Chronic Diarrhea: Diagnosis and Management

Lawrence R. Schiller; Darrell S. Pardi; Joseph H. Sellin

Disclosures

Clin Gastroenterol Hepatol. 2017;15(2):182-193. 

In This Article

Is There Benefit From Categorizing Chronic Diarrhea by Stool Characteristics and Tests?

Recommendations

13. When the differential diagnosis is broad, stool testing to characterize diarrhea can direct further evaluation more precisely. (2c)

14. Stool chemistry tests can be used to categorize diarrhea and should be considered when the diagnosis remains obscure after initial assessment. (2c)

15. Fecal lactoferrin or calprotectin can be used as surrogate measures for fecal leukocytes. (1b) Stool chymotrypsin and elastase may have some utility as screening tests for pancreatic insufficiency. (2b)

The differential diagnosis of chronic diarrhea is lengthy and can be grouped by the kind of diarrhea that is produced: fatty, inflammatory, or watery. Watery stools can be subdivided into secretory and osmotic diarrheas, with different etiologies for each. Inspection of the stools and simple tests including measurement of fecal electrolytes, fat, occult blood, and leukocytes can distinguish these stool types (Supplementary Table 3). Characterizing diarrhea type in a given patient should allow a more focused differential diagnosis.

Stool Electrolytes. Fecal electrolytes can distinguish osmotic and secretory diarrhea on the basis of calculation of the osmotic gap:[46] add fecal sodium and potassium concentrations, double that number to account for unmeasured anions, and subtract that number from 290 mOsm/kg (the expected osmolality of intraluminal contents). Measured stool osmolality is affected by fermentation and should not be used for this determination. A fecal osmotic gap <50 mOsm/kg indicates a secretory diarrhea. If the gap is >75 mOsm/kg, some non-electrolyte contributes substantially to fecal osmolality, indicating an osmotic diarrhea.[46]

A low fecal pH (<7.0) may be due to colonic fermentation of malabsorbed carbohydrates to short chain fatty acids.[46]

Blood or pus in the stool raises the possibility of an inflammatory diarrhea, although their absence does not exclude an inflammatory process.

Steatorrhea indicates a problem with fat absorption because of mucosal disease or luminal factors such as bile acid deficiency, SIBO, or pancreatic insufficiency. Although measurement of quantitative stool fat output on a 48- to 72-hour timed collection is ideal, qualitative stool fat content may be accurately assessed with a Sudan stain on a spot specimen.[47]

A recent study evaluated the utility of measuring stool chemistries in patients referred to a tertiary center for evaluation of chronic diarrhea.[48] In this study, such stool analysis identified 6 patterns of stool composition with important impact on further diagnostic testing ( Table 1 ). However, many of these patients had previous evaluations, and it is likely that the distribution of etiologies might be different than in a population-based sample.

Fecal Lactoferrin and Calprotectin. Microscopy for fecal leukocytes is operator-dependent. Measurement of leukocyte enzymes (lactoferrin or calprotectin) has been proposed as a surrogate for fecal leukocytes as a signal of mucosal inflammation. Fecal calprotectin appears to be more sensitive for this purpose.[49]

Fecal Chymotrypsin and Elastase. Fecal concentrations of the pancreatic enzymes, chymotrypsin or elastase, have been proposed as tubeless tests of pancreatic exocrine function.[50] Most of the studies validating these assays were done in children and suggested that sensitivity and specificity were low (~70%),[51] indicating that these tests might be suitable for screening but not for diagnosing pancreatic insufficiency.

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