Symptom Finder - Hyponatremia
HYPONATREMIA
The physiologic model of intake, absorption, transport, regulation, and excretion lends itself well to developing a list of possible causes of hyponatremia.
Intake: A limited intake of sodium by itself does not usually cause hyponatremia. However, in disorders of the GI tract that cause vomiting or diarrhea, there is often associated hyponatremia. Consequently, pyloric obstruction, cholera, viral gastroenteritis, intestinal obstruction, acute ulcerative colitis, and bacterial dysentery lead to hyponatremia.
Absorption: Absorption of sodium through the intestinal wall is inhibited in malabsorption syndrome, causing hyponatremia.
Transport: In CHF, there is decreased perfusion of the glomeruli, leading to retention of both sodium and water. There is also inappropriate secretion of ADH, causing a greater retention of water than sodium, and thus dilutional hyponatremia is known to occur.
Regulation: The hormone aldosterone regulates the reabsorption of sodium by the kidney; when this is absent, as in Addison disease and other conditions associated with adrenal insufficiency, there is hyponatremia. Diuretics also interfere with the reabsorption of sodium by the kidney, leading to hyponatremia, which is desirable as long as it is not taken to extreme. In the syndrome of inappropriate ADH -secretion, more water than sodium is retained, causing hyponatremia. This syndrome is found in carcinoma of the lung, porphyria, Guillain– Barré syndrome, postoperatively, and other pulmonary and neurologic disorders.
Excretion: Excess sodium is excreted via the kidney. Consequently, in renal failure one would consistently expect salt retention and hypernatremia. In fact, the opposite usually occurs. In acute renal failure, hyponatremia results because more water than sodium is retained, and there is often vomiting that contributes to the hyponatremia because the patient usually replaces the water without adequate salt replacement. In chronic renal failure, there is often hyponatremia because reabsorption of sodium by the distal tubules is impaired. In renal tubular acidosis, hyponatremia occurs because of the interference with the exchange of the hydrogen ion for sodium. Sodium is secreted by the sweat glands. It follows that hyponatremia is found in pathologic diaphoresis and heat exhaustion.
Approach to the Diagnosis
The history may reveal causes of hyponatremia such as the use of diuretics, CHF, malabsorption syndrome, or chronic renal failure. Symptoms of vomiting or diarrhea should also alert one to a GI disorder as the cause. Laboratory tests such as a chemistry panel, serial electrolytes, plasma cortisol, serum and urine osmolality, spot urine sodium, and blood volume may be very helpful.
Other Useful Tests
1. CBC (infection, Addison disease)
2. Urinalysis (acute or chronic nephritis)
3. Serum ADH assay (diabetes insipidus)
4. Plasma renin (aldosteronism)
5. Arterial blood gases (shock, CHF)
6. Endocrinology consult
7. Nephrology consult
8. 24-hour urine aldosterone (Addison disease)
9. Corticotropin stimulation test (Addison disease)
The physiologic model of intake, absorption, transport, regulation, and excretion lends itself well to developing a list of possible causes of hyponatremia.
Intake: A limited intake of sodium by itself does not usually cause hyponatremia. However, in disorders of the GI tract that cause vomiting or diarrhea, there is often associated hyponatremia. Consequently, pyloric obstruction, cholera, viral gastroenteritis, intestinal obstruction, acute ulcerative colitis, and bacterial dysentery lead to hyponatremia.
Absorption: Absorption of sodium through the intestinal wall is inhibited in malabsorption syndrome, causing hyponatremia.
Transport: In CHF, there is decreased perfusion of the glomeruli, leading to retention of both sodium and water. There is also inappropriate secretion of ADH, causing a greater retention of water than sodium, and thus dilutional hyponatremia is known to occur.
Regulation: The hormone aldosterone regulates the reabsorption of sodium by the kidney; when this is absent, as in Addison disease and other conditions associated with adrenal insufficiency, there is hyponatremia. Diuretics also interfere with the reabsorption of sodium by the kidney, leading to hyponatremia, which is desirable as long as it is not taken to extreme. In the syndrome of inappropriate ADH -secretion, more water than sodium is retained, causing hyponatremia. This syndrome is found in carcinoma of the lung, porphyria, Guillain– Barré syndrome, postoperatively, and other pulmonary and neurologic disorders.
Excretion: Excess sodium is excreted via the kidney. Consequently, in renal failure one would consistently expect salt retention and hypernatremia. In fact, the opposite usually occurs. In acute renal failure, hyponatremia results because more water than sodium is retained, and there is often vomiting that contributes to the hyponatremia because the patient usually replaces the water without adequate salt replacement. In chronic renal failure, there is often hyponatremia because reabsorption of sodium by the distal tubules is impaired. In renal tubular acidosis, hyponatremia occurs because of the interference with the exchange of the hydrogen ion for sodium. Sodium is secreted by the sweat glands. It follows that hyponatremia is found in pathologic diaphoresis and heat exhaustion.
Approach to the Diagnosis
The history may reveal causes of hyponatremia such as the use of diuretics, CHF, malabsorption syndrome, or chronic renal failure. Symptoms of vomiting or diarrhea should also alert one to a GI disorder as the cause. Laboratory tests such as a chemistry panel, serial electrolytes, plasma cortisol, serum and urine osmolality, spot urine sodium, and blood volume may be very helpful.
Other Useful Tests
1. CBC (infection, Addison disease)
2. Urinalysis (acute or chronic nephritis)
3. Serum ADH assay (diabetes insipidus)
4. Plasma renin (aldosteronism)
5. Arterial blood gases (shock, CHF)
6. Endocrinology consult
7. Nephrology consult
8. 24-hour urine aldosterone (Addison disease)
9. Corticotropin stimulation test (Addison disease)