HYPERNATREMIA
HYPERNATREMIA: Excerpt from Differential Diagnosis in Primary Care
If an electrolyte profile shows an elevated sodium level, the
physiology model of intake, regulation, and excretion may be applied to
develop a list of possibilities. However, the focus should be on water
intake, transport, regulation, and excretion because this will help recall
most of the possibilities.
Intake. When water intake is diminished in dehydration states,
the sodium level increases.
Regulation. Antidiuretic hormone (ADH) allows for the retention
of water by the distal tubule. When this hormone is reduced or absent, as in
pituitary diabetes insipidus, hypernatremia results. Furthermore, if the
kidney does not respond to ADH, as in renal diabetes insipidus,
hypernatremia results. Aldosterone hormone promotes increased reabsorption
of sodium in the distal tubule in primary aldosteronism, causing
hypernatremia. However, this may be counterbalanced by an increased ADH
secretion and water retention causing the sodium to return to normal.
Excretion. Sodium excretion may be reduced in acute renal
failure but, because water is
retained as well, the plasma sodium is not usually increased. Other causes
of hypernatremia include the administration of normal and hypertonic saline,
prolonged vomiting, and heat exhaustion.
Approach to the Diagnosis
Dehydration can be diagnosed clinically by the tenting of the skin,
mushy eyeballs, and concentrated urine. Laboratory workup includes serial
electrolytes, chemistry panel, serum and urine osmolality, serum ADH, plasma
renin, 24-hour urine aldosterone level, and consultation with an
endocrinologist or a nephrologist. It is wise to withhold all noncritical
drugs until a diagnosis is certain.
Pictures
Book Source Details
- Book Title: Differential Diagnosis in Primary Care
- Author(s): R. Douglas Collins MD, FACP
- Year of Publication: 2007
- Copyright Details: Differential Diagnosis in Primary Care, Copyright © 2007 Lippincott Williams & Wilkins.
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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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