Snakebite Envenomation

Potential medical emergency secondary to bite and subsequent envenomation of an individual that present with either:

Most snakebites do not cause envenomation because either:

  • Insufficient venom is injected
  • The snake is non-venomous

Epidemiology and Risk Factors

Pathophysiology

Venoms are complex protein mixtures that act as toxins via one or more of these effects:

  • Neurotoxins
    Pre- and post-synaptic neuromuscular blockade
    • Post-synaptic blockade reversible with antivenom
    • Pre-synaptic blockade may not be reversible
  • Prothrombin activators
    • Leads to:
      • Consumptive coagulopathy
      • MAHA
      • Cardiovascular collapse
        Likely due to idiosyncratic pulmonary hypertension or PE.
    • Requires antivenom
  • Anticoagulants
    Prevents clotting without consumption.
  • Rhabdomyolysins
    • Direct muscle damage
    • AKI

Aetiology

Pathophysiology by Snake Species
Snake Neurotoxin Prothrombin Activation Anticoagulant Rhabdomyolysin
Brown snake Maybe Yes Maybe
Tiger snake Yes Yes Maybe
Taipan Yes Yes Maybe
Black Yes
Death Adder Yes
Rough-scaled snake Yes
Stephen’s Banded snake Yes
Sea snake Maybe Yes

Clinical Manifestations

Clinical Manifestations by Time Course
Time Since Envenomation <1 hour 1-3 hours >3 hours
General
  • Headache
  • Nausea
  • Vomiting
  • Confusion
  • Regional lymphadenitis
  • ↑ HR
  • ↓ BP
    May precipitate collapse.
  • Shock
Neurotoxin
  • Cranial nerve paresis
  • ↓ VT
  • Truncal paresis
  • Limb paresis
Prothrombin Activation
  • Coagulopathy on laboratory testing
  • Mucosal haemorrhage
  • Venepuncture site haemorrhage
  • DIC
Anticoagulant
  • Coagulopathy on laboratory testing
Rhabdomyolysin
  • Rhabdomyolysis
  • AKI

Features may progress much more rapidly in children.

Local features:

  • Local pain and swelling
  • Myonecrosis
  • Painful lymphadenopathy of draining nodes

Systemic features:

  • Haemodynamic instability
  • GI upset
  • Diaphoresis
  • Headache

Neurotoxicity classically progresses from smaller muscle groups to larger ones:

  • Extra-ocular muscles
  • Bulbar muscles
  • Respiratory muscles
  • Skeletal muscles

Investigations

Bedside:

Laboratory:

  • Venom detection kit
    Performed on blood, urine, or other tissue.
    • Highly sensitive
    • ~25 minutes to run
    • Very high venom concentration may cause a false negative
      Dilute sample and run again if that possiblity exists.

Imaging:

Other:

Diagnostic Approach and DDx

Identification of the snake is helpful but not essential:

  • Venom detection kit should be used to guide antivenom selection
  • Antivenom should be used to cover snakes in that geographical region

Management

  • Pressure-immobilisation bandage
  • Antivenom
  • Resuscitation as required

Resuscitation:

The pressure-immobilisation bandage is designed to ↓ lymphatic and capillary absorption. It is not an arterial tourniquet.

  • Pressure-immobilisation bandage
    • Crepe bandage applied from digits up the limb as far as possible, including the bite site
    • Further immobilisation applied to restrict joints on either side
    • ↓ Absorption by lymphatics by:
      • ↑ Hydrostatic pressure
      • ↓ Skeletal muscle pump
    • Should only be removed once antivenom administered
    • Should not be removed for sampling
      Cut a window over the bite site to sample.
    • Should be reapplied if the patient deteriorates
  • A
    • Intubation if required
  • B
    • Supplemental oxygen or mechanical ventilation as required
  • C
    • Fluid resuscitation as required

Specific therapy:

In general, the dose is two vials of polyvalent antivenom. Dosing is reasonably crude and based mostly on trials in small, cute animals.

  • Pharmacological
    • Antivenom
      • 2-3× dose should be given if critically unwell
      • Can be withheld if clinical situation is mild
      • High risk of immediate hypersensitivity (25%) including anaphylaxis (10%!)
      • Premedication with subcutaneous adrenaline is recommended:
        • 0.01mg/kg in children
        • 0.25mg in adults
      • Administer over 15-30 minutes if situation permits
      • Re-dosing is ineffective
    • Antibiotics
      Consider for contaminated wounds.
  • Procedural
  • Physical

Supportive care:

Antivenom will reverse anticoagulant effects, but not replace lost clotting factors.

  • D
    • Analgesia
      Particularly if rhabdomyolysis.
  • F
    • AKI prevention
      • Aim 1-2mL/kg/hr of urine output
    • Electrolyte derangement
      Rhabdomyolysis.
  • H
    • Coagulopathy treatment

Disposition:

  • Observe for at least 12 hours

Preventative:

Marginal and Ineffective Therapies

  • Heparin
    Not recommended in procoagulant coagulopathy (or for anything else).

Anaesthetic Considerations

Complications

  • Death
  • D
    • Persistent neurological sequelae:
      • Diplopia
      • Anosmia
    • PTSD
  • F
    • AKI
      May progress to CKD. Causes are multifactorial:
      • Pre-renal
        • Sepsis
        • Cardiac failure
        • Thrombotic microangiopathy
      • Intra-renal
        • ATN secondary to pre-renal failure
        • Myoglobinuria
        • Haemoglobinuria
      • Post-renal
        • Haematuria and obstruction

Prognosis

Death is:

  • Due to:
    • Respiratory paralysis
    • Cardiac arrest
    • AKI
    • Haemorrhage
  • Relatively rare:
    • Untreated ~2%
    • Treated ~0.1%

Poor prognostic signs:

  • Massive envenomation
  • Remote location
  • Out-of-hospital collapse
  • Inadequate antivenom therapy

Key Studies

References

  1. Bersten, A. D., & Handy, J. M. (2018). Oh’s Intensive Care Manual. Elsevier Gezondheidszorg.
  2. Isbister GK, Brown SGA, Page CB, McCoubrie DL, Greene SL, Buckley NA. Snakebite in Australia: a practical approach to diagnosis and treatment. Med J Aust. 2013;199(11). Accessed July 12, 2023.