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Detecting And Treating Recluse Spider Bites

Insect bites and stings are a relatively common occurrence with more than 50,000 exposures occurring per year in the United States.1 Slightly less than half of these injuries are spider bites. One of the most clinically significant spiders is the recluse spider, whose bite can progress to ulcerating dermonecrosis at the bite site. 

Brown recluse spiders are part of the genus Loxosceles. They inhabit several areas of the United States including Colorado, southeast Nebraska, Kansas, Oklahoma, Texas, Louisiana, Arkansas, Missouri, Kentucky, Tennessee, Mississippi, Alabama, northern Georgia, southern Ohio, southern Indiana and southern Illinois.2 Studies have reported brown recluse spider bites in California and other western states, but authors believe these to be a misdiagnosis as the brown recluse spider has not established itself outside of its native range.3 Both the hobo spider and the yellow sac spider can cause similar necrotic bites, but these are usually less severe than a recluse spider bite.4

Recluse spiders are rarely aggressive and bites are uncommon. Most bites occur when the spider gets pressed against the skin by clothing, towels, bedding or gloves. Bites most frequently occur at night and in the early morning during warmer months. Frequently, patients do not feel the recluse bite and it does not cause immediate pain.

Brown recluse spiders have several toxins, the most clinically significant being the hemotoxic agent sphingomyelinase D.5 Direct cytotoxicity from this venom component, as well as autoimmune response from cytokines and lymphocytes, theoretically result in the necrosis and systemic symptoms that can arise from recluse spider bites.6 Most recluse spider bites are minor and spontaneously resolve without necrosis. Recluse spider bites can result in the clinical condition of loxoscelism, which is the only proven type of necrotic arachnidism in humans.6 There are two forms of loxoscelism: necrotic cutaneous loxoscelism and viscerocutaneous loxoscelism. A small number of bites produce dermonecrotic skin lesions and an even smaller number of bites produce systemic symptoms. A study by Leach and colleagues found that skin necrosis occurred in 37 percent of recluse spider bites and systemic illness occurred in 14 percent of cases.7

In necrotic cutaneous loxoscelism, symptoms secondary to the recluse spider bite remain localized to the skin. Dermonecrotic skin lesions typically begin with pain and burning at the bite site that progress for two to eight hours after the initial bite occurred. Over the next 12 to 36 hours, symptoms progress with the bite area first becoming pale and the surrounding area becoming red and edematous. The area then develops a bluish, hard, stellate center that becomes progressively more necrotic and eventually sloughs.5,8 The amount of dermal necrosis can be quite extensive with ulcerative necrotic areas up to 40 cm reported.5

In approximately 14 percent of cases, recluse bites result in a combination of local cutaneous and systemic symptoms known as viscerocutaneous loxoscelism.7 Common systemic symptoms include low energy, nausea, vomiting and fever. In advanced cases, the recluse spider hemotoxin can cause destruction of red blood cells, resulting in hemolytic anemia.2 Myonecrosis and rhabdomyolysis from loxoscelism can lead to renal failure.9 Severe bleeding can occur due to destruction of platelets resulting in thrombocytopenia and consumption of clotting factors leading to disseminated intravascular coagulation.2

There are numerous infectious and non-infectious conditions that can produce necrotic wounds similar to the recluse spider bite and physicians misdiagnose an estimated 80 percent of recluse spider bites.5 As I stated previously, the hobo spider and yellow sac spider can cause necrotic bites that are usually less severe than a recluse spider bite.4 Other conditions with symptoms similar to recluse spider bites include: pyoderma gangrenosum, staphylococcal or streptococcal infection, herpes zoster or herpes simplex, diabetic ulcers, fungal infection, chemical burn, Toxicodendron dermatitis, squamous cell carcinoma, vasculitis, syphilis, toxic epidermal necrolysis, erythema multiforme, purpura fulminans, sporotrichosis and Lyme disease.2,10 One of the most common and clinically significant differential diagnoses for recluse spider bites is nosocomial or community-acquired methicillin-resistant Staphylococcus aureus infection.11

A Closer Look At Treatment Options

Despite being one of the most clinically significant spider bites, recluse spider bites have no established treatment protocols. The initial recommended treatments for recluse spider bites includes cleaning the bite site, cold compresses, elevation, immobilization, analgesics, antihistamines and tetanus prophylaxis.12,13 There are other treatment modalities, none of which randomized control studies have shown to provide clinical benefit. These treatments include antibiotics, glucocorticoids, hyperbaric oxygen, surgical intervention and nitroglycerin.

Antibiotics. Dapsone (Aczone, Allergan) has been in use for several decades in the treatment of recluse spider bites. Physicians presumed that dapsone stopped dermonecrosis by inhibiting leukocyte migration, degranulation and cytokine release.14 Animal studies have shown conflicting results and currently there are no studies demonstrating the clinical efficacy of dapsone for the treatment of recluse spider bites.2,15 Additionally, dapsone carries a risk of hemolysis with methemoglobinemia. Authors suspect that dapsone may be effective in treating recluse spider bites that physicians had misdiagnosed as infections.10

Glucocorticoids. One may use both systemic and intralesional glucocorticoids to treat recluse spider bites. Oral glucocorticoids may relieve many of the systemic symptoms that result from recluse spider bites, but intralesional injections have no benefit and can actually delay wound healing.16,17

Hyperbaric oxygen. Hyperbaric oxygen hypothetically slows the dermonecrosis of recluse bites by oxidizing bonds and inhibiting the spider’s hemotoxic venom. Studies evaluating the effect of hyperbaric oxygen for the treatment of recluse spider have shown mixed treatment outcomes with some studies showing clinical benefits and other studies showing no effect18-22

Surgical intervention. Studies have shown no clinical benefit and possible worse clinical outcomes with early surgical excision for the treatment of recluse spider bites.23 Early surgical excision can extend the dermonecrosis and lead to complications including delayed wound healing, secondary infection and scarring.13,14 For larger areas of dermonecrosis resulting from recluse spider bites, delayed surgical intervention including debridement, excision of eschars and split thickness skin grafting may be required.13,14

Nitroglycerin. Nitroglycerin is a suggested treatment to counteract the vasoconstrictive effect of recluse spider bite venom, but animal studies show no benefit of nitroglycerin in decreasing necrosis and that nitroglycerin treatment can lead to increased inflammation and signs of systemic loxoscelism.24       

In conclusion, while recluse spider bites are relatively uncommon, they are clinically significant due to their potential to cause dermonecrosis at the bite site. While most recluse spider bites are minor and spontaneously resolve, they can lead to both necrotic cutaneous loxoscelism and viscerocutaneous loxoscelism. There are numerous infectious and noninfectious conditions that can produce necrotic wounds similar to the recluse spider bite. Methicillin-resistant Staphylococcus aureus infection is one of the most common disorders misdiagnosed as a recluse spider bite.

References

1. Toewe CH II. Bug bites and stings. Am Fam Physician. 1980;21(5):90-5.

2. Swanson DL, Vetter RS. Bites of brown recluse spiders and suspected necrotic arachnidism. N Engl J Med. 2005;352(7):700-7.

3. Vetter RS. Arachnids misidentified as brown recluse spiders by medical personnel and other authorities in North America. Toxicon. 2009;54(4):545-47.

4. Bennett RG, Vetter RS. An approach to spider bites. Erroneous attribution of dermonecrotic lesions to brown recluse or hobo spider bites in Canada. Can Fam Physician. 2004;50(8):1098-101.

5. Swanson DL, Vetter RS. Loxoscelism. Clin Derm. 2006;24(3):213:3):

6. Diaz JH, Leblanc KE. Common spider bites. Am Fam Physician. 2007;75(6):869-873.

7. Leach J, Bassichis B, Itani K. Brown recluse spider bites to the head: three cases and a review. Ear Nose Throat J. 2004;83(7):465-70.

8. Wasserman G, Anderson P. Loxoscelism and necrotic arachnidism. J Toxicol Clin Toxicol. 1983-1984;21(4-5):451-72.

9. Franca FO, Barbaro KC, Abdulkader RC. Rhabdomyolysis in presumed viscero-cutaneous loxoscelism: report of two cases. Trans R Soc Trop Med Hyg. 2002;96(3):287-90.

10. Vetter R, Bush S. The diagnosis of brown recluse spider bite is overused for dermonecrotic wounds of uncertain etiology. Ann Emerg Med. 2002;39(5):544-6.

11. Dominguez TJ. Ites not a spider bite, it’s community-acquired methicillin-resistant Staphylococcus aureus. J Am Board Fam Pract. 2004;17(3):220-6.

12. Wright SW, Wrenn KD, Murray L, Seger D. Clinical presentation and outcome of brown recluse spider bite. Ann Emerg Med. 1997;30(1):28-32.

13. Rees R, Campbell D, Rieger E, King LE. The diagnosis and treatment of brown recluse spider bites. Ann Emerg Med. 1987;16(9):945-9.

14. Sams HH, Dunnick CA, Smith ML, King LE Jr. Necrotic arachnidism. J Am Acad Dermatol. 2001;44(4):561-73.

15. Elston DM, Miller SD, Young RJ 3rd, Eggers J, McGlasson D, Schmidt WH, Bush A. Comparison of colchicine, dapsone, triamcinolone, and diphenhydramine therapy for the treatment of brown recluse spider envenomation: a double-blind, controlled study in a rabbit model. Arch Dermatol. 2005;141(5):595-7.

16. Jansen GT, Morgan PN, McQueen JN, Bennett WE. The brown recluse spider bite: controlled evaluation of treatment using the white rabbit as an animal model. South Med J. 1971;62(10):1194-202.

17. Fardon DW, Wingo CW, Robinson DW, Masters FW. The treatment of brown spider bite. Plast Reconstr Surg. 1967;40(5):482-8.

18. Merchant ML, Hinton JF, Geren CR. Effect of hyperbaric oxygen on sphingomyelinase D activity of brown recluse spider (Loxosceles reclusa) venom as studied by 31P nuclear magnetic resonance spectroscopy. Am J Trop Med Hyg. 1997;56(3):335-8.

19. Maynor ML, Moon RE, Klitzman B, Fracica PJ, Canada A. Brown recluse spider bites: beneficial effects of hyperbaric oxygen. J Hyperb Med. 1992;7(1):89-102.

20. Svendsen FJ. Treatment of clinically diagnosed brown recluse spider bites with hyperbaric oxygen: a clinical observation. J Ark Med Soc. 1986;83(5):199-204.

21. Phillips S, Kohn M, Baker D, et al. Therapy of brown spider envenomation: a controlled trial of hyperbaric oxygen, dapsone, and cyproheptadine. Ann Emerg Med. 1995;25(3):363-8.

22. Hobbs GD, Anderson AR, Greene TJ, Yealy DM. Comparison of hyperbaric oxygen and dapsone therapy for Loxosceles envenomation. Acad Emerg Med. 1996;3(8):758-61.

23. Rees R, Altenbern D, Lynch J, King L. Brown recluse spider bites. A comparison of early surgical excision versus dapsone and delayed surgical excision. Ann Surg. 1985;202(5):659-63.

24. Lowry B, Bradfield J, Carroll R, Brewer K, Meggs W. A controlled trial of topical nitroglycerin in a New Zealand white rabbit model of brown recluse spider envenomation. Ann Emerg Med. 2001;37(2):161-5.

Comments

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I think this is a nice review article. Several of the points in the article run counter to my experience of brown recluse spider bite victims and their treatment, between my residency in Philadelphia and my private practice in Corpus Christi, Texas. First, my mainstay for treatment is to anesthetize the area and reduce the toxin burden in the bite area via sharp debridement, usually with a Fox dermal curette. In comparison with those bites I see that have not been debrided by other practitioners, the extent of the necrosis and the scarring of the site is minimal after early detection and débridement, and can be very extensive and debilitating without. This would include my own bite experience on my right mid-thigh, which I treated. Secondly, my treatment always includes Dapsone, and, again, my experience is that when it isn’t used, the necrosis is far more extensive. We inherited an interesting case during my residency from another hospital and another podiatric group. The man had been bitten by a brown recluse spider (confirmed by the patient as he slapped and killed it while it was on his heel, possibly initiating the bite, ironically). After being bitten, he sought care at his doctor’s office, and was seen the next day by a podiatrist in the locale. After those two days, the necrotic area was already the size of a quarter and he was sent to the E.R. and admitted. The team at the other hospital did no débridement and only placed him on I.V. antibiotics (as he was diaphoretic, showed malaise and lethargy, some tachycardia and had a low-grade fever). He was finally taken to the O.R. for débridement a week after admission, wherein the necrosis had progressed to the lateral calcaneus. After débridement and a flap closure, he was discharged. Three days after discharge, he presented to our facility because his systemic symptoms had returned in full force, he now had a fever of 103° and had a foul smell emanating from the dressing site. I was able to retrieve a sample for bone culture by simply reaching in with a sterile forceps and pulling out a chunk of his calcaneus as the flap closure was completely necrosed. Despite our best efforts, the necrosis continued to the point that it involved the STJ and the entirety of the calcaneus and he consented to a BKA. Although this was only one of several cases of what I would term poorly attended brown recluse spider bites from my residency and private practice, I will continue to advocate aggressive and early débridement, Dapsone and (probably) oral abx as my personal experience with this treatment regimen is vastly different than my experience of outcomes without.
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