Clinical Management

Caution: do not attempt to capture snakes if you are not trained to do so!

Consult

• Which snake species are present in the country where the snake bite took place?

• How does the clinical picture of snakebite envenoming develop? Comparative observations of the various species responsible in the region.

Detailed biological and clinical information on the main culprits in the region

• Acanthophis sp.
• Hoplocephalus sp.
• Notechis scutatus ssp.
• Oxyuranus sp.
• Pseudechis sp.
• Pseudonaja sp.
• Tropidechis carinatus

Comment

Unfortunatelly, tight (arterial) tourniquets are still being applied. They must not be recommended for general use. 

If a pressure bandage but, also, tight (arterial) tourniquets have been applied, 

• they should not be removed until systemic envenoming has been excluded (Ireland et al. 2010, Isbister and Berling 2025)
  or
• after completion of antivenom administration in patients with systemic envenoming (Isbister etal. 2025),
• with gradual removal of a tourniquet to avoid sudden venom influx and respiratory arrest (Pelle et al. 2022).

• Adverse outcomes have been observed in patients with tight pressure bandages left in place for many hours (Little 2023).
• All patients must be observed after removal of the bandage.

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,

Autopharmacological effects

• Chest X-ray
• cCT

Haematological effects

• Hb, Hct
• Clotting time
• PT/aPTT
• TT
• Fibrinogen
• FSP
• D-dimers
• Platelets

• blood film with 24 hours of the bite (schistocytes > 1% is diagnostic of microangiopathic haemolytic anaemia)
• Free haemoglobin in the plasma and urine
• Haptoglobin

• Blood group/blood sample for cross-matching

Neurological effects

• Blood gas analysis
• Forced expiration test (peak expiratory flow)

Muscular effects

• Myoglobin in the serum/urine,
• Serum creatinine kinase (CK, CPK)
• GOT (AST)
• Serum potassium
• serum phosphate
• serum calcium

Cardiac effects

• Blood pressure, pulse
• ECG

Renal effects

• Urine output (balance, hourly)
• Serum creatinine
• Serum potassium
• Serum bicarbonate.

Identification of the culprit

• Snake venom detection kit (SVDK): no longer recommended for the management of snakebite in Australia (Toxicology and toxinology 2020).

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). 

Symptomatic emergency medical treatment and antivenom treatment are complementary strategies.

Antivenom must be secured as early as possible while emergency medical teratment is running.

The aim of symptomatic emergency medical treatment is the rapid correction of critical parameters (fluid balance, blood pressure, oxygenation etc.) and the maintenance of vital functions (respiratory, cardiovascular).

Symptomatic measures help bridge the gap until specific treatment (antivenom) can be administered and starts being effective. If no antivenom is available or if the required effect is not achieved with antivenom, the goal is to employ symptomatic measures until such time as the venom naturally starts losing its activity.

The aim of antivenom treatment is neutralisation of the venom. The success of antivenom treatment depends on the quality of the antivenom, the specific properties of those venom components relevant to envenoming and the time point at which antivenom is administered (neurotoxic envenoming).

See 'Flowchart of the management of snakebite' (reproduced in Isbister and Berling 2025 with permission from Snakebite. In: Therapeutic Guidelines, Melbourne 2020).

Systemic Envenoming

"1. Haemostatic abnormalities: spontaneous systemic bleeding (including evidence of internal haemorrhage – ante-partum, intracranial, gastrointestinal etc.), incoagulable blood (20WBCT) or prolonged clotting time, elevated FDP or D-dimer, thrombocytopenia.

2. Cardiovascular abnormalities: hypotension, shock, cardiac arrhythmia, reduced ejection fraction (echocardiogram).

3. Neurotoxicity (paralysis, fasciculations).

4. Black urine indicating generalized rhabdomyolysis or intravascular haemolysis.

5. In patients with definite signs of local envenoming, the following confirm systemic envenoming: neutrophil leucocytosis, elevated serum enzymes such as creatine kinase and aminotransferases, haemoconcentration, uraemia, hypercreatininaemia, oliguria, hypoxaemia and acidosis.

Severe Local Envenoming. 

In the absence of 1–5 above, the development at any stage of rapidly spreading local swelling that involves more than half the bitten limb within 48 hours of the bite, or extensive blistering or bruising, especially in patients showing the abnormalities listed above under (5) and in patients bitten by species known to cause local necrosis. (...)"

(Warrell 2023).

"Early administration of antivenom should be considered  if the patient has either of

• an early cardiovascular collapse (e.g. hypotension, cardiac arrest or seizure)
• nonspecific systemic symptoms (e.g. vomiting, hedache or abdominal pain)

as antivenom is effective in preventing neurotoxicity and myotoxicity when given within 3 hours of the bite for most snakes." 

(Isbister and Berling 2025, citing Johnston et al. 2013, 2017b, Churchman et al. 2010, Snakebite. In: Therapeutic Guidelines, Melbourne 2020)

If the selected antivenom is not effective, 3 possible causes need to be considered

1. correct identification of the cause, but insufficient dose administered;
2. correct identification of the cause, but inadequate efficacy of the antivenom;
3. incorrect identification of the cause → revision of identification.

See Antivenom treatment.

Isbister and Berling (2025)

Snakebite. In: Therapeutic Guidelines, Melbourne 2020

Assessment of success, indication for continued antivenom treatment of antivenom and complications

See 'Flowchart of the management of snakebite' (reproduced in Isbister and Berling 2025 with permission from Snakebite. In: Therapeutic Guidelines, Melbourne 2020):
Repeat blood tests at 6 hours and 12 hours after giving antivenom, then every 24 hours until effects have resolved.*

*Coagulopathy may not begin to improve until 12 hours after the snake bite.

Repeat clinical examination (as above).

Complications

See Antivenom treatment

Isbister and Berling (2025)

Snakebite. In: Therapeutic Guidelines, Melbourne 2020

Comprehensive ABCDE approach
ICRC Basic Emergency Care: approach to the acutely ill and injured (SAMPLE and ABCDE approach: first module)

The guidance provided addresses major genus- or species-specific specific snakebite envenoming problems.

• Clinical entries: Australian elapids
• Clinical entries: Micropechis ikaheca
• Isbister and Berling (2025)
• Snakebite. In: Therapeutic Guidelines, Melbourne 2020
• Guidelines for the Management of Snakebites, WHO Regional Office SE Asia (Australasian Elapids)

Coagulopathy

• The haemostatic defects caused by Australian elapids are primarily a consequence of prothrombin activation, which leads to defibrin(ogen)ation with reactive fibrinolysis. Thrombocytopaenia occurs with variable frequency and severity.

• • INR is high or unrecordable and aPTT is prolonged.
  • Fibrinogen level is low or undetectable and D-dimer level is 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.

Bleeding

• Bleeding (gingival bleeding, epistaxis, haematemesis, haematuria, etc., haemorrhagic schock; intracranial) occurs in particular in Oxyuranus sp., Pseudonaja sp., Notechis sp. envenoming.

• There is a threat of spontaneous haemorrhage with extensive loss of blood or focal bleeding (e.g. intracranial) as long as the haemostatic defect exists. The risk is even greater if a patient does not receive appropriate treatment at a hospital and is then exposed to trauma, even very minor trauma.

• Loss of large volumes of blood can occur due to blood oozing from the bite wound or from injuries or due to medical or paramedical intervention.

Replacement therapy

Replacement of clotting factors and platelets following antivenom administration to bridge the gap until the antivenom starts being effective, insofar as evident bleeding or the imminent threat of critical bleeding makes this necessary. Also in cases where antivenom is not available or is ineffective and bleeding or the risk of bleeding makes intervention necessary (Warrell 1990b). In all other cases administration of effective antivenom should be a sufficiently effective and quick means of correcting the haemostatic defect. However, it is important to note that replacement of clotting factors and platelets is only effective in the short-term while circulating haemostatically active venom components are still present. Recurrence of venom-induced coagulation abnormalities are an important problem.

• Patients with VICC require blood film with 24 hours of the bite (schistocytes > 1% is diagnostic of microangiopathic haemolytic anaemia); serial creatinine.
• There is limited evidence that antivenom prevents TMA.

• Descending flaccid paralysis classically first involves the eye muscles (ptosis, diplopia and blurred vision), followed by bulbar muscles, respiratory muscle paralysis and limb paralysis.
• Once paralysis is established, it responds only slightly or not at all to antivenom administration. 
• The venoms of Acanthophis sp., Pseudechis papuanus, Oxyuranus sp. contain such venom components. Such paralysis does resolve spontaneously, but very slowly, such that long-term artificial respiration may be necessary. Early administration of antivenom is crucial.
• Antivenom given within 3 to 4 hours after the bite can prevent neurotoxicity. Once generaized paralysis has devloped, recovery may take up to weeks (Johnston et al.2017b, Lalloo et al. 1995).

• Myotoxicity is defined as
  • Local or generalised myalgia and/or muscle tenderness
  • CK level is usually normal (within the laboratory’s reference interval) on admission and rapidly rises over 24–48 hours (peak ranges from 1000U/L in mild cases to >100000U/L in severe cases)
  • Potassium level may also be elevated (>5.0mmol/L) in severe cases, and renal impairment may develop”
    (Isbister et al. 2013)
• Rhabdomyolysis leads to acute kidney injury (AKI). Hyperkalaemia and hypercalcaemia are, however, the more important  determinats of severe complications. 
• The onset of abnormal CK values is, however, delayed (median time to recording the first abnormal CK activity level 11 hours; 34 hours to the peak level) conpared to clinical signs of muscle injury (local or generalised myalgia and/or muscle tenderness) (Johnston and Isbister 2021).
• The delayed increase of CK limits the usefulness of CK to trigger antivenom application since myotoxicity seems to be prevented if antivenom is given 3 hours after the bite in mulga snake envenoming and 6 hours after the bite in red-bellied black snake evnenoming  (Johnston et al. 2013; Isbister et al. 2024).
• Rhabdomyolysis-induced muscle weakness must be differentiated from neurotoxin-induced paralysis.
• Non-envenomned patients may present with elevated CK values, e.g. due to physical activity. Early presentation of elevated CK values which decrease again points towards other causes since myotoxicity-associated elevated CK activity comes in much later (see above) and continues to increase.
• Snake species most commonly associated with myotoxicity are Notechis scutatus ssp., Pseudechis porphyriacus and Pseudechis australis (Johnston and Isbister 2021).

"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).
See 'Muscle injury, rhabodomyolysis' and 'Thrombotic microangiopathy (TMA)' above.

As Australian elapid bites generally do not cause any marked local symptoms of envenoming (exception: Pseudechis sp., Tropidechis carinatus), local complications are extremely uncommon.