The authors of this case report describe a 4-year-old spayed female British shorthaired cat that presented with severe weakness, bradycardia (120 beats/min), hypovolemia, and hypothermia (99 F [37.2 C]). The cat’s systolic blood pressure was measured and was undetectable. The owners reported that the cat had been polyuric and polydipsic beginning four weeks earlier but had become progressively weaker and had stopped eating or drinking one week prior to presentation.
Diagnostic testing. The results of a complete blood count showed lack of a stress leukogram. The following serum chemistry profile abnormalities were found (reference ranges in parentheses):
* pH = 7.14 (7.31 to 7.39)
* Bicarbonate (mmol/L) = 10.4 (15.5 to 23.9)
* Base excess = -19 ( -10.12 to 1.2)
* Sodium (mmol/L) = 121 (141 to 150)
* Potassium (mmol/L) = 8 (3.6 to 4.8)
* Chloride (mmol/L) = 90.8 (110 to 125)
* BUN (mg/dl) = 62.5 (20 to 30)
* Creatinine (mg/dl) = 6.7 (0 to 1.9)
* Phosphorus (mg/dl) = 11.5 (2.5 to 5.9)
The blood glucose concentration was also noted to be at the low end of the reference range. A thoracic radiographic examination revealed microcardia, a narrow caudal vena cava, and pulmonary hypoperfusion. An abdominal ultrasonographic examination revealed a small left adrenal gland; the right adrenal gland could not be visualized.
Treatment. Intravenous crystalloids (0.9% sodium chloride) and hydroxyethyl starch were given as well as sodium bicarbonate to correct the metabolic acidosis. Rewarming measures were also taken. Dextrose was added to the fluids, and fluid content was adjusted according to blood gas analysis results. An ACTH stimulation test was performed at the initiation of therapy. After aggressive therapy and monitoring (continuous echocardiography and blood gas analyses every three hours) over 12 hours, the cat improved and vital parameters normalized. An oral dose of 0.025 mg fludrocortisone given twice daily and 0.3 mg/kg prednisolone given once daily was begun within 24 hours of presentation. Over the next few days the cat continued to improve, and its clinical signs resolved.
Definitive diagnosis. The ACTH stimulation test confirmed a diagnosis of hypoadrenocorticism with both cortisol and aldosterone concentrations not detectable at baseline and after stimulation. At the one-week follow-up visit, mild electrolyte abnormalities were still present, but the results of a physical examination were normal. The prednisolone was discontinued at this time, and the fludrocortisone was continued as before. Two weeks later, the polyuria/polydipsia returned and the prednisolone was reinstituted. The clinical signs resolved, and the cat was maintained on a 0.2 mg/kg once a day prednisolone dose in conjunction with the fludrocortisone.
Addison’s disease is rare in cats, and the cause remains unclear. The clinical presentation and clinicopathologic abnormalities in this case were similar to what we would expect to see in dogs, except for the severe metabolic acidosis. With appropriate diagnosis and treatment, the long-term prognosis in cats with hypoadrenocorticism is favorable.
Link to article: http://jfm.sagepub.com/content/15/10/941 
Sicken J, Neiger R. Addisonian crisis and severe acidosis in a cat: a case of feline hypoadrenocorticism. J Feline Med Surg 2013;15:941-944.