Nice images. The adrenals

Nice images. The adrenals here are not overly mass like… possible stress related but worth testing aldosterone. I havent run an aldosterone level in a while but most labs run them. here is an excerpt from the Curbside guide that has a chapter on hyperaldosteronism (Conn’s syndrome)with the URL to similar cases if you have the digital version on the Curbside you can see how it meshes with our sonopath membership. Cut and paste or click on the url under the chapter heading and it will take you to  cases in sonopath archive (now 20k + cases) that are applicable to the chapter subject.

Heres the link for the Curbside makes for nice x mas gift fyi:)

https://sonopath.com/products/book

Here are some quick notes form my ABVP prep on Hypernatremia

Neuro effects at Na>170

Correct sodium slowly

Hypernatremia: diabetes insipidis or dehydration, salt load, conns syndrome paintball ingestion >>***glycol ingestion> no activated charcoal, gi disease vomiting

Feline Hyperaldosteronism

http://www.sonopath.com/Hyperaldosteronism

Description: Feline hyperaldosteronism can be caused by either a unilateral aldosterone-secreting adrenal tumor or bilateral adrenal hyperplasia. The resultant oversecretion of aldosterone results in hypokalemia, hypernatremia, and metabolic alkalosis. Primary hyperaldosteronism and secondary hyperaldosteronism caused by renal disease may be difficult to differentiate. Hyperaldosteronism is associated with clinical signs that result from systemic hypertension caused by an expansion in blood volume or polymyopathy resulting from hypokalemia. There is no breed predilection and the disease tends to occur in older cats between the ages of 6 and 13 at a mean age of approximately 10 years.

Clinical Signs: The most common clinical sign is hypokalemic polymyopathy, which presents as a ventroflexion of the neck. Other signs are paresis, hind limb weakness, and acute onset blindness.

Diagnostics: The most common laboratory findings are severe hypokalemia and elevated serum creatine kinase activity. Abdominal ultrasonography will show either unilateral or bilateral adrenomegaly and/or an adrenal mass. The diagnosis is confirmed by the presence of severely elevated plasma aldosterone concentrations. Plasma renin concentrations may be decreased or within normal reference range. In animals without markedly elevated aldosterone concentrations, an increased plasma aldosterone-plasma renin ratio may be useful in establishing the diagnosis. A CT scan can be used to detect subtle changes within the adrenal cortex and better delineate the extent of the adrenal mass if surgery is being considered.

Treatment: Treatment of primary hyperaldosteronism resulting from a unilateral adrenal tumor consists of potassium supplementation and administering an aldosterone blocker, such as spironolactone, as well as amlodipine. Once stabilized, surgical removal of the adrenal mass should be considered. In cases of idiopathic adrenal hyperplasia that give rise to hyperaldosteronism, medical treatment is the only option available; however, most cats will eventually succumb to progressive renal insufficiency.

References:

Ash RA, Harvey AM, Tasker S. Primary hyperaldosteronism in the cat: a series of 13 cases. J Feline Med Surg 2005;7:173-82.

Chiaramonte D, Greco DS. Feline adrenal disorders. Clin Tech Small Anim Prac 2007;22:26-31.

Duesberg CA, Nelson RW, Feldman EC, et al. Adrenalectomy for treatment of hyperadrenocorticism in cats: 10 cases (1988-1992). J Am Vet Med Assoc 1995;207:1066-70.

Javadi S, Djajadiningrat-Laanen SC, Kooistra HS, et al. Primary hyperaldosteronism, a mediator of progressive renal disease in cats. Dom Anim Endocrinol 2005;28:85-104.

Im more concerned with

Im more concerned with irregular contour, capsular deviation or escape and unilateral morophological change. I think the smallest one I can remember was in the 8 mm range or so.