Signalment: A ten years old castrated male cat arrived in the intensive care unit after sedation with dexmedetomidine and methadone for diagnostic procedures.

History and main clinical examination findings: The cat had a history of polydipsia and slow recovery after an oncologic surgery done 10 days before. Pre-anaesthetic evaluation and blood exams were normal. At the end of anaesthesia the cat was hospitalized in order to receive fluid therapy and stay in observation. One hour after the extubation the cat was still very lethargic even though atipamezole was administrated at the end of the procedure.

Diagnostic investigations: Heart rate and blood pressure were within the physiological ranges, only the temperature was still low (36°C). After 30 minutes the cat was still very depressed and a venous blood gas analysis was performed to evaluate PCO2and glucose. The results showed a light respiratory acidosis with 7.29 of pH and 56 mm Hg of PCO2, a severe hyperkalaemia (7.9 mEq/L) and hyperglycaemia (279 mg/dL), whereas all the other parameters resulted within the normal ranges.

Therapy: ECG was immediately performed and a widening of the QRS complex was revealed, with normal P waves. A bolus of furosemide 1 mg/kg was administered and blood and urine samples were taken for haematobiochemical exams. Bladder catheterization was done to evaluate urine production. A blood gas exam, repeated after 30 minutes, showed the reduction of the hyperkalaemia to 6.6 mEq/L, the ECG was normal, the temperature was 37.6°C and the cat was responsive. After 3 hours the plasma level of potassium was normalized. The results of the heamatobiochemical exams did not show any alteration with the exception of hyperglycaemia, which resulted normal on the day after.

Discussion: The causes of hyperkalaemia are renal disease, cell death from reperfusion injury, Addison disease, dehydration, diabetes and potassium supplement. All these causes were excluded for this cat. Hyperkalaemia associated to hyperglycaemia is a fatal event reported in big felines after the use of alfa-2-agonists. The mechanism is still unclear and seems related to the inhibition of the release of insulin by the alfa-2-agonist. The cat recovered uneventfully with a symptomatic therapy.