Journal Scan: Case study: The cat that suffered an Addisonian crisis

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May 21, 2014

Overview

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]). Systolic blood pressure was measured and was undetectable. The owners reported that the cat had been polyuric and polydipsic (PU/PD) 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:

pH 7.14
Bicarbonate (mmol/L) 10.4
Base excess -19
Sodium (mmol/L) 121
Potassium (mmol/L) 8
Chloride (mmol/L) 90.8
BUN (mg/dl) 62.4
Creatinine (mg/dl) 6.7
Glucose (mg/dl) 72

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. Therapy consisting of intravenous crystalloids (0.9% sodium chloride) and hydroxyethyl starch was 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 PU/PD 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.

Take-home message

Addison’s disease is a rare condition 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, with the exception of severe metabolic acidosis. With appropriate diagnosis and treatment, the long-term prognosis in cats with hypoadrenocorticism is favorable.

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.

Link to article: http://jfm.sagepub.com/content/15/10/941

Jennifer L. Garcia, DVM, DACVIM, is a veterinary internal medicine specialist at Sugarland Veterinary Specialists in Houston, Texas.