Etiology

Hyperaldosteronism may be of primary or secondary etiology. Secondary hyperaldosteronism occurs as a response to stimulation of the renin–angiotensin–aldosterone system (RAAS) and therefore may occur in any disease that stimulates the RAAS, such as dehydration, hypotension, reduced renal perfusion (most commonly secondary to renal disease), or sodium deficiency (reduced intake or increased loss). In primary hyperaldosteronism (PHA) there is an inappropriate increase in aldosterone secretion, independent of the RAAS. Unilateral adrenocortical neoplasia is the most commonly described cause of PHA in cats, with unilateral adrenal adenomas and carcinomas appearing to have approximately equal incidence. Although rare, bilateral adrenal neoplasms have also been described. Bilateral adrenal hyperplasia³ is also recognized, and in these cases medical management is advised.

Clinical features

The major clinical signs of primary hyperaldosteronism are similar, whether it results from adrenal adenoma, carcinoma or hyperplasia, and they can be divided into two main groups:

Concurrent hyperaldosteronism and hyperprogesteronism has also been reported in some cases of adrenal neoplasia.4,5 In these cases the signs of hyperprogesteronism usually predominate, resulting in very similar clinical signs to those encountered with hypercortisolemia (Fig. 35-2).

Diagnosis

On serum biochemistry, hypokalemia is most often present; however, the degree is variable and normokalemia does not exclude the possibility of primary hyperaldosteronism. Serum sodium concentrations are usually normal or only mildly increased. Creatine kinase is usually elevated in cats with polymyopathy, with the degree of elevation being highly variable. Urea and creatinine may be elevated secondary to hyperaldosteronism, and so the presence of azotemia should not lead the clinician to conclude that hypokalemia and/or hypertension is a consequence of the renal disease itself.

Adrenal masses are rarely visible on radiographs, but if the mass is seen it is more likely to be an adrenocortical carcinoma than an adenoma. Pulmonary metastases can occur, albeit infrequently. In all reported feline cases of primary hyperaldosteronism in which adrenal ultrasonography was performed, unilateral adrenal enlargement with evidence of an adrenal mass was identified, ranging in size from 10–46 mm in diameter (Fig. 35-3). The contralateral adrenal gland may appear normal in appearance or may be unidentifiable. It is, however, vital that the contralateral gland be assessed, because bilateral adrenal neoplasms have been reported. Ultrasonography should also be used to identify the presence and degree of invasion of the caudal vena cava by the tumor or related thrombus, and the presence of metastasis to other organs. Close association of the tumor with the caudal vena cava is usually evident. Other imaging modalities, including MRI (Fig. 35-4), CT, and saphenous venography, have been used in a small number of cases in an attempt to establish the extent of the adrenal mass before undertaking surgery.

Confirmation of diagnosis relies mainly on demonstrating an elevated plasma aldosterone concentration. The assay is widely available at commercial endocrine laboratories and requirements for collection and handling of serum or plasma are routine. Ideally, plasma aldosterone concentration needs to be interpreted together with plasma renin activity, which would be expected to be elevated in cases of secondary hyperaldosteronism. There are difficulties with measuring plasma renin activity and as a consequence demonstration of the presence of adrenocortical neoplasia concurrently with a markedly elevated plasma aldosterone concentration is considered to be sufficient to make a diagnosis of aldosterone-secreting adrenocortical tumor in cats, especially in conjunction with persistent hypokalemia and hypertension. Histopathologic confirmation of the neoplasm together with resolution of clinical signs and plasma aldosterone measurements postoperatively assist in confirming the diagnosis.

If no adrenal mass is present, then non-neoplastic primary hyperaldosteronism should be considered, and this is more difficult to diagnose without assessment of plasma renin activity. Surgical treatment would not be indicated in these cases.

Medical management

Initial treatment of primary hyperaldosteronism is directed at controlling hypokalemia and/or hypertension. Potassium supplementation using potassium gluconate at doses of 2–6 mmol PO q12h has been used; intravenous potassium chloride may be required in more severely hypokalemic cases. Amlodipine besylate (0.625–1.25 mg PO q24h) is the initial treatment of choice for hypertension. Most hypertensive cats become normotensive with the aforementioned amlodipine treatment, but higher doses are sometimes required. Spironolactone, a competitive aldosterone receptor antagonist, is also recommended (2–4 mg/kg PO q24h), for the control of both hypokalemia and hypertension.

Etiology

Hyperadrenocorticism results from chronic cortisol excess, and may occur secondary to iatrogenic cortisol administration, or with naturally occurring disease. Naturally occurring disease can be pituitary dependent, whereby a pituitary neoplasm secretes excessive ACTH with subsequent bilateral adrenocortical hyperplasia and increased cortisol secretion, or it may be adrenal dependent, as a result of a cortisol secreting adrenal neoplasm. Hyperadrenocorticism is rare in cats, but when it does occur the majority of cases (~80%) are pituitary dependent, most commonly as a result of a pituitary adenoma. About 50% are microadenomas (<3 mm diameter) and 50% are macroadenomas (>3 mm diameter). Pituitary carcinoma has only been rarely reported. In reported cases of adrenal-dependent disease, about 50% have been adrenocortical adenomas, and 50% adrenocortical carcinomas.

Clinical features

The major clinical signs are similar, whether hyperadrenocorticism results from adrenal adenoma, carcinoma or hyperplasia. Approximately 75% of cats with hyperadrenocorticism develop secondary diabetes mellitus, and the signs of uncontrolled diabetes mellitus usually predominate, namely polyuria, polydipsia, and polyphagia. Other clinical signs include lethargy, weight loss, an unkempt coat, and abdominal enlargement/pot belly appearance, although this is usually less appreciable than it is in dogs. Failure of hair regrowth, thin skin, and poor wound healing are common dermatologic features. Cushingoid cats may also exhibit severe skin fragility where the skin is so thin that it easily tears (Fig. 35-5). This is a serious complication as resultant wounds heal poorly, and it can also result in life-threatening sepsis.

Stay updated, free articles. Join our Telegram channel

Join