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  1. Terrestrial snakes
  2. Australia and the Pacific Islands
  3. Clinical Flowchart

Clinical Flowchart

Autopharmacological effects

All Australian elapids1
Minutes to 1 hour2
 
Nausea, vomiting, abdominal pain, diarrhoea, arterial hypotension, collapse, cardiac arrest, seizures
 
Cardiovascular failure
1

“Early collapse, cardiovascular collapse, or hypotensive collapse have been reported particularly following bites by brown snakes, but also by tiger snakes (Notechis scutatus ssp.), rough- scale snakes (Tropidechis carinatus), and taipans (Oxyuranus scutellatus).” (Isbister et al. 2025). 
2

Collapse after Australian snake envenoming almost always occurred within 60 minutes of the bite (on average 20 minutes), and was always accompanied by VICC; it most frequently followed brown snake bites.” (Isbister et al 2025, Johnston et al 2017).

It most often happens pre-hospital and immeditae life support is essential.

Local effects

Pseudechis sp.
Notechis scutatus ssp.
Tropidechis carinatus
Minutes to hours
 

Local pain and swelling
 
Painful swelling of the regional lymph nodes
 
(Necrosis)

Haematological effects

Hoplocephalus sp. 
Notechis scutatus ssp.
Oxyuranus sp.
(Pseudechis sp.)
Pseudonaja sp.
Tropidechis carinatus

Within < 1 hours to hours
    
Gingival bleeding
    
Bleeding from wounds remote from the site of the bite
 
Haematemesis, bleeding per rectum, haematuria
     
Systemic bleeding Intracranial bleeding 
(focal neurological deficits, 
meningismus, coma)
 
Hypovolaemia/haemorrhagic shock
       
Cardiovascular failure Renal failure
CNS failure
 
  • Coagulopathy within 1 h 36 min (median; 20 min to 11 h 30 min (range) for first INR > 1.2  in patients with severe envenoming and VICC (Ireland et al. 2010).
  • In settings where resources are immediatelly accessible: INR, aPTT, Fibrinogen, D-dimer
    • INR (high or unrecordable), aPTT (prolonged).
    • Fibrinogen level (low or undetectable), D-dimer level (very high).
      (Isbister et al. 2013)

    • Even severe haemostatic defects that can be detected on laboratory tests may not become clinically evident for a long period, or even not at all. 

  • Within 24 hours: Thrombotic microangiopathy (TMA) / microangiopathic haemolytic anaemia occurs in about 15% of Australian snake envenoming cases and only from snakes that cause VICC (see Clinical entries: Australian elapids)
  • Patients with VICC require blood film with 24 hours of the bite (schistocytes > 1% is diagnostic of microangiopathic haemolytic anaemia); serial creatinine
    (Ismister et al. 2013)

Neurological effects

Acanthophis sp.
(Notechis scutatus ssp.)
Oxyuranus sp.
Pseudechis papuanus
(Pseudonaja sp.)
(Tropidechis carinatus)
Minutes to hours
 
Cranial nerve deficits (ptosis, ophthalmoplegia, dysphagia, dysarthria)
 
Paralysis of the skeletal musculature including the respiratory musculature
 
Respiratory failure

Muscular effects

Notechis scutatus ssp.
(Oxyuranus sp.)
Pseudechis sp.
(Tropidechis carinatus)
Hours
 
Myalgia (at rest, with active/passive movement, upon pressure), dark urine, ECG changes1
 
Signs of paralysis
 
Rhabdomyolysis → acute renal failure
1 Hyperkalaemia (ECG!) and hypercalcaemia are the important  determinats of severe complications. 

Cardiac effects

Pseudonaja sp.1
 Notechis scutatus ssp.
Tropidechis carinatus
Oxyuranus scutellatus 1
Minutes to 1 hour2
 
Nausea, vomiting, abdominal pain, diarrhoea, arterial hypotension, collapse, cardiac arrest, seizures
 
Cardiovascular failure
1

“Early collapse, cardiovascular collapse, or hypotensive collapse have been reported particularly following bites by brown snakes, but also by tiger snakes (Notechis scutatus ssp.), rough- scale snakes (Tropidechis carinatus), and taipans (Oxyuranus scutellatus).” (Isbister et al. 2025). 
2

Collapse after Australian snake envenoming almost always occurred within 60 minutes of the bite(on average 20 minutes), and was always accompanied by VICC; it most frequently followed brown snake bites.” (Isbister et al 2025, Johnston et al 2017).

It most often happens pre-hospital and immeditae life support is essential.

Renal effects

?1,2
Hours to days
 
Flank pain, renal bed sensitive to percussion
 
Urinary output <400 ml/24 h
 
Renal failure2 
1
  • The contribution of direct venom nephrotoxicty is unclear.
2
  • Direct venom nephrotoxicity, renal ischaemia secondary to shock, disseminated intravascular coagulation with thrombotic microangiopathy (TMA), haemoglobinuria, myoglobinuria, and hyperkalaemia contribute to acute tubular necrosis.” (Warrell and Williams 2023).
  • In Australian elapid envenoming, AKI mostly occurs in the context of thrombotic microangiopathy and rhadomyolysis (Johnston et al. 2017a, Isbister and Berling 2025).