Symptom Finder - Hypernatremia
HYPERNATREMIA
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.
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.