Veterinary Medicine - March 2009 - (Page 127)

TABLE 1 Selected Serum Chemistry Proﬁle Results Pre-referral Results Results Obtained at the Referral Hospital Parameter BUN (mg/dl) Creatinine (mg/dl) Albumin (g/dl) Total protein (g/dl) Calcium (mg/dl) Phosphorus (mg/dl) Sodium (mmol/L) Potassium (mmol/L) Day 1 93 2.3 3.5 6.8 14.6 11.6 129 7.5 Reference Range* 6–26 0.4–1.6 2.5–4.5 5–7.5 8.8–12.4 2.2–5.8 138–155 3.5–5.5 Day 7 Presentation 67 1.7 3.2 6 26.8 22.7 138 8.3 Day 8 Morning 39 0.8 3.1 5.8 24.1 18.8 138 5.1 Day 8 Evening Day 9 26 0.4 2.5 4.9 16.8 11.6 138 4.8 24 0.3 2.3 4.4 10.5 7.1 131 3.7 Day 10 Released 36 1 2.8 5.2 9.2 4.5 129 3.2 Day 14 27 0.6 3.4 5.6 9.9 6.5 141 4 Day 31 27 0.3 4.1 6.5 10.9 6.1 144 4.9 Reference Range** 6–25 0.5–1.6 2.7–4.4 5–7.4 8.8–11.4 2.5–6 139–154 3.6–5.5 * Reference range values from Sunrise Veterinary Laboratories, Clearwater, Fla. * * Reference range values from Antech Diagnostics, West Los Angeles, Calif. ratio in this puppy was 16.6. A sodium: potassium ratio < 24 is highly correlated with hypoadrenocorticism.2 We also considered primary hyperparathyroidism and secondary hyperparathyroidism due to renal failure as differential diagnoses for the hypercalcemia. However, because of the owner’s nancial limitations and our strong suspicion of hypoadrenocorticism, we did not measure ionized calcium and parathyroid hormone concentrations. Furthermore, the dog had been receiving a high-quality commercial puppy food and had no known ingestion of toxins such as rodenticides, psoriasis drugs, or excess vitamin D or calcium. DIAGNOSIS AND TREATMENT Initial treatment included a 400-ml bolus of 0.9% sodium chloride solution given intravenously over two hours (30 ml/kg/hr) followed by prednisolone sodium succinate (18.4 mg/kg IV), which was administered immediately after completion of an ACTH stimulation test. Intravenous uid therapy with 0.9% sodium chloride solution was continued at 6.5 ml/kg/hr after the initial bolus. We administered cefazolin (30 mg/kg intravenously, two doses, 10 hours apart) and famotidine (0.75 mg/kg orally b.i.d. for the duration of hospitalization) to prevent sepsis due to bacterial translocation and ulceration secondary to compromised gastrointestinal mucosal integrity, which commonly occurs with hypoadrenocorticism.3 The ACTH stimulation test results were available the next day (day 8) and con rmed hypoadrenocorticism. The resting cortisol concentration was 0.5 µg/dl (reference range = 0.5 to 5.5 µg/ dl), and the two-hour post-stimulation cortisol concentration was 0.4 µg/dl (reference range = 5.5 to 20 µg/dl). We treated the dog with a mineralocorticoid, desoxycorticosterone pivalate (Percorten—Novartis Animal Health; 2.2 mg/kg given intramuscularly), and glucocorticoids. Dexamethasone sodium phosphate (0.22 mg/kg intravenously) was administered once. The patient then began eating, so we switched to treatment with oral prednisone (1.5 mg/kg orally once a day). Clinical signs resolved, and serum chemistry pro le abnormalities, including the hypercalcemia, improved after three days of treatment for hypoadrenocorticism (Table 1, day 9). After four days of hospitalization, the patient was eating well and the ocular discharge had resolved, so the patient was released to the owner. Prednisone (0.73 mg/ kg b.i.d.) and famotidine (0.73 mg/kg b.i.d.) were prescribed as initial home care. We emphasized the importance of strict compliance with future desoxycorticosterone pivalate injections and prednisone dosages. At reevaluation (day 14), the patient was doing well. Its energy level and appetite had improved, and it had gained 1.3 lb (0.6 kg) since being released from hospital. Most serum chemistry pro le results, including the calcium concentration, were normal (Table 1, day 14). VETERINARY MEDICINE March 2009 127

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Veterinary Medicine - March 2009

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