PRIMARY
ALDOSTERONISM
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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