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Two Cases of Brown Recluse Envenomation

Abstract

Objective

Hemostatic abnormalities, including disseminated intravascular coagulation (DIC), are often cited as a common finding in patients following Loxosceles spider envenomation (ie, loxoscelism). The prevalence and severity of coagulopathy, however, particularly following L reclusa (ie, brown recluse) envenomation, is not well described. This study aimed to characterize coagulation laboratory parameters and coagulopathy in patients following L reclusa envenomation.

Methods

We evaluated the coagulation laboratory parameters (eg, prothrombin time, partial thromboplastin time, coagulation factor activity levels, lupus anticoagulant [LA] testing) of 2 patients seen at our institution following brown recluse spider envenomation. We also comprehensively reviewed the literature for all reported cases of brown recluse spider envenomation and assessed patient demographics, clinical presentations, coagulation laboratory parameters, and outcomes.

Results

We identified 2 patients with loxoscelism (1 cutaneous only, 1 systemic with hemolysis) with prolonged partial thromboplastin times but with normal clotting factor levels following envenomation. Literature review identified 263 patients: 12 patients had at least 1 prolonged clotting time, 31 reported a platelet count below 150 × 109/L, and there was clinical concern for DIC in 12 cases. The odds of death were statistically significantly higher in patients with clinical concern for DIC than in cases without concern for DIC or coagulopathy (odds ratio, 82.9 [95% CI, 12.6-433.8]; P < .001).

Conclusions

Following brown recluse spider envenomation, hemostatic perturbations are infrequent and clinical coagulopathy is uncommon, but the odds of death following a brown recluse spider bite are statistically significantly greater if DIC develops, even when compared to individuals with hemolysis without DIC.


Added 11-07-25: Here is a manuscript from colleague Dave McGlasson describing his experiments with the Brown Recluse spider venom: McGlasson DL, Harroff HH, Sutton J, Dick E, Elston, DM.  Cutaneous and systemic effects of varying doses of Brown Recluse spider (Loxoceles reclusa) venom in a rabbit model (Oryctolagus cunniculus).

Abstract

Objective: To ascertain the cutaneous and systemic effects of a single variable dose of Brown Recluse Spider venom (BRSV) in a rabbit model. Cutaneous necrosis is a serious complication of brown spider envenomation. Disseminated intravascular coagulation (DIC) remains the most dreaded complication of brown recluse envenomation in humans. New Zealand white (NZW) rabbits have proved to be a suitable model for the study of therapeutic regimens to prevent skin necrosis after spider bites. We studied the venom’s effects on the skin and the coagulation mechanism in this rabbit model to determine if the NZW rabbit is a suitable model to study both cutaneous and systemic effects of the venom.

Design and Setting: Thirty-six New Zealand white rabbits were divided into three groups. One group received a saline injection, and the other two groups received a 4.0µg/ml or a 10.0µg/ml dose of purified BRSV intradermally into the skin on the dorsum of the back. Samples were collected at baseline, 24, 48 and 72 hours. Tissue specimens were obtained at 72 hours. Measurements included CBC with platelets, PT, APTT, fibrinogen (clottable and immunological), coagulation factors II, V, VII, VIII, IX, X, XI, XII, antithrombin, alpha-2 antiplasmin, protein C, mixing studies, lupus anticoagulant screening, plasminogen, thrombin-anti-thrombin, FDP, d-dimer, and thrombin time.

Interventions: None

Results: The WBC and platelet counts decreased dramatically at 24 hours in the two groups receiving the BRSV. BRSV produced a dose related increase in the APTT. Levels of fibrinogen as well as Factors V, VII, VIII, IX, X, anti-thrombin III, and alpha-2 antiplasmin were greatly increased in response to the BRSV. Protein C decreased at 24 hours and remained low in other time points. Mixing studies corrected the prolonged APTT’s to normal ranges. Factor II, FXI and FXII showed no significant alteration in response to the BRSV.

Conclusions: In the model, both the size and depth of the eschar were dose related. We also observed a dose related elevation in the APTT that corrected with mixing studies. We did not detect a factor deficiency or evidence of a lupus anticoagulant. The assayed coagulation factors were elevated or normal following the BRS envenomation, while Protein C demonstrated a sustained decrease. Although DIC did not occur in the rabbit model, alterations in coagulation factors were evident that could shed light on a human coagulopathy following envenomation. Gross pathology results were consistent with previous studies that used higher doses of BRSV.

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