October's Case of the Month
Hyperaldosteronism in a Domestic Shorthair
Sonographer: Shadawn Salmond-Jimenez DVM
Patient Information:
Age: 14 years
Gender: Spayed Female
Species: Feline
History
Anorexic and lethargic for 2 days. Physical exam included a normal abdominal exam. Bloodwork was unremarkable except for mild hypokalemia of 3.1 mEq/L (range 3.5-5.8) and mild eosinopenia. Spec cPL test was normal. Radiographs showed no evidence of abdominal obstruction or masses.
Image Interpretation
The left adrenal gland was visualized and recognized as having abnormally rounded "plump" shape, increased size (6.5mm), normal position with homogeneous moderately hypoechoic echogenicity. No adrenal invasion into the aorta, phrenic vein thrombosis, or dystrophic mineralization were noted.
The right adrenal gland was visualized and recognized as having normal shape, size (3.2mm), position, and echogenicity.
Diagnosis and Sonographic Analysis:
Unilateral Left Adrenal Enlargement - DDx: differentials include cortical & medullary neoplasia vs. benign hyperplasia
a) Cortical Neoplasia - Adrenal adenocarcinoma = Cushing's Diease (common)
b) Non-functional adenoma vs. myelolipoma vs. hyperplasia
c) Medullary Neoplasia - Pheochromocytoma (rare)
d) Functional adenoma
Case outcome
Resting plasma aldosterone levels were obtained. Results were significantly high at 1461 (normal range 198-388, confirming hyperaldosteronism (likely primary).
Medical management was elected including Spironolactone and Tumil K therapy. Patient was doing great at the time of follow-up six months later, with one episode of diarrhea noted at that time.
Sonographer: Shadawn Salmond-Jimenez, DVM
Brief Overview of Hyperaldosteronism
Hyperaldosteronism (Conn’s syndrome) can be classified as primary or secondary. Primary hyperaldosteronism (PHA) is autonomous, excessive secretion of aldosterone from adrenal diseases (i.e neoplasia or hyperplasia of the adrenal gland). Adrenal masses may be unilateral or bilateral. Secondary hyperaldosteronism occurs with hypersecretion of aldosterone in response to activation of the renin-angiotensin-aldosterone system (RAAS) in response to decreased renal blood flow. Examples include CHF, renal failure, and hepatic failure.
Many patients are presented with clinical signs related to hypokalemia or systemic hypertension.
Clinical signs of hypokalemia do not typically occur until potassium concentration is ≤2.5 mEq/L. Clinical signs related to hypokalemia include muscle weakness, lethargy, cervical ventroflexion, plantigrade stance in the rear limbs, recumbency, inability to jump, and collapse.1 Other signs seen in patients with Primary Hyperaldosteronism include PU/PD, weight loss, anorexia and abdominal pain.1 Since plasma renin activity is difficult to measure, measurement of PAC (plasma aldosterone concentration) may be used alone.1,4,5 Unilateral adrenalectomy is the treatment of choice for confirmed PHA.2,6 Spironolactone is a mineralocorticoid receptor antagonist that has been used to successfully manage PHA. Potassium gluconate is also typically given to help control hypokalemia.2,5,6
(Revised by Kari Rothrock DVM
Original author was Linda Shell DVM, DACVIM (Neurology), 1/31/2008)
Sonographic image of left adrenomegaly (green arrow) in this patient. The enlarged adrenal gland was seen ventrolateral to the aorta. The celiac and mesenteric arteries are seen medial to the gland (blue lines).
Sonographic image of a normal left adrenal gland (greenarrow) in a feline patient dorsomedial to spleen (blue arrow).
Images above are of patients diagnosed with Primary Hyperaldosteronism (Conn’s syndrome).
A special thanks to the staff at Nebel Street Animal Hospital for this interesting case.