Acute diarrhea laboratory findings: Difference between revisions
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{{Acute diarrhea}} | {{Acute diarrhea}} | ||
{{CMG}}; {{AE}} | {{CMG}}; {{AE}}{{Cherry}} | ||
==Overview== | ==Overview== | ||
Laboratory investigations performed in the evaluation of patients with acute diarrhea include spot [[Stool examination|stool analysis]], detection of [[occult blood]], [[white blood cells]], [[stool culture]], quantitative [[Stool examination|stool analysis]], fecal weight, stool osmotic gap, [[Fecal pH test|fecal pH]], [[Fecal fat|fecal fat concentration]] and analysis for [[Laxative|laxative abuse]]. According to the ACG guidelines, [[stool culture]] is done only in cases where the patient is at high risk of spreading the disease to others. [[Stool examination|Stool diagnostic studies]] are performed when symptoms last for >7 days, patient has [[dysentery]] or moderate-to-severe diarrhea and to determine [[etiology]] to enable directed [[pathogen]]-specific therapy. [[Antibiotic sensitivity|Antibiotic sensitivity testing]] for management of acute diarrhea is not advised. | |||
Laboratory | |||
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==Laboratory Findings== | ==Laboratory Findings== | ||
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** [[White blood cells|Fecal leukocytes]] | ** [[White blood cells|Fecal leukocytes]] | ||
** Test for ''[[C. difficile]]'' | ** Test for ''[[C. difficile]]'' | ||
* According to the ACG guidelines, the following points should be kept in mind in the diagnostic evaluation of acute diarrhea patients: | |||
** [[Stool culture]] is done only in cases where the patient is at high risk of spreading the disease to others. | |||
** Stool diagnostic studies are performed in the following cases: | |||
*** Symptoms lasting >7 days | |||
*** [[Dysentery]] | |||
*** Moderate-to-severe diarrhea | |||
*** Determination of [[etiology]] to enable directed [[pathogen]]-specific therapy | |||
** [[Antibiotic sensitivity|Antibiotic sensitivity testing]] for management of acute diarrhea is not advised. | |||
===Laboratory Evaluation of Acute Diarrhea=== | ===Laboratory Evaluation of Acute Diarrhea=== | ||
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=====Stool Osmotic Gap===== | =====Stool Osmotic Gap===== | ||
* The stool osmotic gap is calculated from electrolyte concentrations in [[Human feces|stool]] water by the following formula : 290 - 2([Na+] + [K+]). | * The stool osmotic gap is calculated from [[Electrolyte|electrolyte concentrations]] in [[Human feces|stool]] water by the following formula : 290 - 2([Na+] + [K+]). | ||
* The [[Osmolarity|osmolality]] of stool present in the [[Intestine|distal intestine]] is preferred over [[Feces|fecal]] fluid, as measured osmolality of [[Feces|fecal]] fluid increases with [[Fermentation|bacterial fermentation]] of [[Carbohydrate|carbohydrates]] to osmotically active [[Organic acid|organic acids]]. | * The [[Osmolarity|osmolality]] of stool present in the [[Intestine|distal intestine]] is preferred over [[Feces|fecal]] fluid, as measured osmolality of [[Feces|fecal]] fluid increases with [[Fermentation|bacterial fermentation]] of [[Carbohydrate|carbohydrates]] to osmotically active [[Organic acid|organic acids]]. | ||
* Stool osmotic gap in cases of osmotic diarrhea is characterized by osmotic gaps >125 mOsm/kg and in secretory diarrheas, osmotic gap is <50 mOsm/kg. | * Stool osmotic gap in cases of osmotic diarrhea is characterized by osmotic gaps >125 mOsm/kg and in secretory diarrheas, osmotic gap is <50 mOsm/kg. | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sudarshana Datta, MD [2]
Overview
Laboratory investigations performed in the evaluation of patients with acute diarrhea include spot stool analysis, detection of occult blood, white blood cells, stool culture, quantitative stool analysis, fecal weight, stool osmotic gap, fecal pH, fecal fat concentration and analysis for laxative abuse. According to the ACG guidelines, stool culture is done only in cases where the patient is at high risk of spreading the disease to others. Stool diagnostic studies are performed when symptoms last for >7 days, patient has dysentery or moderate-to-severe diarrhea and to determine etiology to enable directed pathogen-specific therapy. Antibiotic sensitivity testing for management of acute diarrhea is not advised.
Laboratory Findings
Laboratory investigations performed in the workup of patients with acute diarrhea include complete blood count, glucose levels, white blood cells (WBC) detection, urine analysis, calcium levels, Thyroid stimulating hormone (TSH) levels, complete metabolic panel 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
- According to the ACG guidelines, the following points should be kept in mind in the diagnostic evaluation of acute diarrhea patients:
- Stool culture is done only in cases where the patient is at high risk of spreading the disease to others.
- Stool diagnostic studies are performed in the following cases:
- Antibiotic sensitivity testing for management of acute diarrhea is not advised.
Laboratory Evaluation of Acute Diarrhea
Spot Stool Analysis
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 Plesiomonas species.
- In immunocompromised patients, stool culture is included as a part of routine investigations to rule out infection due to bacteria such as Salmonella, Campylobacter, protozoa and fungi.[4]
- Protozoa may detected by the use of fecal enzyme-linked immunosorbent assay (ELISA).[5]
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 includes measurement of:
- Stool weight
- Stool fat content
- Stool osmolality
- Stool electrolyte concentrations
- Magnesium levels
- 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 present in the distal intestine is preferred over fecal fluid, as measured osmolality of fecal fluid increases with bacterial fermentation of carbohydrates to osmotically active organic acids.
- Stool osmotic gap in cases of osmotic diarrhea is characterized by osmotic gaps >125 mOsm/kg and in secretory diarrheas, osmotic gap is <50 mOsm/kg.
- In mixed cases, the osmotic gap lies between 50-125mOsm/kg.[7]
Fecal pH
- A fecal pH of < 5.3 is indicative of carbohydrate malabsorption.
- A fecal pH of > 5.6 may exclude carbohydrate malabsorption as the cause of acute diarrhea.[7]
Fecal Fat Concentration and Output
- In normal subjects, fecal fat ouput is approximately 9% of dietary fat intake (7g/day).
- Fecal fat levels >7g/day are suggestive of steatorrhea.
- Fecal fat concentration of <9.5 g/100 g of stool: Small intestinal malabsorptive syndromes[8]
- Fecal fat concentrations of ≥9.5 g/100 g of stool: Pancreatic and biliary steatorrhea[9]
Analysis for Laxative Abuse
Stool analysis for laxatives is done in the assesment of diarrhea of unknown cause. This includes the following techniques:
- Treatment of 3ml of stool supernatant or urine with a single drop of concentrated NaOH with resulting pink or red color, due to alkalinization is the simplest test for laxatives.
- Analysis of stool using chromatography for emetine, bisacodyl and its metabolites, phenolphthalein, etc may also be performed.
- Calculation of stool osmotic gap may be helpful in pinpointing the laxative responsible for acute diarrhea:
- Stool osmotic gap <50: Sodium sulfate or sodium phosphate[10]
- Stool osmotic gap >125 mOsm/kg: Magnesium laxatives[11]
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.