Newcastle Laboratories

Faecal electrolytes

Clinical Background:

Faecal electrolytes and osmolality are useful in assessing the cause of watery diarrhoea. 

Faecal electrolytes and osmolality are useful in assessing the cause of watery diarrhoea. 

Test Details

  • Discipline:

    Biochemistry

    Biochemistry

  • Specimen Container Adult:

    Faeces in universal container

    Faeces in universal container

  • Specimen Container Paediatric:

    Faeces in universal container

    Faeces in universal container

  • Minimum Volume Adult:

    5 mL liquid faeces

    5 mL liquid faeces

  • Minimum Volume Paediatric:

    5 mL liquid faeces

    5 mL liquid faeces

  • Special Requirement:

    Faeces must be liquid

    Faeces must be liquid

  • Sample Stability:

    After centrifugation:

    at +2° to +8°C      48hr
    at -15° to -20°C    14 days

    After centrifugation:

    at +2° to +8°C      48hr
    at -15° to -20°C    14 days

  • Interpretation:

    The magnitude of the osmolar gap, the difference between the measured faecal osmolality and that contributed by sodium and potassium, calculated by 2(Na+ + K+), indicates the presence or absence of...

    The magnitude of the osmolar gap, the difference between the measured faecal osmolality and that contributed by sodium and potassium, calculated by 2(Na+ + K+), indicates the presence or absence of poorly absorbable solute(s). In osmotic diarrhoea the osmolal gap is typically >30mmol/kg and secretory diarrhoea the osmolal gap <30mmol/kg.

    It is important to note that faecal osmolality may be increased factitiously because carbohydrates may be metabolised by colonic bacteria causing an increase faecal in osmolality. This can be minimised by analysing samples with 24h of receipt or freezing samples until they are analysed.

    Some centres prefer to calculate the faecal osmolal gap by: serum osmolality −[2(Na+ + K+)], the cut off used for this equation has been >100mmol/kg (osmotic) and <100mmol/kg (secretory). This approach is to avoid factitious increases in the osmolal gap due to bacterial fermentation.

    Faecal sodium of >150 mmol/L and an osmolality of >375-400 mmol/kg suggests contamination with concentrated urine.

     

    Osmotic Diarrhoea:

    An osmolal gap >30 mmol/kg indicates osmotic diarrhoea. Faecal potassium concentration and daily excretion rate are usually below the median level in patients with osmotic diarrhoea. Modest increases (2x) in faecal chloride concentration and excretion rate may be observed when faecal sodium is elevated in association with osmotic diarrhoea. Osmotic agents such as magnesium, sorbitol, or polyethylene glycol may be the cause of this. Magnesium concentration of >200mmol/L is frequently associated with decreased faecal sodium and potassium and is an indicator of excessive consumption of magnesium, a common cause of osmotic diarrhoea.

     

    Secretory Diarrhoea:

    An osmolal gap <30 mmol/kg indicates secretory diarrhoea. If sodium concentration or 24h sodium excretion rate is 2-3 times normal and osmotic gap >30 mmol/kg, secretory diarrhoea is also indicated. Agents such as phenolphthalein, bisacodyl or cholera toxin should be suspected. 

    For very low stool osmolality, consider factitial diarrhoea.

    Normal or low faecal sodium in association with high faecal 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 gastrointestinal tract that might be induced by agents such as cholera toxin or hypersecretion of vasointestinal peptide.

     

    Congenital chloride losing diarrhoea (chloridorrhoea)

    Congenital chloride diarrhoea (CLD) is a rare autosomal recessive disorder that has a high incidence inFinland(1:20,000-1:43,000),Poland,Saudi ArabiaandKuwait. High faecal chloride concentration (>90 mmol/L) is the standard for diagnosis of CLD, although DNA analysis is also available.

    It presents with persistent secretory diarrhoea, polyhydramnios and intractable diarrhoea from birth. The watery diarrhoea has a high Cl- content and low pH and may cause dehydration and hypochloraemic metabolic alkalosis. CLD may be fatal if not adequately treated. Long-term prognosis is generally favourable, but complications such as renal disease, hyperuricaemia, inguinal hernias, spermatoceles, and sub-fertility are possible

    CLD is caused by mutations in the SLC26A3 gene, encoding a Na+-independent Cl/HCO3- exchanger. The diagnosis is generally made on the basis of high faecal chloride concentration in patients with serum electrolyte homoeostasis corrected by salt substitution.

     

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  • Routine Contact Name:

    Duty Biochemist

  • Routine Telephone:

    Freeman: 0191 244 8889
    RVI: 0191 282 9719

    Freeman: 0191 244 8889
    RVI: 0191 282 9719

  • Routine Email:

Availability:

Available daily during full access hours
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Turn Around:

Within 1 day

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