have been reported.23
Antivenom. Antivenom is probably the best treatment for envenomation. If administered within the first 24 hours, it should significantly decrease the size of the lesions. However, antivenom is still not commercially available.7

    Hyperbaric oxygen. Hyperbaric oxygen therapy has been used successfully in the management of necrotic wounds,24-27 but not in all cases.28 It is thought to be useful in the treatment of brown recluse spider bites through two different mechanisms. First, the hypoxic nature of nonhealing wounds suggests a strong relationship between healing and oxygen supply.29-31 Sheffield and Dunn32 showed that wound oxygen tension is elevated with hyperbaric treatments. The second mechanism of action directly involves the venom, possibly inactivating its necrotizing component. Sphingomyelinase-D digests the intercellular matrix, allowing the venom to spread; hypothetically, hyperbaric oxygen therapy denatures the sphingomyelinase-D.24 One study disputes this theory33; however, the sphingomyelinase-D was not tested at clinical levels. Controlled animal and human studies are still needed to conclusively demonstrate the efficacy of hyperbaric oxygen therapy.

    The absolute contraindications to hyperbaric therapy include chemotherapy, uncontrolled seizure disorders, a history of spontaneous pneumothorax, pregnancy, and anabuse.34 Bangasser26 suggests that if the diagnosis is made within the first 48 hours, the patient is usually treated once a day at 2.0 ATA for 120 minutes. The average number of treatments is five; a series can range from two to 18 treatments. Hyperbaric oxygen therapy is recommended until the spread of the erythematous area stops. After this time, hyperbaric treatment is unnecessary unless indicated for wound healing, such as in the preservation of a skin graft.

Case Study

    Ms. B, a 24-year-old Caucasian woman in excellent health, was bitten by a spider on the medial right thigh at 7:30 am. The bite was not very painful so she dressed and attended school. As the day progressed, the pain gradually increased. By noon, the area of erythema was approximately 5 cm. That afternoon she saw her local physician who provided no treatment. Throughout the evening, the pain — described as a burning scalding sensation — increased. She was unable to sleep and developed a fever of 102o F with shaking chills.

    Ms. B saw her physician the next morning and was immediately referred to the Osteopathic Medical Center of Texas Hyperbaric Medicine Department. She brought in a carcass of a Loxosceles species, probably a reclusa. The patient appeared acutely ill. She had a fine macular rash extending over her trunk and extremities. On the medial aspect of her right thigh, a 10-cm ecchymotic area was indurated and exquisitely tender (see Figure 2). The patient noted a 3-mm shallow pit with very dark discoloration as the point of the bite. Her initial laboratory values were normal with a hemoglobin of 12.5 g.

    The patient was started on Ringers Lactate at 80 mL/h; 12.5 mg Benadryl (Warner-Lambert, Morris Plain, NJ) every 4 hours; Dapsone 100 mg by mouth twice a day, morphine IV, and 125 mg of methylprednisolone sodium succinate IV (Solu-medrol, Pharmacia & Upjohn, Peapack, NJ). The patient was immediately cleared for hyperbaric oxygen therapy and treated at 2.4 atmospheres absolute (ATA, a pressure equivalent to 45 feet of sea water) for 90 minutes, twice daily, until the lesion stopped expanding (see Figure 3).

    On the second day, the patient developed tenderness along the superficial femoral vein and tender inguinal lymphadenopathy. Ultrasonography revealed no intraluminal clots and the symptoms gradually subsided. Her hemoglobin fell precipitously to 8.4 g/dL, possibly due to intravascular hemolysis — a reaction to the venom that can occur or an uncommon side effect of Dapsone. The antibiotic was held and vigorous hydration preserved renal function. Dapsone was reinstated without further incident. By the fifth day, a leathery eschar began to form (see Figure 4). The twice-daily hyperbaric oxygen treatments were stopped after 7 days and the patient was discharged to home care to continue daily wound care with a topical antimicrobial preparation (Iodosorb, Healthpoint, Fort Worth, Tex.) and daily hyperbaric oxygen therapy. By the tenth day, the eschar had begun to shed (see Figure 5). Once a good granulation bed was established (see Figure 6), hyperbaric therapy was discontinued and an autologous split-thickness skin graft was applied with 100% take (see Figure7).

Discussion

    The consequences of a L. reclusa bite may take many forms, from minor bite discomfort to a fatal illness. Identifying the spider is extremely important for confirmation of the diagnosis, although it is usually made on the basis of history and symptoms. Many therapies have been tried and the medical community is still not settled on the best treatment. Clinicians agree, however, that early and aggressive surgery should be avoided.19

    Supportive care for severe wounds, especially with systemic involvement, is also extremely important. Dapsone has been used worldwide as a treatment for leprosy20 and was found to be effective in other skin disorders.35 Dapsone was first used in 1985 for brown recluse spider bites with considerable success. Of 31 patients studied, only one required skin grafting.19 However, Dapsone must be used with caution and patients must be watched for complications such as methemaglobinemia36 and agranulocytosis.

    The benefit of steroids in systemic loxoscelism has not been proven but they may be administered acutely (4 to 5 days) to stop red cell destruction by the venom.37 Wilson and King14 suggest that systemic steroids in doses of 1 to 2 mg/kg/day be given in cases of suspected loxoscelism and that steroids may be useful in children.38 Other therapeutic interventions such as antibiotics should be reserved for secondary infections39 and following appropriate cultures and sensitivities.

    Clinical presentation. Making a definitive diagnosis of loxoscelism is difficult because most patients neither feel nor see the spider. The physician must deal with circumstantial evidence. Many wounds are misdiagnosed as L. reclusa bites even though the patient lives outside the geographical distribution of this spider.2 Identification of the spider by an entomologist provides the most definitive diagnosis. However, the patient is often unaware of the bite because it requires no care.5 If the patient cannot produce the spider, obtaining a complete bite history and evaluating any signs or symptoms that have developed are important. The diagnosis is usually based on a clinically consistent lesion and a geographical location consistent with the presence of brown recluse spiders.5

    Russell13 suggests that a general relationship exists between the level of the pain of envenomation and the severity of the clinical manifestations. The age and general health of the patient also will influence the severity of the reactions.4 Thus, an individual may not notice a bite, which would then not be reported to a physician, or a mild reaction such as the formation of a small (5 mm) erythematous papule might be seen as a temporary irritation.5 The only symptom usually observed during the first 8 hours is local pain.4

    A second clinical category is characterized by a cytotoxic reaction. Anderson40 described a particular characteristic of the loxosceles bite as a blue-gray halo that spreads around the puncture site and a small bleb that develops within the first 24 hours. The bleb ruptures, causing necrosis in the next 3 to 4 days, followed by eschar formation between 5 and 7 days.4 Between 7 and 14 days, the eschar falls off and leaves an ulceration.41 Ulcerations may vary from 1 cm to 30 cm and take 6 weeks to 4 months to heal.5 Lesions in the fatty areas tend to be more extensive and have more scar formation.14

    The third clinical category is systemic involvement that occurs 24 to 48 hours after the bite. These symptoms include fever, chills, weakness, edema, nausea, vomiting, joint pain, petechial eruptions, convulsions, and hemolysis.42, 43 These symptoms warrant hospitalization, close observation, and treatment.5

Conclusion

    Brown recluse envenomations can be a diagnostic dilemma given the variety of clinical responses. No consensus exists within the medical community regarding therapy. However, for rapidly advancing, necrotizing lesions potentially associated with an envenomation, the authors advise vigorous treatment. This should include high-dose steroids, Dapsone (if the patient is not of Mediterranean descent), hyperbaric oxygen therapy if the lesion is expanding and this therapy is available, symptomatic care, and close observation if acute care hospitalization is not indicated at the time of presentation.