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491.e2 Hyperaldosteronism, Primary

Hyperaldosteronism, Primary Client Education
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BASIC INFORMATION
concentration and low plasma renin activ-
ity points to primary hyperaldosteronism. TREATMENT
Definition Abdominal ultrasonography is usually employed Treatment Overview
Autonomous hypersecretion of aldosterone from to visualize abnormalities in size or structure Treatment is directed at resolving clinical signs
neoplastic or hyperplastic adrenocortical (zona of the adrenal gland(s). associated with hypertension and hypokalemia
glomerulosa) tissue by normalizing plasma potassium concentration
Differential Diagnosis and arterial blood pressure. Surgical excision
Synonyms Combination of findings (e.g., hypokalemia, is warranted if an adrenal tumor is identified.
Conn’s syndrome, low-renin (hyper)aldosteronism hypertension) can be inappropriately attributed If adrenalectomy is not possible, medical
to concurrent chronic kidney disease alone treatment with aldosterone receptor blockers
Epidemiology For adrenal mass: should be initiated.
SPECIES, AGE, SEX • Cortisol or sex hormone–secreting adrenal
• Rare in dogs tumor Acute General Treatment
• Increasingly recognized in cats; currently • Pheochromocytoma • Oral potassium supplementation or
considered the most common feline adre- • Nonfunctional adrenal mass intravenous administration of potassium-
nocortical disorder For hyperaldosteronism: supplemented fluids for correction of plasma
• Middle-aged and older animals • Secondary to hypovolemia, chronic kidney potassium concentration (p. 516)
• No sex predisposition disease, heart failure, or severe hepatic • Persistent arterial hypertension due to
dysfunction primary hyperaldosteronism is best managed
ASSOCIATED DISORDERS For hypokalemia (p. 1240): with the calcium channel blocker amlodipine.
Arterial hypertension and/or hypokalemia. In • Fasting • Spironolactone, an aldosterone receptor
cats, associated with progressive loss of kidney • Potassium shift from extracellular to intracel- blocker, at a starting dosage of 1-2 mg/kg
function lular fluid (e.g., alkalosis) PO q 12h
• Gastrointestinal losses (vomiting and/or
Clinical Presentation diarrhea) Chronic Treatment
DISEASE FORMS/SUBTYPES • Excessive renal losses (e.g., osmotic diuresis) • Surgical excision of an adrenal tumor is
• Adrenocortical tumor recommended if there is no evidence of
• Bilateral adrenocortical hyperplasia Initial Database abdominal or thoracic metastasis.
• CBC, routine biochemical profile, uri- • Chronic medical management with spirono-
HISTORY, CHIEF COMPLAINT nalysis, total thyroxine: frequent findings lactone and oral potassium supplementation
Episodic weakness and lethargy occur. In are hypokalemia, elevated plasma creatinine can be successful at managing clinical signs
cats, cervical ventroflexion and loss of vision concentration, low-normal plasma phosphate if surgery is not feasible.
are common. Polyuria/polydipsia is the main concentration. Plasma sodium is generally • Chronic kidney disease should be addressed
presenting clinical sign in dogs. within reference range because water reten- (pp. 167 and 169).
tion results in sodium dilution.
PHYSICAL EXAM FINDINGS • Abdominal ultrasonography: possible unilat- Possible Complications
Muscular weakness (dogs and cats), cervical eral adrenal mass ± intraabdominal metasta- • The major potential complication of
ventroflexion (cats), loss of vision due to retinal sis. Cats with primary hyperaldosteronism unilateral adrenalectomy is perioperative
detachment and/or retinal and intravitreal secondary to adrenal hyperplasia may have hemorrhage.
hemorrhages (cats) grossly normal adrenal glands on abdominal • There are no reports of postoperative
imaging. hypoaldosteronism occurring after exci-
Etiology and Pathophysiology • Thoracic radiographs: possible metastasis sion of an aldosterone-secreting adrenal
• Occurs as a result of autonomous hypersecre- from adrenal adenocarcinoma. tumor.
tion of aldosterone from unilateral or bilateral • Systolic arterial blood pressure: usually
adrenocortical neoplasia or from hyper- > 160-180 mm Hg Recommended Monitoring
plasia of adrenocortical zona glomerulosa • Blood gas analysis: may reveal metabolic • Successful surgical management of primary
tissue alkalosis hyperaldosteronism due to an adrenal tumor
• Mineralocorticoid excess leads to increased should result in resolution of hypokalemia
renal potassium excretion (causing hypoka- Advanced or Confirmatory Testing and arterial hypertension and normalization
lemia), increased renal sodium and water • Plasma aldosterone concentration (PAC): of plasma aldosterone concentration.
resorption (causing arterial hypertension), high-normal or increased. • If chronic medical management is under-
and suppression of renin secretion. • Plasma renin activity (PRA) may be decreased taken, serial electrolyte and blood pressure
or within the reference range. In theory, monitoring is recommended.
DIAGNOSIS increased PRA excludes a diagnosis of
primary hyperaldosteronism. PROGNOSIS & OUTCOME
Diagnostic Overview • An increased PAC/PRA ratio may be
Primary hyperaldosteronism should be con- useful in establishing the diagnosis in dogs • After complete removal of a benign, uni-
sidered in all middle-aged and older cats with or cats without markedly elevated plasma lateral, mineralocorticoid-producing tumor,
hypokalemic muscle weakness and/or systemic aldosterone concentration. the prognosis can be excellent without
hypertension. In dogs, polyuria/polydipsia may • CT or MRI can be used for detecting subtle medication.
be a reason to explore the possibility of primary changes in the adrenal cortex and to better • Prognosis is guarded in cases of adenocar-
hyperaldosteronism. The combination of a delineate the extent of an adrenal mass cinoma because metastasis can occur. If no
high-normal or elevated plasma aldosterone preoperatively. metastases are seen at surgery, prognosis

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