Stool osmotic gap

Stool osmotic gap is an measurement of the difference in solute types between serum and feces, used to distinguish among different causes of diarrhea.

Feces is normally in osmotic equilibrium with blood serum, which the human body maintains between 290–300 mOsm/kg.[1] However, the solutes contributing to this total differ. Serum is mostly sodium and potassium salts, while the digestive tract contains significant amounts of other compounds. Stool osmotic gap is a measure of the concentration of those other compounds.

Stool osmotic gap is calculated as 290 mOsm/kg − 2 × (stool Na + stool K).[2] 290 mOsm/kg is the presumed stool osmolality, and the measured concentration of sodium and potassium cations is doubled to account for the corresponding anions which must be present.

A normal gap is between 50 and 100 mOsm/kg,[3] corresponding to the concentration of other solutes such as magnesium salts and sugars.

A low stool osmotic gap suggests secretory diarrhea, wherein the digestive tract is hyperpermeable and losing electrolytes, while a high gap suggests osmotic diarrhea, wherein the digestive tract is unable to absorb solutes from the chyme, either because the digestive tract is hypopermeable (e.g. due to inflammation), or non-absorbable compounds (e.g. Epsom salt) are present.[4] The reason for this is that secreted sodium and potassium ions make up a greater percentage of the stool osmolality in secretory diarrhea, whereas in osmotic diarrhea, other molecules such as unabsorbed carbohydrates are more significant contributors to stool osmolality.

High osmotic gap (>100 mOsm/kg) causes of osmotic diarrhea include celiac sprue, chronic pancreatitis, lactase deficiency, lactulose, osmotic laxative use/abuse, and Whipple's disease.

Low osmotic gap (<50 mOsm/kg) causes of secretory diarrhea include toxin-mediated causes (cholera, enterotoxigenic strains of E. coli) and secretagogues such as vasoactive intestinal peptide (from a VIPoma, for example). Uncommon causes include gastrinoma, medullary thyroid carcinoma (which produces excess calcitonin), factitious diarrhea from non-osmotic laxative abuse[5] and villous adenoma.

References

  1. Topazian M, Binder HJ (May 1994). "Brief report: factitious diarrhea detected by measurement of stool osmolality". N. Engl. J. Med. 330 (20): 1418–9. doi:10.1056/NEJM199405193302004. PMID 8159195.
  2. Greenberger, Norton J. "Diarrhea: Approach to the Patient With Lower GI Complaints". Merck Manual Professional. Retrieved 2009-04-10.
  3. Ghosh, Amit K.; Habermann, Thomas (2007). Mayo Clinic Internal Medicine Concise Textbook. Informa Healthcare. p. 228. ISBN 978-1-4200-6749-1.
  4. Shiau YF, Feldman GM, Resnick MA, Coff PM (June 1985). "Stool electrolyte and osmolality measurements in the evaluation of diarrheal disorders". Ann. Intern. Med. 102 (6): 773–5. doi:10.7326/0003-4819-102-6-773. PMID 3994188.
  5. Oster, JR; Materson, BJ; Rogers, AI (1980). "Laxative abuse syndrome". The American Journal of Gastroenterology. 74 (5): 451–8. PMID 7234824.

Further reading

  • Duncan, A; Robertson, C; Russell, RI (April 1992). "The fecal osmotic gap: technical aspects regarding its calculation". The Journal of Laboratory and Clinical Medicine. 119 (4): 359–63. PMID 1583385.
  • Eherer, Andreas J.; Fordtran, John S. (August 1992). "Fecal osmotic gap and pH in experimental diarrhea of various causes". Gastroenterology. 103 (2): 545–551. doi:10.1016/0016-5085(92)90845-P. PMID 1634072.
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