title: Thrombotic microangiopathy from Australian brown snake (Pseudonaja) envenoming.
abstract: BACKGROUND
  Australian brown snake (genus Pseudonaja) envenoming causes a venom-induced consumptive coagulopathy (VICC). A proportion of cases go on to develop thrombotic microangiopathy characterized by thrombocytopenia, microangiopathic haemolytic anaemia (MAHA) and acute renal failure (ARF).
  
  
  OBJECTIVE
  The aim of the study was to define better the natural history and empirical treatments for thrombotic microangiopathy in brown snake envenoming.
  
  
  METHODS
  A review of brown snake bites recruited to the Australian Snakebite Project (ASP), a national multicentre study of snake envenoming was undertaken. Serial data are recorded on clinical effects and laboratory results, including measurement of venom concentrations. We describe cases of thrombotic microangiopathy and compare these to cases without thrombotic microangiopathy.
  
  
  RESULTS
  From 32 cases of brown snake envenoming with severe VICC, four (13%) developed thrombotic microangiopathy, we also included two cases of thrombotic microangiopathy from prior to ASP. All six developed severe thrombocytopenia (<20 x 10(-9)/L), worst 3 days after the bite and resolving over a week, MAHA with fragmented red blood cells on the blood film and five developed anuric ARF requiring dialysis and lasting 2-8 weeks. All six received antivenom, which was delayed compared with other brown snake-envenoming cases. Four were treated with plasmapheresis. The severity and recovery of the thrombocytopenia, anaemia and renal function were similar with and without plasmapheresis. The median length of stay for MAHA cases was 14 days (interquartile range (IQR) 12-14) compared to 1.8 days (IQR 1.3-2) for all other cases.
  
  
  CONCLUSIONS
  Thrombotic microangiopathy resulting from brown snake bite appears to have a good prognosis and management should focus on early antivenom therapy and supportive care including dialysis. The role of plasmapheresis is yet to be defined.
authors.affiliation: Tropical Toxinology Unit, Menzies School of Health Research, Charles Darwin University, Darwin, Northern Territory, Australia. geoffrey.isbister@menzies.edu.au
authors.forename: G K
authors.initials: GK
authors.lastname: Isbister
authors.forename: M
authors.initials: M
authors.lastname: Little
authors.forename: G
authors.initials: G
authors.lastname: Cull
authors.forename: D
authors.initials: D
authors.lastname: McCoubrie
authors.forename: P
authors.initials: P
authors.lastname: Lawton
authors.forename: F
authors.initials: F
authors.lastname: Szabo
authors.forename: J
authors.initials: J
authors.lastname: Kennedy
authors.forename: C
authors.initials: C
authors.lastname: Trethewy
authors.forename: G
authors.initials: G
authors.lastname: Luxton
authors.forename: S G A
authors.initials: SG
authors.lastname: Brown
authors.forename: B J
authors.initials: BJ
authors.lastname: Currie
mesh_terms: D058186:Acute Kidney Injury / Q000209:etiology / Q000628:therapy; D000328:Adult; D000369:Aged, 80 and over; D000743:Anemia, Hemolytic / Q000209:etiology / Q000628:therapy; D000818:Animals; D001315:Australia; D004211:Disseminated Intravascular Coagulation / Q000209:etiology* / Q000628:therapy; D017815:Elapidae; D006801:Humans; D008297:Male; D012909:Snake Bites / Q000150:complications* / Q000628:therapy; D013921:Thrombocytopenia / Q000209:etiology / Q000628:therapy