Presumptive Fluphenazine‐induced Hepatitis and Urticaria in a Horse

Abstract

4-year-old Standardbred gelding (450 kg) was examined because of depression, poor appetite, and suspected liver disease. Eight days before examination, the horse had won a race. The next day, depression, muscle stiffness, and transient pyrexia (39.0uC) were observed. The horse was treated with single doses of flunixin meglumine a (1 mg/kg IV), phenylbutazone b (0.2 mg/kg PO), methocarbamol c (4.4 mg/kg PO), Nacetylcysteine d (6.6 mg/kg PO), and 5 L lactated Ringer’s solution IV. A CBC and serum biochemical profile performed 4 days before presentation revealed neutrophilia and moderate increases in serum concentration of the hepatic enzyme activities (Table 1). Moderate urticaria (hives) was present over the trunk of the horse. On examination, the horse was quiet but alert and was in good body condition. Initial physical examination revealed mild jaundice and mild clinical dehydration. The heart rate (36 bpm), respiratory rate (12 bpm), and rectal temperature (37.6uC) were within normal reference limits. Multiple raised, edematous, nonpruritic nodules (3–5 mm diameter), consistent with urticaria were observed over the trunk and the neck. Auscultation and percussion of the thorax and the abdomen was unremarkable. Neurologic examination was unremarkable. This was the only horse of 19 on the farm affected. Thirty-three days before referral, the horse had been empirically administered a single dose of a long-acting parenteral preparation of fluphenazine decanoate e (0.28 mg/kg IM) as a tranquilizer to control anxious behavior. The gelding had daily access to 2 species of weeds, which were estimated to occupy approximately 20% of the turnout paddock area. No grass was available in the paddock because of overgrazing. Nineteen other horses shared the same turnout paddock and had the same management. All horses had access over a fence to lush grass, which had been sprayed with a surfactant-free glyphosphate product f the week the subject horse was administered fluphenazine. Serum biochemical profiles conducted on the herdmates, 2 days before examination, revealed serum activity of hepatic enzymes and concentration of total bilirubin within reference limits. No other horses in the barn had been administered fluphenazine decanoate. Vaccines administered to the horse included equine influenza, rhinopneumonitis, tetanus toxoid, and West Nile virus. The last dose of which had been administered approximately 8 weeks before referral. Clinicopathologic abnormalities were limited to hyperbilirubinemia, increased serum activity of hepatic enzymes (glutamate dehydrogenase [GLDH], aspartate aminotransferase [AST], gamma-glutamyl transferase [GGT], and alkaline phosphatase [AP]), and increased total bile acids concentration (Table 1). These findings were interpreted as indicative of impaired bile circulation and active hepatocellular damage. No changes compatible with an inflammatory process were identified. Plasma fibrinogen and blood ammonia concentrations were not determined at that time. Transabdominal ultrasound examination revealed normal hepatic architecture. A fecal bacterial culture for Salmonella spp. was negative. The initial therapy consisted of lactated Ringer’s solution (60 mL/kg/d IV), trimethoprim-sulfadioxine g (24 mg/kg IV q12h), and flunixin meglumine (1 mg/kg IV q24h). The diet was restricted to first-cut grass hay to avoid high dietary protein content. Taxonomic classification of the weed plant species reported by the owner revealed that the predominant plant was ‘‘redroot pigweed,’’ Amaranthus retroflexus (80% of weeds in paddock), and the other was ‘‘Lamb’s quarter,’’ Chenopodium album (20% of weeds in paddock). A. retroflexus has been associated with severe renal disease in cattle, 1 and C. album has been associated with nitrate toxicosis in cattle. 2 To the authors’