QJM, Vol 89, Issue 1 25-35, Copyright © 1996 by Oxford University Press
DG Lalloo, AJ Trevett, J Black, J Mapao, A Saweri, S Naraqi, D Owens, AS Kamiguti, RA Hutton, RD Theakston and DA Warrell
Thirty-two patients with enzyme-immunoassay-proven death adder (Acanthophis
sp.) bites were studied in Port Moresby, Papua New Guinea. Eighteen were
envenomed; local signs were rare and none had incoagulable blood, but all
except one had signs of neurotoxicity. Five (27.7%) envenomed patients
required intubation and ventilation. One patient developed renal failure,
previously undescribed following death adder bites. Laboratory
investigations showed mild prolongation of prothrombin and partial
thromboplastin times in some patients. In vitro studies showed that the
venom contains anticoagulant activity, but does not cause fibrinogenolysis.
In contrast to taipan envenoming, neurotoxicity did not progress after
antivenom administration, and there was reversal of neurotoxicity, evident
within 6 h, in three severely envenomed patients treated less than 12 h
after the bite. One patient treated with antivenom and anticholinesterases
had the most dramatic response to treatment; the optimum management of
bites by this species may include prompt treatment with both antivenom and
anticholinesterases in addition to effective first aid.
ORIGINAL PAPERS
Neurotoxicity, anticoagulant activity and evidence of rhabdomyolysis in patients bitten by death adders (Acanthophis sp.) in southern Papua New Guinea
Department of Clinical Sciences, University of Papua New Guinea, Port Moresby.
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