title: Death adder envenoming causes neurotoxicity not reversed by antivenom--Australian Snakebite Project (ASP-16).
abstract: BACKGROUND
  Death adders (Acanthophis spp) are found in Australia, Papua New Guinea and parts of eastern Indonesia. This study aimed to investigate the clinical syndrome of death adder envenoming and response to antivenom treatment.
  
  
  RESULTS
  Definite death adder bites were recruited from the Australian Snakebite Project (ASP) as defined by expert identification or detection of death adder venom in blood. Clinical effects and laboratory results were collected prospectively, including the time course of neurotoxicity and response to treatment. Enzyme immunoassay was used to measure venom concentrations. Twenty nine patients had definite death adder bites; median age 45 yr (5-74 yr); 25 were male. Envenoming occurred in 14 patients. Two further patients had allergic reactions without envenoming, both snake handlers with previous death adder bites. Of 14 envenomed patients, 12 developed neurotoxicity characterised by ptosis (12), diplopia (9), bulbar weakness (7), intercostal muscle weakness (2) and limb weakness (2). Intubation and mechanical ventilation were required for two patients for 17 and 83 hours. The median time to onset of neurotoxicity was 4 hours (0.5-15.5 hr). One patient bitten by a northern death adder developed myotoxicity and one patient only developed systemic symptoms without neurotoxicity. No patient developed venom induced consumption coagulopathy. Antivenom was administered to 13 patients, all receiving one vial initially. The median time for resolution of neurotoxicity post-antivenom was 21 hours (5-168). The median peak venom concentration in 13 envenomed patients with blood samples was 22 ng/mL (4.4-245 ng/mL). In eight patients where post-antivenom bloods were available, no venom was detected after one vial of antivenom.
  
  
  CONCLUSIONS
  Death adder envenoming is characterised by neurotoxicity, which is mild in most cases. One vial of death adder antivenom was sufficient to bind all circulating venom. The persistent neurological effects despite antivenom, suggests that neurotoxicity is not reversed by antivenom.
authors.affiliation: School of Medicine Sydney, University of Notre Dame Australia, Darlinghurst, New South Wales, Australia.
authors.forename: Christopher I
authors.initials: CI
authors.lastname: Johnston
authors.forename: Margaret A
authors.initials: MA
authors.lastname: O'Leary
authors.forename: Simon G A
authors.initials: SG
authors.lastname: Brown
authors.forename: Bart J
authors.initials: BJ
authors.lastname: Currie
authors.forename: Lambros
authors.initials: L
authors.lastname: Halkidis
authors.forename: Richard
authors.initials: R
authors.lastname: Whitaker
authors.forename: Benjamin
authors.initials: B
authors.lastname: Close
authors.forename: Geoffrey K
authors.initials: GK
authors.lastname: Isbister
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000818:Animals; D000997:Antivenins / Q000008:administration & dosage*; D001315:Australia; D001774:Blood Chemical Analysis; D002648:Child; D002675:Child, Preschool; D017815:Elapidae; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006801:Humans; D007440:Intubation; D008297:Male; D008875:Middle Aged; D009422:Nervous System Diseases / Q000139:chemically induced / Q000473:pathology* / Q000628:therapy*; D012121:Respiration, Artificial; D012909:Snake Bites / Q000473:pathology* / Q000628:therapy*; D012910:Snake Venoms / Q000097:blood; D016896:Treatment Outcome; D055815:Young Adult
chemical_list: D000997:Antivenins; D012910:Snake Venoms