Objective: To describe the clinical signs, clinicopathologic abnormalities, treatment, complications and outcome, and to identify risk factors for death in cats envenomed by Vipera palaestinae (Vp).
Design: Retrospective study.
Setting: Veterinary teaching hospital.
Animals: Eighteen client-owned cats envenomed by Vp.
Interventions: None.
Measurements and main results: All envenomations occurred during the hot season (May to October), mostly in young (<4 years, 66%) domestic shorthair, outdoor or indoor-outdoor cats. Clinical signs included tachypnea (>40/min, 100%), lameness (78%), depression (71%), fang penetration marks (55%), hypothermia (<37.5°C, 43%), hematoma at the envenomation site (27%), tachycardia (>220/min, 20%), and bradycardia (<140/min, 20%). Hematologic abnormalities included thrombocytopenia (89%), hemoconcentration (33%), and leukocytosis (33%). The activated partial thromboplastin and prothrombin times were prolonged in 100% and in 93% of the cats at presentation to a veterinarian, and remained prolonged 12-24 hours later in 92% and in 77% of the cats, respectively. Cats displayed increased serum creatine kinase activity (100%) and hyperglycemia (89%). Four cats (22%) did not survive. Median hospitalization time was 2 days. Variables associated with death included lower body weight (P = 0.01), lower initial rectal temperature (P = 0.02), lower initial hematocrit (P < 0.001) and 12-24 hours later (P = 0.001), and lower total plasma protein at 12-24 hours following presentation (P = 0.001). There was no association between death and administration of antivenom (10 mL/cat), fresh frozen plasma, or corticosteroids.
Conclusions: Cats are at least as susceptible as dogs to Vp envenomation. Lower body weight, rectal temperature, and hematocrit at presentation were associated with nonsurvival.
Keywords: antivenom; coagulation; feline; snakebite; viper.
© Veterinary Emergency and Critical Care Society 2014.