Elapid snake envenomation Flashcards
(5 cards)
What are the venom components and their activity
Enzymes acting on the coagulation pathway
- can have either procoagulant or anticoagulant activity
Phospholipases A2 enzymes
- hemotoxic
- myotoxic
- neurotoxic
- oedematogenic, hypotensive, cytotoxic
Neurotoxins
- alpha-neurotoxins bind to post-synaptic nicotinic Ach receptors causing flaccid paralysis associated with some elapid envenomation
- beta-neurotoxins have phospholipase A2 activity and cause pre-synaptic depletion of synaptic vesicles after initially increasing miniature end-plate potentials
What are the clinical signs of envenomation in cats
The predominant activity of venom (i.e., neurotoxicity, myotoxicity, coagulopathy) will depend on the species of snake, season, diet and geographical location
Common clinical signs:
- flaccid paralysis, weakness
- mydriasis, decreased PLR
- tachypnoea and dyspnoea
What is the main differential for elapid snake envenomation
The clinical signs can look like those of tick paralysis
- both result in lower motor neuron signs
However, paresis and paralysis is generally slower in onset in cases of tick paralysis, tacking 2 or more days to result in recumbency
Tick paralysis is also not associated with coagulopathy, hemolysis, pigmenturia or marked elevations in CK
What are the clinical pathology findings in snake envenomation
Hemoglobinuria, hematuria, myoglobinuria
Increased serum CK activity
- in cats, the CK level is often normal at admission, increasing over 24-48h to 100000 IU/L or higher
- a six-figure CK result in the absence of obvious trauma or severe hypokalemia is virtually diagnostic for tiger snake envenomation
Clotting times may be normal or prolonged
- prolonged clotting times are a common feature of elapid snake envenomation but have different pathophysiology
What is the goal of antivenom treatment
Antivenom does not reverse the clinical effects of venom
- it acts to prevent unbound circulating venom binding to target proteins and worsening any clinical effect
