The principal action of aldosterone is to conserve body sodium. Under the influence of this hormone, the kidneys excrete less sodium and more potassium and hydrogen. Excessive production of aldosterone, which occurs in some patients with functioning tumors of the adrenal gland, causes a distinctive pattern of bio-chemical changes and a corresponding set of clinical manifesta-tions that are diagnostic of this condition.
Patients with aldosteronism exhibit a profound decline in the serum levels of potassium (hypokalemia) and hydrogen ions (alka-losis), as demonstrated by an increase in pH and serum bicarbon-ate level. The serum sodium level is normal or elevated depending on the amount of water reabsorbed with the sodium. Hypertension is the most prominent and almost universal sign of aldosteronism, although it is the primary cause in less than 1% of cases of hyper-tension (Tierney et al., 2001).
Hypokalemia is responsible for the variable muscle weakness, cramping, and fatigue in patients with aldosteronism, as well as an inability on the part of the kidneys to acidify or concentrate the urine. Accordingly, the urine volume is excessive, leading to polyuria. Serum, by contrast, becomes abnormally concentrated, contributing to excessive thirst (polydipsia) and arterial hyper-tension. A secondary increase in blood volume and possible di-rect effects of aldosterone on nerve receptors, such as the carotid sinus, are other factors producing the hypertension.
Hypokalemic alkalosis may decrease the ionized serum cal-cium level and predispose the patient to tetany and paresthesias. Trousseau’s and Chvostek’s signs can be used to assess neuro-muscular irritability before overt paresthesia and tetany occur.
Glucose intolerance may occur because hypokalemia interferes with insulin secretion from the pancreas.
In addition to a high or normal serum sodium level and low serum potassium level, diagnostic studies indicate high serum aldos-terone levels and low serum renin levels. The measurement of the aldosterone excretion rate after salt loading is a useful diagnostic test for primary aldosteronism. The renin–aldosterone stimula-tion test and bilateral adrenal venous sampling are useful in dif-ferentiating the cause of primary aldosteronism. Antihypertensive medication may be discontinued up to 2 weeks prior to testing.
Treatment of primary aldosteronism usually involves surgical re-moval of the adrenal tumor through adrenalectomy. Hypokalemia resolves for all patients after surgery, but hypertension may persist. Spironolactone may be prescribed to control hypertension.
Adrenalectomy may be used in treating adrenal tumors, primary Cushing’s syndrome, and aldosteronism. For adrenal tumors, all of the endocrine disturbances associated with a hypersecreting tumor of the adrenal cortex or medulla can be relieved completely by surgical removal of the involved gland.
Adrenalectomy is performed through an incision in the flank or the abdomen. In general, the postoperative care resembles that for other abdominal surgery. However, the patient is susceptible to fluctuations in adrenocortical hormones and requires admin-istration of corticosteroids, fluids, and other agents to maintain blood pressure and prevent acute complications. If the adrena-lectomy is bilateral, replacement of corticosteroids will be life-long; if one adrenal gland is removed, replacement therapy may be temporarily necessary because of suppression of the remaining adrenal gland by high levels of adrenal hormones. A normal serum glucose level is maintained with insulin, appropriate intravenous fluids, and dietary modifications.
Nursing management in the postoperative period includes fre-quent assessment of vital signs to detect early signs and symptoms of adrenal insufficiency and crisis or hemorrhage. Explaining all treatments and procedures, providing comfort measures, and pro-viding rest periods can reduce the patient’s stress and anxiety level.
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