C53-42 When Venoms Cross Paths: Brown Snake Antivenom Reversing Pygmy Mulga Envenomation

Introduction Snake bites remain a global issue. We present a case of Pygmy Mulga envenomation that was successfully treated with brown snake antivenom. Case report A sixty-six-year-old male, professional snake breeder, with history of hypertension, presented thirty minutes after sustaining a snake bite, on his finger, during a feeding attempt. Shortly after arrival, he experienced bleeding from gums, abdominal cramps, nausea, and disorientation. On exam, he was tachycardic, otherwise hemodynamically stable. Inspection of the bite site revealed fang marks, localized erythema and edema, no compartmental restriction or impaired mobility. Gingival bleeding was evident. Laboratory findings demonstrated elevated creatine kinase (peak 1311 IU/L), elevated liver enzymes, total bilirubin 2.5mg/dL, INR 1.4, D-Dimer 1200 ug/mL (normal <500). Troponin, fibrinogen, platelet counts, and renal function were normal. As a professional snake breeder, he carried Antivenom with him. Upon discussion with toxicologists and poison control center, a total of 2000 U of Brown snake Antivenom was administered; he received intravenous fluids for nontraumatic rhabdomyolysis, and empiric antibiotics. Due to neurotoxic effects resembling Myasthenia, vital capacity and negative inspiratory force were monitored every six hours. Five hours later, he experienced worsening digital swelling and paresthesia, that improved significantly with diluted Polyvalent Snake Antivenom 80,000 Units, administered over two hours. Fibrinogen and INR were monitored for potential worsening of coagulopathy. Fortunately, his recovered well without sequalae, over five days. Discussion Envenomation by Pygmy Mulga is rare. In addition to non-specific symptoms, anticoagulant coagulopathy, myotoxicity, and hemolysis were the most common effects. Bleeding at intravenous sites, gingiva were common compared to major hemorrhage. Neurotoxicity ranges from blurred vision, ptosis, slurred speech to seizures, coma. Rarely cardiac arrest was reported. Mild nonspecific symptoms can be seen early in the course, despite significantly high venom concentrations in serum, as in our patient. Access to antivenom is lifesaving, especially when given within two hours. Serial measurements of venom and antivenom concentration (serum or urine) pre- and post-treatment may be useful, particularly in the setting of clinical deterioration. The only antivenoms effective for Pygmy Mulga are brown snake antivenom and the polyvalent snake antivenom, often expensive and has limited supply in the United States. Early presentation and prompt administration of antivenom along with critical care monitoring led to relatively rapid recovery without potential complications. Our case illustrates the importance of early treatment with antivenom in fatal snake bites to mitigate progression to life threatening coagulopathy and hemorrhage. This abstract is funded by: None