INTRODUCTION: Rattlesnakes cause the majority of snake bites reported in the United States. According to AAPCC, there are approximately 7000-8000 snake bites in the US, and 300000-400000 snake bites internationally. We present a rare case of a patient with systemic envenomation.
CASE PRESENTATION: A 58-year-old woman was brought in by ambulance after reporting a rattlesnake bite to her left leg. EMS noted facial swelling, hypotension, tachycardia, and tachypnea. In the ED, she developed dyspnea with rapidly progressive respiratory distress. Direct laryngoscopy revealed laryngeal edema, and a nasotracheal airway was secured. The left leg was dusky and ecchymotic with progressive edema. Patient developed diffuse fasciculations and oozing from all access sites; labs revealed platelets of 7,000, hemoglobin of 17.4, white blood cells 12,900. Antivenom was initiated and patient was admitted to the ICU. In the ICU, fasciculations increased, horizontal nystagmus was noted and rhabdomyolysis developed secondary to myokymia. Hourly administration of antivenom was continued for 12 hours, at which point myokymia, nystagmus, and DIC had resolved, and local reaction stabilized. Antivenom was tapered to maintenance dosing until hospital day 3 when patient was extubated. On day 4, patient developed altered mental status and hypoxic respiratory distress requiring reintubation. Labs revealed recurrence of DIC. Cryoprecipitate, FFP, and antivenom were administered. Supportive care for renal and respiratory failure continued until day 13 when patient was successfully extubated.
DISCUSSIONS: Patients with systemic envenomation present with a wide spectrum of symptoms, from mild local pain and erythema, to dyspnea, hematemesis or neurologic symptoms. The most extreme cases involve laryngeal edema-induced airway compromise, DIC, and myokymia (fasciculations) resulting in rhabdomyolysis. Venom-induced thrombocytopenia may also exist with or without defibrination, caused by direct conversion of fibrinogen to an unstable fibrin clot. Laryngeal edema and stridor occur due to capillary leak caused by systemic circulation of venom. Pit-viper venom increases the permeability of the capillary membranes, resulting in the extravasation of electrolytes, albumin, and red cells into the envenomated site. This process may also occur in the lungs, myocardium, kidneys, peritoneum, and rarely, the central nervous system. Altered permeability of red-cell membranes may result in hemolysis. Edema, hypoalbuminemia, and hemoconcentration are followed by pooling of blood and fluids in the microcirculation, resulting in hypovolemic shock and lactic acidosis. Renal failure may result from hypotension, intravascular hemolysis, a syndrome resembling disseminated intravascular coagulation, or nephrotoxic effects of components of venom.Management in the field consists of keeping the site of envenomation immobilized and below the level of the heart, without tournicates and suction devices. The currently used antivenom is Polyvalent Crotalidae Ovine Immune Fab (FabAV, CroFab). Its use is recommended for any degree of envenomation. The optimal length of antivenom infusion has not been established, however, the initial dose is 4-6g immediately, then another 4-6g one hour later if the patient has not yet responded, then 2g every six hours for three doses. More doses may be necessary if symptoms or laboratory abnormalities persist. Clinical improvement may be seen even with administration of antivenom more than 6 hours after envenomation. Mortality from systemic envenomation has been reduced to 0.28% with administration of anti-venom. Patients should also receive tetanus prophylaxis. Antibiotics are not recommended.
CONCLUSION: Systemic envenomation is the most common cause of mortality due to rattle snake bites. Systemic envenomation requires very frequent administration of anti-venom and aggressive respiratory and cardiovascular support in order to ensure survivial.
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