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 25-28 September, 2018 | Singapore
included hypertriglyceridaemia, mild hyperglycaemia, hyperbilirubinaemia, hyperglobulinaemia and hypocholesterolaemia 4.
Reported complications of Viper envenomation in dogs include bacterial infections (clostridial or other), local necrosis, upper respiratory airway obstruction due
to laryngeal edema, acute renal failure, coagulation disorders namely venom-induced consumptive coagulopathy (VICC) and death 3. For dogs with Vp envenomation, the reported mortality rate in the literature is relatively low (3.7-6%) 3,4.
Venom-induced hemostatic abnormalities, potentially culminating in venom-induced consumptive coagulopathy (VICC), include thrombin inhibition and activation, increased fibrinolysis, hypofibrinogenemia, release of kinins, endothelial damage, and platelet aggregation, destruction and dysfunction. Viper- envenomed dogs commonly develop VICC, its frequency increasing over time during hospitalization. Although VICC is similar to DIC in many ways, it differs from
the former by a rapid onset and resolution, different mechanism of initiation and it is not usually resulting
in end-organ effects. Venom-induced hemostatic abnormalities, potentially culminating in venom-induced consumptive coagulopathy (VICC), include thrombin inhibition, increased fibrinolysis, hypofibrinogenemia, release of kinins, endothelial damage, and platelet aggregation, destruction and dysfunction.
Cats are considered more resistant to snakebites than other animals9. However several studies published in the last decade have shown that mortality rate cats varied between 6-22%. Although bleedings are not so common in cats, haemostatic abnormalities were reported in all cats expressed by elongated aPTT in 100% and PT in 93% of the cats. Several RF were identified including; lower rectal temperature (P=0.02, 35.90 C vs. 38.00 C), lower haematocrit (29 vs. 44%, P<0.001) upon admission and lower haematocrit 24 hrs post admission (22 vs. 33%, P=0.001). In our emergency department we see 2-6 cases of cat’s snakebites a year, as compared to 30-40 cases of dogs with snakebite. The discrepancy between dogs and cats for the limited cases might be the caution and the ability of cats to cope with snakes, cats are not referred to medical treatment since they do not show clinical signs nor are outdoor cats. Based on our limited experience, the diagnosis of cats with snake bites is not as obvious as in dogs. As the time lag from the snakebite to admission in cats is usually longer than in dogs, the most common clinical signs are local swelling with severe hematoma, which might develop over the 24-48 h post snakebite, depression and shock. Hematological findings are hemoconcentration, thrombocytopenia, hypoproteinemia, hemolysis and consequent anemia, and the appearance of peripheral nucleated red blood cells. Disseminated intravascular coagulation also is
a common complication in cats with snakebites with dramatic elongation of the PT and aPTT but relatively slight clinical signs that are characteristic to DIC in other species.
The clinical outcome following envenomation,
however, is highly variable, partly depending on its anatomical location and the amount of venom delivered. Accordingly, clinical signs may remain local in up to 49% of human cases, limited to pain, hemorrhage, edema and regional lymphadenopathy, while in other cases in humans and dogs, systemic clinical signs may ensue, including shock, cardiac arrhythmias and bleeding. The reported mortality rate in humans is low, ranging from 0.5% to 2%, whereas in dogs it may reach 15%. Different VP-specific antivenin treatment protocols, the result of lower availability and financial constraints in veterinary medicine, may partly account for the discrepancy. Retrospective studies of VP envenomations in humans, unlike studies in dogs, espouse the use of specific antivenin to improve outcome, although robust evidence is lacking.
Different treatment regimes are used for VP envenomation in different (human or veterinary) institutions. These include antibiotics, antihistamines, steroids and specific antivenin 10. Dosing and timing are controversial, and may vary in different medical institutions. The Hebrew University Veterinary Treating Hospital (HUVTH) treatment protocol includes:
1. Fluid therapy
- Crystalloids- 10-20 mL/kg as a bolus.
- Colloids / Fresh frozen plasma when DIC is suspected or when total solids (TS) are low (below 4 g/dL), as needed.
2. Antimicrobial therapy (ampiciline 25 mg/kg
q8h for 5 days) to prevent clostridial or other infection that may have been transferred by the snake’s teeth.
3. Antihistamine - Diphenhydramine (2 mg/kg q8h for 24 h), only after hypersensitivity skin test for the antivenom has been completed.
4. Steroids - The use of glucocorticosteroids in snakebites has always been controversial. They are used in cases of shock and severe edema, particularly when in the larynx area, as they may minimize and/or prevent further endothelial damage. However, steroids may slow and dimin- ish antivenom activity and increase the risk for bacterial infection. Some clinicians believe that the use of steroids is contraindicated in snake- bites 10. In a retrospective study of 327 dogs with snakebite it has been shown that glucocorticoid
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43RD WORLD SMALL ANIMAL VETERINARY ASSOCIATION CONGRESS AND 9TH FASAVA CONGRESS














































































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