Veterinary Medicine - March 2009 - (Page 129)

hyperparathyroidism, acute and chronic renal failure, vitamin D toxicosis, nutritional secondary hyperparathyroidism, granulomatous diseases, neoplasia (e.g. carcinomas, lymphoma, multiple myeloma, melanoma), hyperthyroidism, and spurious laboratory results.14 Mild elevations in serum calcium concentrations (11 mg/dl) may occur in dogs up to 3 months of age because of normal bone growth.13 A small percentage of normal young dogs may have serum calcium concentrations as high as 12 mg/dl, possibly as high as 15 mg/dl.13 One published reference range for serum calcium concentrations in pediatric dogs is 10.6 to 11.7 mg/dl.15 No calcium or vitamin D supplements had been added to the high-quality commercial diet of the patient in this report. Total serum calcium is the sum of ionized calcium (the biologically active form), protein-bound calcium, and complexed calcium. Spurious hypercalcemia can occur because of lipemia, hemolysis, dehydration, and acidosis and can also occur in young animals, postprandial samples, and samples containing EDTA anticoagulant.16 This puppy’s calcium concentration was measured and veri ed at a commercial veterinary laboratory from a fasted, nonlipemic, nonhemolyzed sample that contained no anticoagulant. Dehydration may have increased the total serum calcium concentration in this patient. Ionized calcium concentrations help differentiate between spurious and true hypercalcemia. However, as previously stated, the nancial limitations of the owners prevented this additional testing. In this patient, primary hyperparathyroidism and secondary hyperparathyroidism due to renal failure were initially considered as differential diagnoses for hypercalcemia. Ideally, ionized calcium and parathyroid hormone concentrations would have been measured. However, because of the rapid, complete, and sustained resolution of hypercalcemia after treatment for hypoadrenocorticism, we thought no further testing was indicated. Treating hypercalcemia Hypercalcemia is best managed by treating the underlying cause. However, emergency measures to lower serum calcium concentrations are indicated while diagnostic test results are pending if the calcium-phosphorus product is > 60.13 Saline diuresis promotes renal excretion of calcium. The additional ltered sodium competes with calcium for renal tubular reabsorption, so an increase in sodium results in enhanced calciuresis.14 After dehydration is corrected, furosemide is administered to inhibit calcium reabsorption in the thick ascending limb of the loop of Henle, which enhances calcium excretion.14 Furosemide was not required in this case because the hypercalcemia and hyperphosphatemia resolved in a few days with rehydration and treatment for Addison’s disease. Glucocorticoids increase renal calcium excretion, decrease calcium resorption from bone, and decrease absorption of calcium from the intestinal tract. However, premature glucocorticoid administration may confound diagnostic test results for hypoadrenocorticism and lymphoma.14 Three forms of glucocorticoids were administered in this puppy. Prednisolone sodium succinate, a rapidly acting injectable glucocorticoid with a short half-life, was initially used when the puppy was obtunded. The subsequent injectable dose was with dexamethasone sodium phosphate, a slower-onset and longer-acting glucocorticoid. Once the puppy was eating, oral prednisone was administered and injectable glucocorticoids were discontinued. Hydrocortisone, prednisone, and prednisolone cross-react in the cortisol assay, so these glucocorticoid preparations must not be given before the ACTH stimulation test is completed.17 is poor. When the solubility product of serum calcium and phosphorus is > 60 in dogs, soft tissue mineralization may occur, which can quickly result in renal and cardiac damage.13 CONCLUSION In an Addisonian patient, hypercalcemia is not in itself remarkable. What is remarkable in the patient reported here is both the severity of the hypercalcemia (26.8 mg/dl) and the calcium-phosphorus product (608) on presentation and the dramatic improvement with treatment for hypoadrenocorticism. REFERENCES 1. Faulks RD, Lane IF. Qualitative urinalysis in puppies 0 to 24 weeks of age. J Am Anim Hosp Assoc 2003;39(4):369-378. 2. Adler JA, Drobatz KJ, Hess RS. Abnormalities of serum electrolyte concentrations in dogs with hypoadrenocorticism. J Vet Intern Med 2007;21(6):1168-1173. 3. Feldman BF, Nelson RW. Hypoadrenocorticism (Addison’s disease). In: Canine and feline endocrinology and reproduction. 3rd ed. St. Louis, Mo: Saunders, 2004;394-439. 4. Lathan P, Tyler J. Canine hypoadrenocorticism: diagnosis and treatment. Compend Contin Educ Pract Vet 2005;27(2):121-132. 5. Simm PJ, McDonnell CM, Zacharin MR. Primary adrenal insuf ciency in childhood and adolescence: advances in diagnosis and management. J Paediatr Child Health 2004;40(11):596-599. 6. Perry R, Kecha O, Paquette J, et al. Primary adrenal insuf ciency in children: twenty years experience at the Sainte-Justine Hospital, Montreal. J Clin Endocrinol Metab 2005;90(6):3243-3250. 7. Peterson ME, Kintzer PP, Kass PH. Pretreatment clinical and laboratory ndings in dogs with hypoadrenocorticism: 225 cases (1979-1993). J Am Vet Med Assoc 1996;208(1):85-91. 8. Lathan P, Tyler J. Canine hypoadrenocorticism: pathogenesis and clinical features. Compend Contin Educ Pract Vet 2005;27(2):110-120. 9. Peterson ME, Feinman JM. Hypercalcemia associated with hypoadrenocorticism in sixteen dogs. J Am Vet Med Assoc 1982;181(8):802-804. 10. Willard MD, Schall WD, McCaw DE, et al. Canine hypoadrenocorticism: report of 37 cases and review of 39 previously reported cases. J Am Vet Med Assoc 1982;180(1):59-62. 11. Walser M, Robinson BHB, Ducket JW Jr. The hypercalcemia of adrenal insuf ciency. J Clin Invest 1963;42(4):456-465. 12. Smith SA, Freeman LC, Bagladi-Swanson M. Hypercalcemia due to iatrogenic secondary hypoadrenocorticism and diabetes mellitus in a cat. J Am Anim Hosp Assoc 2002;38(1):41-44. 13. Schenck PA, Chew DJ, Nagode LA, et al. Disorders of calcium: hypercalcemia and hypocalcemia. In: DiBartola SP, ed. Fluid therapy in small animal practice. 3rd ed. St. Louis, Mo: Saunders Elsevier, 2006;122-194. 14. Feldman BF, Nelson RW. Hypercalcemia and primary hyperparathyroidism. In: Canine and feline endocrinology and reproduction. 3rd ed. St. Louis, Mo: Saunders, 2004;660-715. 15. Miller E. Diagnostic studies and sample collection in neonatal dogs and cats. In: Bonagura JD, Kirk RW, eds. Kirk’s current veterinary therapy XII small animal practice. Philadelphia, Pa: WB Saunders Co, 1995;26-30. 16. Feldman EC. Disorders of the parathyroid glands. In: Ettinger SJ, Feldman EC, eds. Textbook of veterinary internal medicine diseases of the dog and cat, Volume 2. St. Louis, Mo: Elsevier Saunders, 2000;1508-1535. 17. Kemppainen RJ, Behrend EN. CVT Update: interpretation of endocrine diagnostic test results for adrenal and thyroid disease. In: Bonagura JD, ed. Kirk’s current veterinary therapy XIII small animal practice. Philadelphia, Pa: WB Saunders Co, 2000;321-324. Prognosis The prognosis for hypercalcemia tends to correlate with its cause, severity, and especially the solubility product of serum calcium and phosphorus. If the underlying cause cannot be treated, the prognosis VETERINARY MEDICINE March 2009 129

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Veterinary Medicine - March 2009

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