Sorted By Test Name - Mayo Medical Laboratories

NAFT
60032
NABF
8039
NAF
8374
2007 Chapter 53, Part VI, pp 961-971
Sodium, 24 Hour, Feces
Clinical Information: The concentration of sodium in fecal water and the rate of excretion per 24
hours 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 or 24-hour
excretion rate is 2 to 3 times normal, secretory diarrhea may be the cause, and agents such as
phenolphthalein, bisacodyl, or cholera toxin should be suspected.
Useful For: Determining the cause of chronic diarrhea
Interpretation: 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.
Reference Values:
0-15 years: not established
> or =16 years: 0-19 mEq/24 hour
Clinical References: 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
Sodium, Body Fluid
Reference Values:
Not applicable
Clinical References: Tietz Textbook of Clinical Chemistry. Edited by Burtis and Ashwood.
Philadelphia, WB Saunders Co, 1994
Sodium, Random, Feces
Clinical Information: 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
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