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Acute STEMI successfully treated with chest compression and defibrillation

organ failure. Therefore, high levels of fibrin degradation product and D-dimer after snakebite suggest that there are other causes of coagulopathy rather than venom-induced coagulopathy. Actually, coagulopathy shown in our case was responsive to proper administrations of antibiotics and transfusion, not additional use of antivenin. Because of the snake venom’s potent bactericidal activity, wound infection after snakebite is rare, but it is significantly increased if the wound is complicated with haematoma or necrosis. Our patient also had extensive swelling and petechia of the affected extremity that extended to the inguinal area. Recent study of snake normal flora reported that 406 bacteria were isolated from the mouth swabs of 72 snake species inhabited in Hong Kong, of which 11 cases (2.7%) were Acinetobacter species. According to the study by Garg et al., Acinetobacter species accounted for 3.8% of whole bacterial species cultured from 53 infected wounds after snakebites. Wound infection after snakebite might have originated from the snake normal flora and environmental contaminations. We did not perform bacterial culture from snakebite wound. Systemic infection after snakebite could be secondarily caused by poor clinical condition such as hypotension or bile stasis because of severe stress. Our patient also showed elevated bilirubin levels during the hospital stay. Therefore, it was uncertain if Acinetobacter bacteremia shown in our patient originated from the snake normal flora of the oral cavity or environmental contaminations. All of these are our limitations.