Results of CBC and serum chemistry analysis revealed a high urea nitrogen (110 mg/dl) with a normal creatinine concentration(1.9 mg/dl), as well as hyperphosphatemia (14.0 mg/dl). The urine specific gravity was 1.020 with an inactive sediment. Serum electrolyte changes included moderate hypercalcemia (calcium = 13.3 mg/dl), mild hyponatremia (sodium = 134 mEq/L), marked hyperkalemia (potassium = 8.8 mEq/L), and a low Na:K ratio (15.9).
I submitted a resting cortisol concentration to the lab and started the dog on intravenous 0.9% NaCl, ampicillin, and famotidine. By the next morning, the dog was eating well and was much brighter. Repeat chemistry panel showed resolution of the azotemia (BUN = 30 mg/dl and creatinine = 0.9 mg/dl). However, hyperkalemia (potassium = 7.0 mEq/L), hyponatremia (sodium = 135 mEq/L), and low Na:K ratio (19.2) persisted. The resting cortisol concentration was very low at 0.2 μg/dl.
The dog continued to do well and was eating well with no vomiting on continued fluid therapy. However, 12 hours after stopping the IV fluids, the dog again became anorexic, depressed, and hypothermic.
Is this puppy an Addisonian? Do I have to do an ACTH stimulation test to confirm the diagnosis or is that resting cortisol low enough to diagnose Addison's disease? Should I start her on Percorten-V and prednisone?
The owner is limited financially. What's the cheapest way to treat her?
I would strongly recommend that you perform an ACTH stimulation test ASAP to confirm Addison's disease, given that it's a lifelong disease that is quite expensive to control and treat. There are other conditions that could produce hyponatremia and hyperkalemia and mimic true Addison's disease (e.g., whipworms causing pseudo-Addison's)(1). Although this dog probably does have Addison's disease based on the clinical signs and low basal cortisol concentration (2), I've seen other dogs that appeared to be Addisonian that turned out not to be when the ACTH stimulation test was done.
The hypercalemia is also consistent with Addison's disease and develops in 25% of dogs in adrenal crisis (3). If the ACTH stimulation test confirms Addison's disease, the serum calcium should normalize within a day or two of glucocorticoid and mineralocorticoid replacement. If not, a workup for hypercalcemia should also be considered.
Addison's disease, not matter what drugs given, is an expensive disease to treat. Although desoxycorticosterone pivalate (Percorten-V) is the most effective mineralocorticoid replacement in most dogs, fludrocortisone acetate (Florinef) also works well in most cases. If you have use generic fludrocortisone prepared by a compounding pharmacy, the drug generally costs much less to maintain an Addison's dog that does Percorten-V.
- Graves TK, Schall WD, Refsal K, et al. Basal and ACTH-stimulated plasma aldosterone concentrations are normal or increased in dogs with trichuriasis-associated pseudohypoadrenocorticism. Journal of Veterinary Internal Medicine 1994;8:287-289.
- Lennon EM, Boyle TE, Hutchins RG, et al. Use of basal serum or plasma cortisol concentrations to rule out a diagnosis of hypoadrenocorticism in dogs: 123 cases (2000-2005). Journal of the American Veterinary Medical Association 2007;231:413-416.
- Peterson ME, Feinman JM. Hypercalcemia associated with hypoadrenocorticism in sixteen dogs. Journal of the American Veterinary Medical Association 1982;181:802-804.
An ACTH stimulation test confirmed hypoadrenocorticism, based on an undetectable basal cortisol (less than 0.1 μg/dl) with no response to ACTH stimulation (post-ACTH cortisol - 0.2 μg/dl). Maxine has had an excellent clinical response to treatment with generic fludrocortisone (20 μg/kg)and low daily doses of prednisone (0.1 mg/kg). All of the serum electrolytes imbalances, including the hypercalcemia, hyperkalemia, and hyponatremia were completely resolved at the dog's initial 2-week recheck.