Snakebite in Small Animals: Advice to Clinicians

Snake envenomation can look deceptively mild at first and then deteriorate quickly. This page distils our emergency and critical care team’s guidance into a rapid, practical reference. 

Outcomes are unpredictable; stable patients can crash, and severe cases can still recover - so the focus here is on early objective monitoring, airway protection where indicated, and clear triggers for transfer if intensive care is needed. 

VSOS provides 24/7 specialist oversight, ICU monitoring, invasive ventilation, and ambulance transfer from your Veterinary practice (including for anaesthetised patients). Use the checklist below to streamline decision-making, set owner expectations, and avoid delays that can cost patients their best window for a good outcome.

• If a bite is suspected but unconfirmed:
  • Coagulation tests (PT/aPTT).
  • CK (creatinine kinase).
  • Collect urine (>  2 h & < 12 h from bite) fora Snake Venom Detection Kit. A
    negative does not rule out envenomation?
  • If all negative - Monitor in hospital and reassess all test in 1 - 4 hrs

1. No clinical signs, but owner suspects possible snake bite.
2. Preparalytic signs witnessed by owner but appears stable now
3. Moderate clinical signs -Weakness, ataxia, reduced responsiveness, laboured breathing, nausea, pupil dilation, tachycardia, pain, mild cutaneous bruising.
4. Severe signs - Collapse, very poor responsiveness, discoloured urine, severe myalgia/tremoring, seizures, severe laboured breathing, hypercapnia, failing ventilation, hypoxia, severe bruising, petechiae, ecchymoses.

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• Venomous snakes in New South Wales are the Eastern Brown Snake, Tiger Snake, Red Bellied Black Snake and Death Adder.

• Multivalent Tiger/Brown antivenom is effective at neutralising Tiger, Brown and Red Bellied Black Snake venom.

• Death adder antivenoms are not routinely stocked local requires a specific antivenom from human hospitals.

• When to give:

  • Confirmed, witnessed envenomation or evolving coagulopathy/clinical signs supportive of snake envenomation.

  • If the bite is uncertain. Admit, observe and repeat PT/aPTT, CK and SVDK.

  • Mild/moderate signs - Give 1-2 vials and monitor for progression.

  • Severe signs - Given 2 vials straight away. May require 4-8 vials total depending on progression of signs.

• Cats - Not all cats receive antivenom by default; timing and presentation guide the decision. Cats have much higher resistance to envenomation than dogs and so can survive without antivenom (~ 50 - 70% survival).

• Coagulopathy/bleeding: skin, cavities, lungs.
• Renal risk: track creatinine and its trend (AKI concern, particularly with browns).
• Respiratory failure: some cases require ventilatory support.
• Prognosis messaging: unpredictable, stable can crash; severe can recover. Set expectations early.

Eastern Brown Snake (Pseudonaja spp.)

Major toxin effects: potent procoagulant (VICC), neurotoxin (progressive paralysis), cardiovascular collapse. 

Common clinical signs:

• Sudden collapse, often with a “collapse ? apparent recovery ? deterioration” pattern
• Weakness, ataxia, hindlimb wobbliness
• Tachycardia initially; may later become bradycardic pre-arrest
• Vomiting, salivation, restlessness
• Coagulopathy: bleeding from venepuncture sites, mucosal bleeding (though less commonly than RBBS)
• Dilated pupils, reduced menace
• Respiratory difficulty, progressing to respiratory failure
• Death can occur rapidly (as little as 30-60 min in severe cases without treatment)

Tiger Snake (Notechis spp.)

Major toxin effects: potent presynaptic neurotoxin (LMN flaccid paralysis), procoagulant venom (VICC), myotoxin (rhabdomyolysis)

Common clinical signs:

• Flaccid paralysis, starting with hindlimbs and moving forward
• Dilated, unresponsive pupils (early and prominent)
• Difficulty swallowing, drooling, regurgitation
• Voice change, weak or altered bark
• Coagulopathy: prolonged clotting times, bleeding tendency
• Muscle tremors, fasciculations
• Dark urine (myoglobin)
• Respiratory paralysis is the usual cause of death if untreated
• Often more neurotoxic signs than RBBS, and more bleeding compared with brown snake in dogs

Red-Bellied Black Snake (Pseudechis porphyriacus) 

Major toxin effects: myotoxin (rhabdomyolysis), anticoagulant (bleeding), haemolysin (haemolysis

Common clinical signs:

• Local swelling atbite site (more common than in brown snake bites)
• Dark red or brown urine (myoglobinuria from muscle breakdown)
• Vomiting, hypersalivation
• Weakness, hindlimb ataxia (less sudden collapse than brown snakes)
• Muscle pain, stiffness
• Coagulopathy, though usually milder than brown and tiger snakes
• Acute kidney injury secondary to myotoxicity
• Respiratory compromise in severe cases
• Dogs often survive longer before collapse than with brown snake envenomation

Death Adder (Acanthophis spp.)

Major toxin effects: extremely potent postsynaptic neurotoxin (LMN paralysis).

Common clinical signs:

• Rapid-onset LMN flaccid paralysis
• Marked cranial nerve signs:
  • dilated pupils
  • absent menace
  • decreased gag reflex
  • drooling
• Weakness - recumbency - complete paralysis
• Minimal or no bleeding disorders
• No major myolysis (urine usually not discoloured)
• Respiratory failure due to paralysis (primary cause of death)

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• Explain the unpredictable course & importance of early antivenom therapy.
• Discuss need for serial coagulation tests, possible antivenom, and monitoring for bleeding, AKI, and respiratory compromise.
• Prepare for potential ICU-level care and, in some cases, ventilation.
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• Evidence of respiratory compromise, creatinine/AKI, progressive coagulopathy
• Unclear antivenom strategy/availability
• Anticipated need for continuos ICU monitoring, blood transfusions or mechanical ventilation