Interpretive Handbook

The concentration of sodium in fecal water and the rate of excretion are dependent upon 3 factors:

-Five% to 10% of the normal daily dietary load of sodium passes into the gastrointestinal (GI) tract

-Sodium is passively transported from serum and other vascular spaces to equilibrate fecal osmotic pressure with vascular osmotic pressure

-Certain rare toxins (cholera toxin) cause sodium transport into fecal water

Fecal osmolality is normally in equilibrium with vascular osmolality, and sodium is the major affector of this equilibrium. Fecal osmolality is normally 2 x (sodium + potassium) unless there are exogenous factors inducing a change in this ratio, such as the presence of other osmotic agents (magnesium sulfate, saccharides), or drugs inducing secretions, such as phenolphthalein or bisacodyl.

If the relationship between osmolality, potassium, and sodium (see equation above) indicates an osmotic gap, diarrhea may be osmotically induced by exogenous agents such as magnesium sulfate or saccharides. If there is no osmotic gap but sodium concentration is 2 to 3 times normal, secretory diarrhea may be the cause, and agents such as phenolphthalein, bisacodyl, or cholera toxin should be suspected.

Determining the cause of chronic diarrhea

Typically, stool sodium is similar to serum since the gastrointestinal (GI) tract does not secrete water. A useful formula is 2x (stool sodium + stool potassium) = stool osmolality + or - 30 mOsm.

Increased fecal sodium content or daily excretion rate with normal fecal potassium and no osmotic gap indicates secretory diarrhea.

Normal fecal sodium and potassium in the presence of an osmotic gap (>30 mOsm/kg) suggests osmotic diarrhea.

Normal or low fecal sodium in association with high fecal potassium suggests deterioration of the epithelial membrane or a bleeding lesion.

High sodium and potassium in the absence of an osmotic gap indicate active electrolyte transport in the GI tract that might be induced by agents such as cholera toxin or hypersecretion of vasointestinal peptide.

If sodium concentration or 24-hour sodium excretion rate is 2 to 3 times normal and osmotic gap >30 mOsm/kg, secretory diarrhea may be the cause. Agents such as phenolphthalein, bisacodyl, or cholera toxin should be suspected.

For very low stool osmolality, consider factitial diarrhea.

This test will be performed on watery feces (diarrhea) only.

In the event a formed stool is submitted, the test will not be performed and the report will indicate: "A formed stool specimen was submitted for analysis. This test was not performed because it only has clinical value if performed on a naturally occurring watery stool specimen."

High concentrations of gadolinium and iodine are known to interfere with most metals tests. If either gadolinium- or iodine-containing contrast media has been administered, a specimen must not be collected for 96 hours.

0-15 years: not established

> or =16 years: 0-159 mEq/kg

1. Phillips S, Donaldson L, Geisler K, et al: Stool composition in factitial diarrhea: a 6-year experience with stool analysis. Ann Intern Med 1995;123:97-100

2. Ho J, Moyer T, Phillips S: Chronic diarrhea: the role of magnesium. Mayo Clin Proc 1995;70:1091-1092