No abstract

Case summary A 2-year-old castrated male domestic shorthair cat was presented for evaluation of acute and progressive neurologic signs 2–4 h after exposure to baclofen. The suspected ingested dose was 2.1 mg/kg. On admission, the cat was tetraplegic with stuporous mentation, and venous blood gas analysis showed mild hypercapnia (PvCO2 43.4 mmHg) raising concern for hypoventilation. Owing to the acute nature of the ingestion, severity of the clinical signs and reported history of chronic kidney disease, hemodialysis was recommended to remove the toxin. A 5 h hemodialysis session was performed using an intermittent platform without hemoperfusion. At the beginning of hemodialysis, worsening hypoventilation and hypercapnia (PvCO2 88.6 mmHg) required endotracheal intubation and manual ventilation initially, followed by mechanical ventilation. At the end of the dialysis session, the cat was breathing spontaneously and disconnected from the ventilator. The cat was ambulatory and alert 1 h after the end of dialysis. After an additional 12 h of monitoring, the cat had full return of neurologic function and was discharged from hospital. Serum baclofen concentration measured prior to, during and after hemodialysis showed a 77.7% reduction in baclofen levels immediately after hemodialysis. Relevance and novel information This is the first report of baclofen toxicity in a cat successfully treated with hemodialysis and mechanical ventilation simultaneously. Treatment with hemodialysis therapy and mechanical ventilation could be considered in cases of acute baclofen toxicosis to improve outcome and reduce the length of the hospital stay.

Manganese is a common component of human joint supplements and may be a source of ingestion and subsequent toxicosis in dogs. Although hepatotoxicity secondary to manganese toxicosis has been reported in dogs before, no descriptions of successful management of manganese toxicosis has been reported in veterinary literature. A 5 yr old spayed female Shetland sheepdog and a 5 yr old female Shetland sheepdog were evaluated following accidental ingestion of a joint supplement. Consultation with a toxicologist revealed concern for manganese toxicosis resulting in hepatic injury. Both dogs developed subsequent acute liver injury, despite decontamination and initial management with N-acetylcysteine and cholestyramine. The patients were managed with calcium ethylenediaminetetraacetic acid, paraaminosalicylic acid, allopurinol, Vitamin E, ginkgo biloba, and S-adenosylmethionine/silybin. Liver values returned to normal in both dogs. Manganese exposure was confirmed with urine manganese analysis in one dog and fecal examination in the other dog. A previous case report detailed the fatal manganese toxicosis in a dog; this case report describes the successful management of severe acute hepatic injury secondary to manganese toxicosis. The combination of medications used above may be used for successful treatment of manganese toxicosis in dogs.