Envenoming by the rough-scaled snake (Tropidechis carinatus): a series of confirmed cases

Melissa Gan, Margaret A O’Leary, Simon G A Brown, Tamara Jacoby, David Spain, Alan Tankel, Chris Gavaghan, Peter Garrett and Geoffrey K Isbister
Med J Aust 2009; 191 (3): 183-186.


Objective: To describe demographic, geographical and clinical features of envenoming by the rough-scaled snake (RSS) (Tropidechis carinatus).

Design, setting and participants: Prospective cohort study of RSS snakebite victims, recruited between January 2004 and December 2008, as part of the Australian Snakebite Project. RSS envenoming cases were confirmed by snake identification and/or venom-specific enzyme immunoassay.

Main outcome measures: Clinical and laboratory features of envenoming.

Results: There were 24 confirmed cases of RSS envenoming, nearly all occurring in coastal areas between northern New South Wales and south-eastern Queensland. Twenty-three patients had local bite-site effects and 17 had at least three non-specific systemic effects (eg, nausea, headache). All 24 had venom-induced consumption coagulopathy (VICC), and 19 had an international normalised ratio > 3.0. Six had bleeding from the bite site or intravenous cannula site, 10 had blood detected on urinalysis, and one had a major intra-abdominal haemorrhage. Mild neurotoxicity developed in two patients, and one patient developed myotoxicity with generalised myalgia, myoglobinuria and a peak creatine kinase level of 59 700 IU/L. Twenty-three patients were treated with antivenom (21 with tiger snake antivenom, two with polyvalent antivenom). Free venom was undetectable in 19 of 20 blood samples taken after antivenom administration.

Conclusion: RSS envenoming occurs predominantly in coastal areas of northern NSW and southern Queensland, and within this range, most envenoming is due to the RSS rather than tiger snakes. Clinically it is characterised by VICC, with mild neurotoxicity and myotoxicity in some cases. Tiger snake antivenom appears to be effective against RSS envenoming.

  • Melissa Gan1
  • Margaret A O’Leary2
  • Simon G A Brown3,4,5
  • Tamara Jacoby3,4
  • David Spain1
  • Alan Tankel6
  • Chris Gavaghan7
  • Peter Garrett8
  • Geoffrey K Isbister9

  • 1 Emergency Department, Gold Coast Hospital, Gold Coast, QLD.
  • 2 Department of Clinical Toxicology and Pharmacology, Calvary Mater Hospital, Newcastle, NSW.
  • 3 Centre for Clinical Research in Emergency Medicine, Western Australian Institute for Medical Research, Perth, WA.
  • 4 Centre for Medical Research, University of Western Australia, Perth, WA.
  • 5 Department of Emergency Medicine, Royal Perth Hospital, Perth, WA.
  • 6 Emergency Department, Coffs Harbour Base Hospital, Coffs Harbour, NSW.
  • 7 Emergency Department, Lismore Base Hospital, Lismore, NSW.
  • 8 Intensive Care Unit, Nambour Base Hospital, Nambour, QLD.
  • 9 Tropical Toxinology Unit, Menzies School of Health Research, Charles Darwin University, Darwin, NT.


We wish to acknowledge the many clinicians and laboratory staff involved in recruiting and collecting data for the ASP and, in particular, for patients recruited to our cohort by Robert Bonnin, Mark Coghlan, David Ward, Andrew Parkin, Colin Page and Julian White. We also thank clinical toxicologists at poisons information centres around Australia for referring additional cases, and acknowledge the help of many nurses, doctors and laboratory staff in recruiting patients and collecting samples. We thank the Hunter Haematology Research Group for doing the clotting factor assays. Our study was supported in part by a National Health and Medical Research Council (NHMRC) project grant. Geoffrey Isbister is supported by an NHMRC clinical career development award and Simon Brown by an NHMRC career development award.

Competing interests:

None identified.

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