Snake bite envenomation
Snake-bite envenomation is a relatively common event in cats, often associated with high outdoor activities. Although the clinical presentation may vary depending on the species of snake and the amount of toxin absorbed, cats often present with lethargy, vomiting, and profound mental depression. Cats are considered more resistant to envenomation compared with dogs or humans and may respond to conservative treatment alone. In one study in Australia, ninety-one percent of cats survived following the administration of antivenom whereas 66% of cats survived without antivenom.
Brown snake venom consists of procoagulants, pre and post synaptic neurotoxins, haemolysins, myotoxins and cytotoxins resulting in a wide range of clinical signs in envenomated patients. Venom-induced pathological changes are primarily the result of thrombi(clot) formation in peripheral and central circulature. Venom-induced changes can be observed in the lungs, kidneys and muscle tissue. Coral snake venom is primarily neurotoxic with little local tissue reaction or pain at the bite site. The net effect of the neurotoxins is a curare like syndrome. Clinical signs are related to marked hemolysis with severe anemia and hemoglobinuria. Pit Viper snakes cause systemic clinical manifestations encompassing a wide variety of problems including pain, weakness, dizziness, nausea, severe hypotension, and thrombocytopenia. Rattlesnake envenomation often affects the cat forelimbs, resulting in paresis.
Onset of clinical signs vary from one to sixty minutes post-bite. Feline patients should be observed closely over a period of 24 hrs. Cats often initially show a weakness and ataxia. Other signs often inconsistent or transient include intermittent weak struggling, lethargy, tachypnoea, dyspnoea, haematuria, plaintive vocalisation, absent pupillary light reflex, disorientation, mydriasis, posterior paresis, generalised paresis, ataxia, salivation, bleeding from bite site and or coma. Often tail movement is retained despite the cat being paralysed.
Diagnosis can be made on visualising the snake bite or use of a commercial snake venom detection kit. Accuracy of these tests are usually > 95% although vlood samples should be taken within 12 hours post-envenomation after which urine samples may be more sensitive.
Treatment regimes consist of supportive IV fluids, corticosteroids and if available, antivenom. The antivenom should be gently warmed to room temperature, diluted up to 1 in 10 in 0.9% saline or Hartmans and administered SLOWLY over 20-30 minutes by the IV route. An appropriate dose of adrenaline (0.1mL of 1:1000) should be given intravenously in cases of serum reaction in cats.
With rattlesnake envenomation, mortality rates are around 15%.
The only definitive treatment for coral snake envenomation is the administration of antivenin (M. fulvius).
- ↑ Michal MT & Eran L (1999) Suspected Vipera palaestinae envenomation in three cats. Vet Hum Toxicol 41(3):145-148
- ↑ Mirtschin PJ et al (1998) Snake bites recorded by veterinary practices in Australia. Aust Vet J 76(3):195-198
- ↑ Jacoby-Alner TE et al (2011) Histopathological analysis and in situ localisation of Australian tiger snake venom in two clinically envenomed domestic animals. Toxicon Jul 29
- ↑ Peterson ME (2006) Snake bite: coral snakes. Clin Tech Small Anim Pract 21(4):183-186
- ↑ Peterson ME (2006) Snake bite: pit vipers. Clin Tech Small Anim Pract 21(4):174-182
- ↑ Ong RK et al (2010) Prospective determination of the specificity of a commercial snake venom detection kit in urine samples from dogs and cats. Aust Vet J 88(6):222-224
- ↑ Moisidis AV et al (1996) Snake envenomation in cats and its detection by rapid immunoassay. Aust Vet J 74(2):143-147
- ↑ Australian Veterinary Serum Laboratory
- ↑ Julius TM et al (2012) Retrospective evaluation of neurotoxic rattlesnake envenomation in dogs and cats: 34 cases (2005-2010). Journal of veterinary emergency and critical care 22:460-469