A 13-year-old intact male mixed-breed dog with a left-sided adrenal gland mass presented for an anesthetized computed tomography scan to aid with surgical planning. The dog had previously undergone transvenous implantation of a single-chamber, right-sided permanent pacemaker placed for treatment of a high-grade second-degree atrioventricular block. The pacemaker mode was changed from variable rate response (ventricular pacing, ventricular sensing, inhibited response, and rate modulation) to fixed demand (ventricular pacing, ventricular sensing, and inhibited response) in preparation for anesthesia, and the rate was set to 95 beats minute[-1]. The dog was premedicated with intravenous (IV) butorphanol tartrate (0.3 mg kg[-1]) and anesthesia was induced with propofol (1.25 mg kg[-1], IV) and midazolam (0.3 mg kg[-1], IV). Anesthesia was maintained with isoflurane delivered in oxygen. Following induction of anesthesia, there was a decrease in the mean arterial blood pressure from 108 mmHg to 45 mmHg, which was effectively treated with a bolus of lactated Ringer's solution (5 mL kg[-1], IV) and infusions of dopamine (12 μg kg[-1] minute[-1]) and norepinephrine (0.1 μg kg[-1] minute[-1]). After starting dopamine and norepinephrine infusions, mean arterial blood pressure increased to 80 mmHg, and the ventricular rate decreased to 60 beats minute[-1]. Interrogation of the pacemaker revealed a change in T-wave morphology, which resulted in T-wave oversensing. Decreasing the lead sensitivity of the pacemaker corrected oversensing and restored the paced ventricular rate to 95 beats minute[-1].

Amantadine is an N-methyl-D-aspartate receptor antagonist commonly used as part of multimodal analgesia in dogs with chronic pain. Although adverse effects are not well documented in veterinary medicine, hypoglycaemia has been reported in humans following amantadine use. This case report highlights a 14.5-year-old female Labrador Retriever referred for investigation of episodic weakness associated with documented hypoglycaemia. The dog was being administered gabapentin, paracetamol, and amantadine for chronic lumbosacral pain. Initial diagnostic investigation, including haematology, biochemistry, and adrenocorticotropic hormone stimulation test, did not identify an underlying cause of hypoglycaemia. Continuous glucose monitoring confirmed recurrent hypoglycaemic episodes. Amantadine was discontinued during glucose monitoring, after which the hypoglycaemia gradually resolved. No further episodes of weakness or hypoglycaemia were reported during a 20-month follow-up period. Other causes of hypoglycaemia, including hypoadrenocorticism and toxin exposure, were considered unlikely based on diagnostic findings and clinical course, although insulinoma was not definitively excluded. A temporal association between amantadine administration and hypoglycaemia, together with resolution following drug discontinuation, suggests a potential causal relationship. This case represents the first report of suspected amantadine-associated hypoglycaemia in a dog and highlights the need to consider this drug as a possible cause of hypoglycaemia in dogs.