Is it an Emergency?

Inquire

• time of the bite,
• local pain,
• nausea, vomiting, abdominal pain.

Assess

• state of consciousness.

Measure

• blood pressure/pulse,
• respiratory rate,
• oxygen saturation (pulse oximeter),
• 20WBCT (bedside test).
  (in settings where resources are immediatelly accessible, go directly to 'Laboratory and physical investigations' below)

Observe/investigate

• bite marks,
• extent and intensity of local swelling,
• enlargement and painfulness of regional lymph nodes,
• swelling in the facial region, including the larynx/pharynx (angio-oedema),
• conjunctival oedema,
• clinical signs of a pleural effusion, pulmonary oedema,
• clinical signs of shock,
• bleeding in the region of the swelling,
• bleeding from bite marks and other injuries,
• gingival bleeding,
• blood-stained sputum, vomit ("coffee ground vomitus"), stools (melaena) or urine,
• acute abdomen (intra-abdominal bleeding!),
• focal neurological deficits, meningismus (intracranial bleeding!),
• cranial nerve deficits, such as ptosis, ophthalmoplegia, dysphagia, dysarthria,
• paralysis of the skeletal musculature including the respiratory musculature (→ respiratory insufficiency/respiratory failure),
• myalgia with active and passive movement and upon pressure,
• dark-brown/red urine (differential diagnosis haemoglobinuria) (rhabdomyolysis!),
• flank pain and renal bed sensitive to percussion,

Varibility of symptoms and degree of envenoming

The symptoms and degree of envenoming depend not only on the amount of venom injected and numerous other variables, but also on the time that has elapsed since the bite. This variable factor must be taken into account when making the following decisions:

• exclusion of envenoming 
• the time interval between clinical examinations
• emergency care (see below)

Local signs & symptoms

Local effects are uncommon in Australian snakebite and are minimal for bites by brown snakes.
More significant local signs can occur in bites from black snakes, tiger snakes and rough-scaled snakes.

Early cardiovascular / hypotensive collapse (autopharmacological / cardial effects)

Probably in all Australian elapid envenoming to varying degrees.
Collapse almost always occurred within 60 minutes of the bite (on average 20 minutes), and was always accompanied by VICC.” (Isbister et al 2025, Johnston et al 2017).
Early collapse, cardiovascular collapse, or hypotensive collapse have been reported following bites by brown snakes, tiger snakes (Notechis scutatus ssp.), rough- scale snakes (Tropidechis carinatus), and taipans (Oxyuranus scutellatus). 
It most often happens pre-hospital and immeditae life support is essential.

Non-clottable blood and bleeding

Clinically evident signs of a haemostatic defect may be absent. Nonetheless defibrin(ogen)ation may be present to such a degree that the blood is completely incoagulable.
Haemostatic defects are frequent and severe. Bleeding (gingival bleeding, epistaxis, haematemesis, haematuria, etc., haemorrhagic schock; intracranial) occurs in particular in Oxyuranus sp., Pseudonaja sp., Notechis scutatus ssp. envenoming.

Thrombotic microangiopathy (TMA)

Thrombotic microangiopathy occurs in about 15% of Australian snake envenoming cases and only from snakes that cause VICC and develops within 24 hours of the bite.

Descending paralysis / Respiratory failure

Descending paralysis in cluding respiratory failure occurs mainly in Acanthophis sp., Pseudechis papuanus, Oxyuranus sp. envenoming. Such paralysis does resolve spontaneously, but very slowly, such that long-term artificial respiration may be necessary. 

Muscle injury, rhabdomyolysis

Uncommon in Australian elapid envenoming, myotoxicity is, however, the main problem in black snake (Pseudechis porphyriacus and Pseudechis australis) and a significant part of tiger snake (Notechis scutatus ssp.) envenoming (Johnston and Isbister 2021).

Acute kidney injury (AKI)

In Australia elapid envenoming, AKI mostly occurs in the context of thrombotic microangiopathy and rhadomyolysis (Johnston et al. 2017a, Isbister and Berling 2025).
See 'Muscle injury, rhabdomyolysis' and 'Thrombotic microangiopathy (TMA)' above).

Monitoring for signs and symptoms that would indicate systemic envenoming for at least 12h. Laboratory parameters (INR, aPTT and CK) and neurological reassessments identify severe envenoming in almost all patients within 12 hours of the bite (Ireland et al. 2010, Isbister and Berling 2025).
See also 'Suggested clinical pathway for observation and blood testing of patients with suspected snake bite' (Ireland et al. 12010).

At least hourly

• state of consciousness,
• ptosis,
• heart rate and rhythm,
• blood pressure,
• respiratory rate,
• bleeding,
• local swelling,
• other newly appearing signs and symptoms.

6-hourly (or more frequently if there is cause for suspicion)

• 20WBCT (bedside test),
• labortaory-based clotting tests (see above),
• CK, GOT (AST),
• urine output.

The absence of signs of envenoming in the first hours after the bite does not exclude the possibility that a relevant injection of venom has taken place. There may be a long delay before systemic signs of envenoming develop. Moreover, the continued absorption of venom from the region around the site of the bite can lead to renewed symptoms of systemic envenoming even after successful administration of antivenom (e.g correction of the haemostatic defect).