Acute diarrhea laboratory findings: Difference between revisions
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=====Stool Osmotic Gap===== | =====Stool Osmotic Gap===== | ||
* The osmotic gap is calculated from electrolyte concentrations in stool water by the following formula : 290 - 2([Na+] + [K+]). | * The stool osmotic gap is calculated from electrolyte concentrations in stool water by the following formula : 290 - 2([Na+] + [K+]). | ||
* The osmolality of stool within the distal intestine should be used for this calculation rather than the osmolality measured in fecal fluid, because measured fecal osmolality begins to increase in the collection container almost immediately when carbohydrates are converted by bacterial fermentation to osmotically active organic acids. | * The osmolality of stool within the distal intestine should be used for this calculation rather than the osmolality measured in fecal fluid, because measured fecal osmolality begins to increase in the collection container almost immediately when carbohydrates are converted by bacterial fermentation to osmotically active organic acids. | ||
* Osmotic diarrheas, where electrolytes account for most of stool osmolality, are characterized by osmotic gaps >125 mOsm/kg, whereas secretory diarrheas where nonelectrolytes account for most of the osmolality of stool water, typically have osmotic gaps <50 mOsm/kg. In mixed cases, such in modest carbohydrate malabsorption (in which most of the carbohydrate load is converted to organic anions that obligate the fecal excretion of cations including Na+ and K+), the osmotic gap may lie between 50 and 125.<ref name="pmid1634072">{{cite journal| author=Eherer AJ, Fordtran JS| title=Fecal osmotic gap and pH in experimental diarrhea of various causes. | journal=Gastroenterology | year= 1992 | volume= 103 | issue= 2 | pages= 545-51 | pmid=1634072 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1634072 }} </ref> | * Osmotic diarrheas, where electrolytes account for most of stool osmolality, are characterized by osmotic gaps >125 mOsm/kg, whereas secretory diarrheas where nonelectrolytes account for most of the osmolality of stool water, typically have osmotic gaps <50 mOsm/kg. In mixed cases, such in modest carbohydrate malabsorption (in which most of the carbohydrate load is converted to organic anions that obligate the fecal excretion of cations including Na+ and K+), the osmotic gap may lie between 50 and 125.<ref name="pmid1634072">{{cite journal| author=Eherer AJ, Fordtran JS| title=Fecal osmotic gap and pH in experimental diarrhea of various causes. | journal=Gastroenterology | year= 1992 | volume= 103 | issue= 2 | pages= 545-51 | pmid=1634072 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1634072 }} </ref> | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
Overview
An elevated/reduced concentration of serum/blood/urinary/CSF/other [lab test] is diagnostic of [disease name].
OR
Laboratory findings consistent with the diagnosis of [disease name] include [abnormal test 1], [abnormal test 2], and [abnormal test 3].
OR
[Test] is usually normal among patients with [disease name].
OR
Some patients with [disease name] may have elevated/reduced concentration of [test], which is usually suggestive of [progression/complication].
OR
There are no diagnostic laboratory findings associated with [disease name].
Laboratory Findings
Laboratory investigations performed in the workup of patients with acute diarrhea include Complete blood count (CBC), glucose levels, white blood cells (WBC) detection, urine analysis, calcium levels, Thyroid stimulating hormone (TSH) levels, Liver function tests (LFTs), Blood urea nitrogen (BUN) / creatinine levels, Hepatitis serologies and stool examination.
- Stool examination includes the following:
- Stool culture
- Stool electrolytes
- Stool osmolality
- Ova and parasites
- Fecal lactoferrin
- Fecal leukocytes
- Test for C. difficile
Laboratory Evaluation of Acute Diarrhea
Spot Stool Analysis
- Stool spot analysis is preferred over 24 hour stool collection as it is less cumbersome.
Occult Blood
- A positive test result suggests the presence of inflammatory bowel disease and acute causes of bloody diarrhea.[1]
- Fecal occult blood positivity may also be associated with diarrhea due to idiopathic secretory diarrhea, laxative abuse, and microscopic colitis.[2]
White Blood Cells
- Wright's staining and microscopy is the standard method for the detection of white blood cells (WBCs) present in stool.
- Neutrophils in the stool present in patients having acute infectious diarrhea may be detected by latex agglutination test.[3]
Stool Culture
- In immunocompetent patients with acute diarrhea, stool culture is not routinely performed.
- If the patient has a history of swimming in streams or ponds and consuming untreated water from wells, stool culture may be performed to evaluate the patient for Aeromonas or Pleisomonas species.
- In immunocompromised patients, stool culture is included as a part of routine investigations to rule out infection due to bacteria such as Samonella, Campylobacter, protozoa and fungi.[4]
Quantitative Stool Analysis
- A 48 or 72-hour quantitative stool collection may sometimes may be useful in the evaluation of acute diarrhea in patients.
- Full analysis of the collection includes measurement of:
- Stool weight
- Stool fat content
- Stool osmolality
- Stool electrolyte concentrations
- Magnesium concentration and output
- Stool pH
- Stool occult blood
- Fecal chymotrypsin
- Fecal elastase activity
- Prior to collection period, patient should eat a regular diet containing adequate amounts of calories and fat. All medications, especially antidiarrheal medications should be avoided.
Fecal Weight
- Stool weight is also a useful index in the diagnosis of acute diarrhea.
- Stool weight of >200g/day is considered diarrheal.
- Low stool weight with increased frequency of stools may be indicative of incontinence or pain.
- Cessation of diarrhea with fasting is indicative of osmotic diarrhea caused by nonabsorbable substances or secretory diarrhea due to laxatives.[6]
Stool Osmotic Gap
- The stool osmotic gap is calculated from electrolyte concentrations in stool water by the following formula : 290 - 2([Na+] + [K+]).
- The osmolality of stool within the distal intestine should be used for this calculation rather than the osmolality measured in fecal fluid, because measured fecal osmolality begins to increase in the collection container almost immediately when carbohydrates are converted by bacterial fermentation to osmotically active organic acids.
- Osmotic diarrheas, where electrolytes account for most of stool osmolality, are characterized by osmotic gaps >125 mOsm/kg, whereas secretory diarrheas where nonelectrolytes account for most of the osmolality of stool water, typically have osmotic gaps <50 mOsm/kg. In mixed cases, such in modest carbohydrate malabsorption (in which most of the carbohydrate load is converted to organic anions that obligate the fecal excretion of cations including Na+ and K+), the osmotic gap may lie between 50 and 125.[7]
Fecal pH
- A fecal pH of < 5.3 indicates that carbohydrate malabsorption (such as that associated with lactulose or sorbitol ingestion) is a major cause of diarrhea.
- A pH of > 5.6 argues against carbohydrate malabsorption as the only cause and malabsorption syndrome that involves fecal loss of amino acids and fatty acids in addition to carbohydrate, have a higher fecal pH.[7]
Fecal Fat Concentration and Output
- The upper limit of fecal fat output measured in normal subjects (without diarrhea) ingesting normal amounts of dietary fat is approximately 7 g/day (9% of dietary fat intake)and values more than this signify the presence of steatorrhea.
- A fecal fat concentration of <9.5 g/100 g of stool more likely to be seen in small intestinal malabsorptive syndromes because of the diluting effects of coexisting fluid malabsorption.[8]
- A fecal fat concentrations of ≥9.5 g/100 g of stool were seen in pancreatic and biliary steatorrhea, in which fluid absorption in the small bowel is intact.[9]
Analysis for Laxatives
Analysis for laxatives should be done early in the evaluation of diarrhea of unknown etiology. The simplest test for a laxative is alkalinization of 3 mL of stool supernatant or urine with one drop of concentrated sodium hydroxide and a pink or red color is a positive result. Stool water can be analyzed specifically for phenolphthalein, emetine and bisacodyl and its metabolites, using chromatographic or chemical tests. Urine can be analyzed for anthraquinone derivatives.
- If stool electrolyte analysis suggests secretory diarrhea (osmotic gap <50), the patient may have ingested a laxative capable of causing secretory diarrhea, such as sodium sulfate or sodium phosphate ingestion.[10]
- If stool electrolyte analysis suggests osmotic diarrhea (osmotic gap >125 mOsm/kg), magnesium (Mg2+) laxatives may have been ingested.[11]
- If fecal osmolality is significantly less than 290 mOsm/kg (the osmolality of plasma), water or hypotonic urine has been added to the stool.
- If the osmolality is far above that of plasma, hypertonic urine may have been added to stool. Urinary contamination can be confirmed by a finding of high monovalent cation concentration (e.g., [Na+] + [K+] > 165, physiologically impossible in stool water) and a high concentration of urea or creatinine in stool water.
Tests for Bacterial Overgrowth
- The gold standard for diagnosis of bacterial overgrowth has been quantitative culture of an aspirate of luminal fluid and specifically a positive jejunal culture (>106 organisms/mL) in chronic diarrhea patients can be considered evidence of clinically significant bacterial overgrowth in the upper small intestine.[12]
- A breath test using [14C] glycocholate is used to test bacterial overgrowth. The radiolabeled conjugated bile acid is deconjugated by the bacteria, and the 14C in the side chain is metabolized to 14CO2, which is exhaled.
- Another 14C-breath test using [14C] xylose, nonradioactive glucose and nonradioactive lactulose have been developed to test bacterial overgrowth.[13]
- An elevated concentration of hydrogen in breath after overnight fasting also has been proposed as an insensitive but specific marker of small intestinal bacterial overgrowth. This elevated hydrogen concentration may also be seen in patients with malabsorption syndrome.
- An abnormal Schilling II test result (radiolabeled B12 given with intrinsic factor) that normalizes after therapy with broad-spectrum antibiotics has also been considered as a test for small intestinal bacterial overgrowth (the so-called Schilling III test).[14]
References
- ↑ Viana Freitas BR, Kibune Nagasako C, Pavan CR, Silva Lorena SL, Guerrazzi F, Saddy Rodrigues Coy C; et al. (2013). "Immunochemical fecal occult blood test for detection of advanced colonic adenomas and colorectal cancer: comparison with colonoscopy results". Gastroenterol Res Pract. 2013: 384561. doi:10.1155/2013/384561. PMC 3844264. PMID 24319453.
- ↑ Fine KD (1996). "The prevalence of occult gastrointestinal bleeding in celiac sprue". N Engl J Med. 334 (18): 1163–7. doi:10.1056/NEJM199605023341804. PMID 8602182.
- ↑ Kane SV, Sandborn WJ, Rufo PA, Zholudev A, Boone J, Lyerly D; et al. (2003). "Fecal lactoferrin is a sensitive and specific marker in identifying intestinal inflammation". Am J Gastroenterol. 98 (6): 1309–14. doi:10.1111/j.1572-0241.2003.07458.x. PMID 12818275.
- ↑ Friedman M, Ramsay DB, Borum ML (2007). "An unusual case report of small bowel Candida overgrowth as a cause of diarrhea and review of the literature". Dig Dis Sci. 52 (3): 679–80. doi:10.1007/s10620-006-9604-4. PMID 17277989.
- ↑ Koontz F, Weinstock JV (1996). "The approach to stool examination for parasites". Gastroenterol Clin North Am. 25 (3): 435–49. PMID 8863034.
- ↑ Fordtran JS (1967). "Speculations on the pathogenesis of diarrhea". Fed Proc. 26 (5): 1405–14. PMID 6051321.
- ↑ 7.0 7.1 Eherer AJ, Fordtran JS (1992). "Fecal osmotic gap and pH in experimental diarrhea of various causes". Gastroenterology. 103 (2): 545–51. PMID 1634072.
- ↑ Bo-Linn GW, Fordtran JS (1984). "Fecal fat concentration in patients with steatorrhea". Gastroenterology. 87 (2): 319–22. PMID 6735076.
- ↑ Hammer HF (2010). "Pancreatic exocrine insufficiency: diagnostic evaluation and replacement therapy with pancreatic enzymes". Dig Dis. 28 (2): 339–43. doi:10.1159/000319411. PMID 20814209.
- ↑ Carlson J, Fernlund P, Ivarsson SA, Jakobsson I, Neiderud J, Nilsson KO; et al. (1994). "Munchausen syndrome by proxy: an unexpected cause of severe chronic diarrhoea in a child". Acta Paediatr. 83 (1): 119–21. PMID 8193462.
- ↑ Fine KD, Santa Ana CA, Fordtran JS (1991). "Diagnosis of magnesium-induced diarrhea". N Engl J Med. 324 (15): 1012–7. doi:10.1056/NEJM199104113241502. PMID 2005938.
- ↑ Saad RJ, Chey WD (2013). "Breath Testing for Small Intestinal Bacterial Overgrowth: Maximizing Test Accuracy". Clin Gastroenterol Hepatol. doi:10.1016/j.cgh.2013.09.055. PMID 24095975.
- ↑ Corazza GR, Menozzi MG, Strocchi A, Rasciti L, Vaira D, Lecchini R; et al. (1990). "The diagnosis of small bowel bacterial overgrowth. Reliability of jejunal culture and inadequacy of breath hydrogen testing". Gastroenterology. 98 (2): 302–9. PMID 2295385.
- ↑ "Schilling test of vitamin B12 absorption". Br Med J. 1 (5639): 300–1. 1969. PMC 1982167. PMID 5762651.