• Pseudonaja nuchalis: Western brown or gwardar
• Pseudonaja affinis: Dugite
• Pseudonaja textilis: Common or eastern brown snake
• Pseudonaja guttata: Speckled brown
• Pseudonaja modesta: Five-ringed brown
• Pseudonaja ingrami: Ingram’s brown
• Pseudonaja tanneri: Tanner’s brown
• Pseudonaja inframacula: Peninsulabrown

• Patients may present asymptomatic with no obvious bite site
• Non‑specific features of envenoming include headache, nausea, vomiting and abdominal pain
• Systemic envenoming may be heralded by pre‑syncope or sudden collapse. Early death occurs rarely, probably secondary to directcardiotoxicity
• The hallmark of brown snake envenoming is a severe defibrinating coagulopathy. This may manifest clinically as bleeding gums, persistent haemorrhage at venesection sites or intracerebral haemorrhage
• Renal failure occurs in a small percentage of patients and oliguria may be present from the time of envenoming
• Microangiopathic haemolytic anaemia is a rare complication
• Rhabdomyolysis does not occur and significant neurotoxicity is rare despite the presence of a neurotoxin in the venom. Mild diplopia and ptosis are observed occasionally.

• Apply a pressure immobilisation bandage (PIB)
• Transport to a hospital capable of providing definitive care
• Contact Poisons Information Service 13 11 26

Resuscitation and supportive care

• Brown snake envenoming is a potentially life‑threatening emergency and patients should be managed in an area capable of cardiorespiratory monitoring and resuscitation
• Potential early life‑threats that require immediate intervention include:
  • Hypotension
  • Severe coagulopathy with uncontrolled haemorrhage

• In cardiac arrest secondary to brown snake envenoming, undiluted antivenom, administered as a rapid IV push, may be life‑saving. The optimal resuscitation dose is 10 ampoules (10 x 1000 units)

Antivenom

• CSL Brown Snake Antivenom is the definitive treatment of envenoming. Systemic envenoming, as evidenced by collapse or objective evidence of coagulopathy, is treated with an initial dose of five ampoules (5 x 1000 units).
• Brown snake antivenom doses currently recommended are based on clinical experience and consensus. Recommendations may change as improved data is acquired regarding venom, antivenom and target‑organ interactions in human cases
  
• The use of blood products (FFP or cryoprecipitate) in patients with profound coagulopathy without evidence of uncontrolled haemorrhage. This is not currently recommended.

• The diagnosis of envenoming is based on the correlation of history, clinical features and laboratory data
• Envenoming is diagnosed if there is a history of collapse, objective clinical evidence of defibrinating coagulopathy, or laboratory abnormalities consistent with brown snake envenoming during 12hours of observation
• Routine laboratory investigations following snakebite include: FBE, EUC, CK and coagulation profile (INR, aPTT, fibrinogen, d‑dimer) at presentation and at intervals thereafter
• The defibrinating coagulopathy of brown snake envenoming is characterised by:
  • Elevated aPTT (>180 seconds) and INR (>10)
  • Undetectable fibrinogen
  • Elevated d‑dimer and fibrin degradation products
  • Variable thrombocytopenia

• Deteriorating renal function and microangiopathic haemolytic anaemia (MAHA) may occur as indicated by raised lactate dehydrogenase (LDH) and fragmented red blood cells on blood film
• The Snake Venom Detection Kit (SVDK) is not used to diagnose envenoming. Instead, it is used to determine the correct monovalent antivenom where one or more snake types could be responsible for the observed clinical features.

• Tiger snake and brown snake envenoming may be indistinguishable, early in the course, as both feature defibrinating coagulopathy. However, in tiger snake envenoming, paralysis and rhabdomyolysis evolve over the ensuing hours
• Taipan envenoming also features a severe defibrinating coagulopathy, but it is usually associated with early paralysis andrhabdomyolysis
• Black snake envenoming is associated with a mild anticoagulant coagulopathy, normal fibrinogen levels and myolysis (raised CK).

• Patients with no clinical features and no laboratory evidence of coagulopathy at 12 hours are not envenomed and may be discharged. Discharge should not occur at night
• Envenomed patients should be monitored for a further 24 hours following successful correction of coagulopathy with antivenom. This timeframe is sufficient to determine whether renal failure or MAHA is developing. If renal function and blood counts remain stable at the end of that time discharge may occur.

• Visual identification is NOT accurate
• The majority of patients bitten by brown snakes do not become envenomed
• In the early stages, brown snake envenoming may be indistinguishable from tiger snake envenoming
• Early collapse after a brown snake bite is virtually pathognomic of envenoming
• All patients should be managed in a hospital equipped with sufficient antivenom stocks (10 ampoules) to definitively treat potential envenoming.

Sutherland SK, Tibballs J. Australian animal toxins: the creatures, their toxins and care of the poisoned patient. South Melbourne: Oxford University Press, 2001. [Reference]

Murray L, Daly F, Little M, Cadogan M. Toxicology Handbook. Elsevier 2006 [Reference]

White J. Why do people still die from brown‑snake bites? Emergency Medicine 2000; 12:204–206. [Reference]

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