Use of Ketamine for the Management of Refractory Status Epilepticus in a Dog

Abstract

A n 8-year-old, intact male Yorkshire terrier weighing 2.8 kg was presented with a history of recurrent, tonic-clonic seizures. Seizure episodes began 4 weeks before presentation, occurred 1–2 times a day and lasted 20 seconds to 2 minutes. CBC, biochemistry, and bile acid determinations were normal, and the animal had been treated with phenobarbital a (5.4 mg/kg PO q12h) and diazepam b (0.5 mg/kg rectally after each seizure). The frequency and duration of convulsions had gradually increased despite therapy and, on the 3 days before presentation, the dog was having 4–6 seizures daily, lasting between 1 and 4 minutes with postictal phases of lethargy and ataxia lasting up to 30 minutes after each event. There were no apparent preictal signs. Five days before presentation, the referring veterinarian reported the dog had developed horizontal nystagmus with fast phase toward the left, ataxia in all 4 limbs with normal spinal reflexes, abnormal conscious propriocep-tion in all 4 limbs, circling to the left, and head pressing. The dog also had been urinating and defecating in the house and appeared to have problems recognizing familiar people. The neuroanatomic localization there-fore was multifocal but included the central vestibular system and forebrain. The dog was presented after a generalized tonic-clonic seizure of 30 minutes duration, despite administration of 2 doses of 0.5 mg/kg diazepam rectally in a period of 15 minutes. Initial assessment identified seizures with generalized tonic-clonic muscular activity, a patent airway, in-creased salivary secretions in the mouth and pharynx, spontaneous breathing, and a heart beat with peripheral pulses. There were congested mucous membranes, a short capillary refill time, tall and narrow pulses, tachycardia (190 beats per minute), and no murmurs or other abnormal cardiac sounds. Respiratory assessment indicated tachypnea (40 breaths per minute), but respiratory effort was difficult to assess due to ongoing involuntary muscular contractions, and increased in-spiratory noises were attributed to secretions in the mouth and upper airways. Lung sounds were normal. Abdominal palpation was unremarkable, but there were cyclic fast contractions of the abdominal wall (2–3 contractions per second). Rectal temperature was 40.6uC (105uF), and Doppler systolic blood pressure was 180 mm Hg. Intranasal diazepam (0.5 mg/kg) reduced motor activity sufficiently to establish vascular access and obtain blood for CBC, biochemistry, blood ammonia concentration, and serum phenobarbital concentration. Initial laboratory results indicated acidemia (venous pH 7.332; normal range, 7.360–7.440), metabolic acidosis (base excess 28 mEq/L; normal range, 23–+2), hyper-lactatemia (64.8 mg/dL [7.2 mmol/L]; normal range, 5.4–22.5 [0.6–2.5]) and hypoglycemia (40 mg/dL [2.2 mmol/L]; normal range, 70–110 [3.3–6.1]). The CBC was normal. An IV bolus of 0.5 g/kg glucose was administered over 5 minutes. Maintenance fluid therapy was started using a crystalloid c supplemented with 2.5% dextrose. IV thiamine d (100 mg) was given also. Seizure activity recurred 15 minutes later and diazepam was given again (0.5 mg/kg IV) followed by a continuous rate infusion (0.25 mg/kg/h, increasing to 0.5 mg/kg/h), which failed to eliminate all muscular activity. Propofol e