Neurotoxicity, anticoagulant activity and evidence of rhabdomyolysis in patients bitten by death adders (Acanthophis sp.) in southern Papua New Guinea

Thirty-two patients with enzyme-immunoassay-proven death adder (Acanthophissp.) bites were studied in Port Moresby, Papua New Guinea. Eighteen wereenvenomed; local signs were rare and none had incoagulable blood, but allexcept one had signs of neurotoxicity. Five (27.7%) envenomed patientsrequired intubation and ventilation. One patient developed renal failure,previously undescribed following death adder bites. Laboratoryinvestigations showed mild prolongation of prothrombin and partialthromboplastin times in some patients. In vitro studies showed that thevenom contains anticoagulant activity, but does not cause fibrinogenolysis.In contrast to taipan envenoming, neurotoxicity did not progress afterantivenom administration, and there was reversal of neurotoxicity, evidentwithin 6 h, in three severely envenomed patients treated less than 12 hafter the bite. One patient treated with antivenom and anticholinesteraseshad the most dramatic response to treatment; the optimum management ofbites by this species may include prompt treatment with both antivenom andanticholinesterases in addition to effective first aid.