A 31-year-old African American male without any significant medical history presented to the emergency department with complaints of left arm pain, vomiting, and dark urine. One week prior to his presentation, he felt a sudden burning sensation to his arm and then developed redness, swelling, and pain. Two days later, the pain became worse, and he noticed a vesicle to the area without any discharge. This was followed by the development of non-bloody, non-bilious emesis and flank pain. His urine became dark one day prior to his presentation to the ED.
He worked at a recycling center and had to frequently reach into piles of material that were kept outside. No one else at his house had reported a rash or insect bites, and no spiders were seen in his house. He denied being on any medications, any drug use, any recent travel, or personal or family history of hemolytic anemia or autoimmune diseases.
His vitals upon presentation consisted of the following: temperature 36.7˚C, heart rate 80 beats per minute, blood pressure 106/70 mmHg, and a respiratory rate of 18 breaths per minute with an oxygen saturation of 99% on room air. Examination revealed scleral icterus with pale conjunctivae and a mildly tender upper abdomen. He was jaundiced but did not have hepatosplenomegaly. There was a dark bullous area with surrounding erythema and ecchymosis to his left arm (image). The site was tender without induration or drainage. There were no other rashes. The remainder of his examination was unremarkable.
ED laboratories revealed a hemoglobin and hematocrit (H/H) of 8.6 gm/dL and 23.8% with a normal platelet count, 166 K/mm3.
His total bilirubin was 14.1 mg/dL, with an AST of 78 Units/L and ALT of 30 Units/L. He had an INR of 1.19, PT 14.9 sec, aPTT 30.9 sec, creatinine 1.09 mg/dL, reticulocyte count 4.2%, LDH 935 units/L, haptoglobin 8.6 mg/dL (normal 27-220), fibrinogen 714 mg/dL (170-500), d-dimer 0.9 mcg/ml, and a urinalysis (UA) with 15 RBCs/hpf. Other labs including myoglobin and serum iron were unremarkable.
The patient was admitted to the hospital with presumed hemolytic anemia from a brown recluse envenomation. He was started on a normal saline infusion with sodium bicarbonate. He was transfused two units of pRBCs later that day when his H/H declined to 5.2/14.4. Further testing including a coombs test and serum antineutrophil cytoplasmic ab (ANCA) were negative. Over the next three days, he received a total of six units of pRBC due to continued hemolysis. The patient did not receive dapsone, antibiotics, or hyperbaric therapy. Hematology was consulted, agreed with the diagnosis of a brown recluse envenomation, and did not recommend any other therapy. He was discharged on hospital day number six with a stable hemoglobin, normal bilirubin, and normal UA.
The brown recluse spider has been reported throughout the US but predominantly in the South – often in storage areas, attics and basements. They range from 1-3 cm in size, and often have violin-like markings on their upper backs.
Brown recluse envenomations can be pruritic, painful, and erythematous. In severe cases, the wound can progress, including hyperesthesias, bullae, ulceration, necrosis, and formation of an eschar1, though it’s notable that other processes, from other insect and animal bites to MRSA infections, can cause similar findings.
Classically, the lesion from brown recluse envenomation is referred to as the “red, white, and blue” sign due to the central, necrotic area, surrounded by an area of blanching ischemia, which is surrounded by an area of erythema. Loxoscelism (systemic illness) is rare, and more commonly seen in children; it can cause nausea, fevers/chills, malaise, arthralgias, hemolysis, coagulopathy, disseminated intravascular coagulation, acute tubular necrosis , renal failure, and, rarely, death1,2,4,5. Systemic loxoscelism generally occurs 24-72 hours after the envenomation. Wound size is not related to the probability of developing systemic loxoscelism1. In North America, the incidence of systemic illness is rare. Treatment includes tetanus prophylaxis and local wound care. A Mexican company called Bioclon® has developed horse-harvested antibodies to sphingomyelinase D, a toxin common to Loxosceles species in the Americas. The antivenom is said to quickly reverse systemic effects6, though it has not been rigorously studied and is not yet available in the US. A similar Bioclon® product, for scorpion envenomations, recently received FDA approval.
There is no proven role for dapsone, steroids, hyperbaric oxygen, nitroglycerin, or early surgical excision. Antibiotics are indicated only if superinfection is present.1,3
1. Andersen RJ, Campoli J, Johar SK, Schumacher KA, Allison EJ Jr. Suspected brown recluse envenomation: a case report and review of different treatment modalities. J Emerg Med. 2011 Aug;41(2):e31-7.
2. Rees RS, O’Leary JP, King LE Jr. The Pathogenesis of Systemic Loxoscelism following Brown Recluse Spider Bites. J Surg Res. 1983 Jul;35(1):1-10.
3. Swanson DL, Vetter RS. Bites of brown recluse spiders and suspected necrotic arachnidism. N Engl J Med. 2005 Feb 17;352(7):700-7.
4. Rosen JL, Dumitru JK, Langley EW, Meade Olivier CA. Emergency department death from systemic loxoscelism. Ann Emerg Med. 2012 Oct;60(4):439-41.
5. McDade J, Aygun B, Ware RE. Brown recluse spider (Loxosceles reclusa) envenomation leading to acute hemolytic anemia in six adolescents. J Pediatr 2010;156:155-7.
6. Bilger, B. Spider Woman. New Yorker 2007; March 5: 66-73.