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Symptoms: Fever and Wound

Sande, Margaret MD

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doi: 10.1097/01.EEM.0000526106.56567.46
    brown recluse spider bite
    brown recluse spider bite:
    brown recluse spider bite

    A 50-year-old man presented with a wound to his right inner thigh, and is concerned that a spider may have bitten him. His vitals were notable for a temperature of 100.5°F but otherwise unremarkable. As the physician in triage, you promptly asked him to show you the site so you can disposition him within your department appropriately, anticipating cellulitis or a drainable abscess.

    The patient said he felt a stinging sensation on his leg, followed by a localized burning discomfort, two days earlier after going through a box of old clothes to be donated. The site subsequently became itchy, red, swollen, and more painful. He began to worry when a bloody blister appeared, and he noted malaise, chills, and nausea at presentation.

    Find the diagnosis and case discussion on p. 32.

    Loxosceles spiders cause an envenomation resulting in dermonecrosis and, more rarely, a systemic reaction or death. They can be found worldwide. The most common in the United States is the brown recluse spider, which is most prevalent in the southern, central, and midwestern states. South American Loxosceles counterparts cause more notable morbidity and mortality secondary to more toxic venom. Only 100 of the 2,566 U.S. envenomations in 2001 thought to be secondary to Loxosceles required admission or further treatment, according to the American Association of Poison Control Centers' Toxic Exposure Surveillance System. (Ann Emerg Med 2004;44[6]:608.)

    Nonarachnologists often misidentify these spiders because dark forms on the spider bodies are mistakenly assumed to be a fiddle pattern. (Toxicon 2003;42[4]:413.) Poison centers are a resource for consulting an arachnologist if a patient presents with the spider in question. The majority of patients only experience a mild inflammatory reaction, and necrosis is unlikely to develop if no lesion is visible two to three days after the bite. (J Am Acad Dermatol 2001;44[4]:561.) A series of 111 Vanderbilt University patients followed up after suspected envenomation found that 37 percent developed a necrotic lesion, 14 percent exhibited systemic illness, five percent warranted hospital admission, three percent ultimately required delayed skin grafting, and no deaths or serious complications were reported. (Ann Emerg Med 1997;30[1]:28.)

    The mechanism of action of the venom is incompletely understood. A core component of it is sphingomyelinase D, but the enzyme hyaluronidase is responsible for the gravity-dependent spread of the lesion, a classic exam finding. The venom also precipitates intravascular clotting, which exacerbates tissue hypoxia. A polymorphonucleocyte infiltration ultimately results. Secondary infection is rare, though a generalized rash and swelling with associated lymphangitis can be mistaken for cellulitis. (Ann Emerg Med 2004;44[6]:608.)

    Mild constitutional symptoms can be seen with uncomplicated cutaneous loxoscelism, though the early phase of the systemic illness known as viscerocutaneous loxoscelism can look the same. This systemic response can be associated with disseminated intravascular necrosis, hemolysis, thrombocytopenia, and rhabdomyolysis, which ultimately leads to renal failure and is most commonly seen 48-72 hours after envenomation. For those exhibiting systemic symptoms, laboratories to evaluate for hemolysis—free haptoglobin, lactate dehydrogenase, and indirect bilirubin—can guide the need for active management. Creatinine kinase and a urinalysis to screen for rhabdomyolysis are also helpful. (Ann Emerg Med 2004;44[6]:608.)

    Treatments proposed include dapsone and colchicine for leukocyte inhibition, steroids, antivenin, hyperbaric oxygen, and wound irrigation. Dapsone is the most commonly cited treatment, but it can have severe adverse effects such as cholestatic jaundice, hepatitis, methemoglobinemia, and hemolytic anemia. Colchicine can lead to bone marrow suppression with aplastic anemia, agranulocytosis, or thrombocytopenia, among others. Studies of the utility of dapsone have several limitations, and a double-blind, randomized, controlled trial has yet to be performed. Reviews suggest that systemic corticosteroids may be useful for viscerocutaneous loxoscelism but not for cutaneous loxoscelism. Four commercial Loxosceles antivenins are utilized most frequently in South America for systemic loxoscelism. None are available in the United States, and no large-scale prospective studies have been undertaken to demonstrate their utility. (Ann Emerg Med 2004;44[6]:608.)

    Nonpharmacotherapies include hyperbaric oxygen and wound irrigation. Hyperbarics were touted as a means to promote neovascularization, but animal data are conflicting. Basic wound irrigation may be of benefit because residual active venom has been found to be present in wounds up to five days after envenomation. (Acad Emerg Med 2001;8[4]:309.)

    After screening labs, including a complete blood count, comprehensive metabolic panel, coagulation studies, free haptoglobin, lactate dehydrogenase, creatinine kinase, and urinalysis, which were found to be unremarkable, this patient was discharged with strict return precautions if systemic symptoms worsened (including discolored urine/hematuria) and asked to return for a recheck in 12-24 hours. He was worried about the need for preventive treatment or antibiotics for the wound, and we reassured him that systemic treatments don't demonstrate clear efficacy and secondary wound infection is unlikely.

    On his return visit, a colleague reported that he had developed a sunken blue necrotic center, which was irrigated and referred to the toxicology and dermatology clinics of a local academic center. His systemic symptoms had resolved. His wound was healed by secondary intention over several weeks, and a scar formed; grafting was not necessary.

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