A retrospective evaluation of Vipera palaestinae envenomation in 18 cats: (2006-2011)

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).

Retrospective study.

Veterinary teaching hospital.

Eighteen client-owned cats envenomed by Vp.

None.

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.

Cats are at least as susceptible as dogs to Vp envenomation. Lower body weight, rectal temperature, and hematocrit at presentation were associated with nonsurvival.