A 3-month-old male intact Somali cat weighing 0.63 kg presented to the Small Animal Hospital of the University of Bern for evaluation of seizures. Approximately 4 weeks previously, the cat had been bitten in the head by a dog. Immediately after, the cat had one generalised seizure and was ataxic for 24 h. Two weeks later, the cat began having intermittent tonic-clonic seizures on a daily basis. It also showed opisthotonus and tremors. Upon evaluation by its primary veterinarian, blood sampling revealed hypoglycaemia as the only abnormality. The cat received subcutaneous fluid therapy, including glucose supplementation, and was discharged with no additional treatment. The cat did not have any more seizures; however, its mental dullness persisted and, according to the owner, it was blind. The cat lived indoors in an apartment with one dog and 10 other cats, four of which were littermates. It was up to date on vaccinations and had been recently dewormed.
Upon evaluation at the University Hospital, 4 weeks after the dog bite, physical examination showed a small-statured cat with proportional appearance. It was moderately apathic. Apart from mild hypothermia (37.6 C), clinical parameters were all within normal limits. On neurological examination, the cat was severely obtunded and showed mild-to-moderate ataxia. Postural reactions were absent on all four limbs. Menace response and nasal sensation were absent bilaterally. The evaluation of the remaining cranial nerves proved normal. The neuroanatomical location was forebrain and cerebellum. At that time point, differential diagnoses included metabolic disorders such as portosystemic shunt or hypoglycaemia, viral encephalitis, TBI, storage disorders and congenital malformation of the brain or the heart.
Emergency blood work revealed normoglycaemia (4.2 mmol/l; reference interval [RI] 3.2-5.7 mmol/l). Complete blood count (CBC) was unremarkable. A serum biochemistry panel showed a slightly elevated urea (15.4 mmol/l; RI 6.5-12.2 mmol/l) with normal creatinine (112 mumol/l; RI 52-138 mumol/l) and mild hyperkalaemia (5.3 mmol/l; RI 3.1-4.9 mmol/l). Pre- and post-prandial bile acids were within the RI (1.7 mumol/l and 1.5 mumol/l, respectively; RI 0-15 mumol/l). A faecal examination, including direct examination and centrifugation flotation, was negative. Four hours after admission, repeat blood sampling revealed marked hypoglycaemia (<1.5 mmol/l) using a portable glucose meter (AlphaTRAK; Abbott Animal Health). Hypoglycaemia was confirmed in the laboratory using a biochemistry analyser.
An intravenous (IV) bolus of 50% glucose (0.5 ml diluted 1:3 in 0.9% sodium chloride solution) resulted in clinical improvement. The cat was more alert and ambulatory. An IV 5% glucose continuous rate infusion (sodium chloride 0.9% w/v and glucose 5% w/v solution for injection [G25; B Braun Medical]) was commenced.
Given the history of head trauma a few weeks prior, MRI of the brain and a cerebrospinal fluid analysis were undertaken, both of which were unremarkable. General anaesthesia was uneventful. However, 12 h later, the cat's general condition suddenly deteriorated and it was found in lateral recumbency, stuporous, hypothermic (36 C) and hypoglycaemic (<1.5 mmol/l). Following the administration of an IV bolus of 0.5 ml 50% glucose, the cat's stupor and hypothermia rapidly resolved. It was more alert and started eating. Frequent feedings every 2-3 h were instituted, and the cat's glycaemia was monitored every 4 h. Over the next 48 h, glucose substitution was slowly decreased and finally stopped. The cat's condition was good, with no neurological deficits, and its blood glucose remained stable, between 3.2 and 6.5 mmol/l. Four days after initial presentation, the cat was discharged with instructions to feed the cat frequent meals throughout the day, and to contact us if the cat showed any clinical signs.
Two weeks after discharge, the cat was presented again with stupor, hypothermia and with severe hypoglycaemia (<1.5 mmol/l). For the first time, the owner recognised that the cat was smaller and lighter than his littermates. Also, the cat was more lethargic and not as active as the others. On physical examination, it was noted that the cat's haircoat was woolly and contained fewer primary guard hairs.
CBC showed a mild anaemia (haematocrit 22%; RI 27-47%), mild leukopenia (3.8 x 109/l; RI 6.5-15.4 x 109/l) with neutropenia (1.6 x 109/l; RI 2.5-12.5 x 109/l) without left shift or toxic changes. Serum biochemistry panel revealed slightly elevated urea (14.1 mmol/l; RI 6.5-12.2 mmol/l) with normal creatinine (81 mumol/l; RI 52-138 mumol/l). Both fasting serum cortisol (2.18 microg/dl; RI 0.50-8.80 microg/dl) and post-ACTH stimulation (6.72 microg/dl; RI 0.50-8.80 microg/dl) were within the RIs. Total thyroxine concentration was also normal (19.8 mmol/l; RI 16-46 mmol/l). Insulin concentrations were unmeasurably low (<1 mU/l; RI 5-30 mU/l). As before, the cat's condition responded rapidly to IV glucose substitution and was discharged 3 days later. The serum IGF-I concentration was significantly low (<25 ng/ml; RI >50 ng/ml). Blood sampling and measurements were repeated twice and the results verified, confirming a presumptive diagnosis of juvenile pituitary hyposomatotropism. Concentrations of IGF-1 from four other Somali cats, (two littermates of the same age, one adult half-sister and one adult unrelated cat) were also determined and were all within normal limits: 394 ng/ml (sibling 1), 614 ng/ml (sibling 2), 406 ng/ml (half-sister) and 561 ng/ml (unrelated Somali cat). When the owner brought the other siblings for blood sampling, the small stature, mental dullness and haircoat abnormalities of the cat became obvious (Figures 1 and 2).
Given that porcine GH is not available in Europe, no hormonal replacement therapy was offered to the owner. The owner was recommended to check the cat's glycaemia at home, using a portable glucose meter, once daily for 1 week, and then once weekly for 4 weeks, and whenever the cat showed neurological signs. The glucose concentration was always normal and the cat did not show neurological signs. However, the cat's physical retardation and woolly haircoat with secondary hair retention persisted.
One year after initial presentation, the owner reported that the cat showed polyuria and polydipsia. The cat was found to be mildly azotaemic (creatinine 178 mumol/l [RI 52-138 mumol/l] and urea 19.6 mmol/l [RI 6.5-12.2 mmol/l]) and urinalysis showed isosthenuria Specific Gravity (SG 1.010) and alkalinuria (pH 7.9) without proteinuria. Arterial blood pressure was normal. An abdominal ultrasound showed normal renal size, shape and internal architecture. There was very mild bilateral pyelectasia (left renal pelvis: 2 mm; right renal pelvis: 1.7 mm; RI <1 mm). Urine culture was negative. Ten days later, alkalinuria and renal pyelectasia persisted. Given the suspicion of a pyelonephritis, treatment with amoxicillin-clavulanate (20 mg/kg orally q12h) was prescribed. Two weeks after starting antibiotic therapy, kidney values, urinalysis and ultrasound findings were re-checked, all of which remained unchanged. Antibiotic therapy was then discontinued. Kidney values stayed stable for the following 6 weeks. The cat was diagnosed with chronic kidney disease (CKD) IRIS stage 2 without proteinuria and hypertension.