Short bowel and how to avoid them

A high stomal output is defined as a stoma that produces more than 1.5 L per day.11 Although stomal output may be high due to a short bowel with a small intestinal length of <200 cm, it is important to recognise that there are other causes.¹⁰ It is also important to be aware that the stomal output must be considered in proportion to the intake. For example, 1.5 L per day is high stomal output for a patient drinking 500 ml per day, but it is not high for a patient who has an oral intake of 3 L per day.  

Other causes of a high output state include:

• Intermittent mechanical obstruction due to adhesions or complications such as stomal stenosis
• Intra-abdominal sepsis
• Enteritis (this may be infective [e.g. due to Clostridium difficile], inflammatory, ischaemic or autoimmune [e.g. coeliac disease])
• Changes in medications, including the starting of prokinetics or the weaning of opiate medications or steroids
• Bowel wall oedema associated with hypoalbuminaemia

The consequences of short bowel include:

• Sodium and water depletion (dehydration) 
• Hypomagnesiaemia
• Weight loss
• Deficiencies of trace minerals (e.g. copper, zinc, selenium), fat-soluble vitamins and vitamin B12

It is important to measure serum magnesium and random urine sodium concentrations in all patients who have a jejunostomy. Often just urea and creatinine concentrations are measured and they can be normal in patients with mild dehydration (see mistake 3). The magnesium concentration is often not measured and hypomagnesaemia can present as muscle cramps when levels are very low. Hypomagnesaemia can be detected early, prior to becoming symptomatic, and so prevented (see mistake 4). 

Our suggested algorithm for assessing and managing patients with high stomal output is shown in figure 1.

Figure 1 | Suggested algorithm for assessing and managing high stomal output.

Dehydration in patients with short bowel occurs if stomal output is greater than 1.5 L per day.¹⁰ It is a common misconception that if a patient has normal blood parameters of renal function, including urea and creatinine levels, this excludes dehydration. These values are often affected by the fact that patients may be sarcopenic and their creatinine and urea levels may be below the normal range. As a result, when the creatinine concentration is above the normal range, this indicates that there is significant renal impairment. We would suggest that a combination of several parameters—symptoms, signs and laboratory test results—be used to assess a patient for dehydration (figure 2).

The symptoms and signs of dehydration are well known but often overlooked; however, a urine sodium level of <20 mmol/L reflects dehydration or sodium depletion, and can identify patients with dehydration earlier than other parameters. The aim of treatment should be to keep the urine sodium concentration >20 mmol/L and urine output to  >800 ml/day.¹⁰

Figure 2 | Parameters that can be used to assess for dehydration.

The fluid secretions of the proximal small bowel total more than 4 L,¹⁸ and the majority of this fluid is absorbed in the distal small bowel and colon. In short bowel, the absence of the absorptive distal bowel results in patients being in a secretory state. Hypotonic fluid or solutions with a sodium content of <90 mmol/L lead to a net secretion of sodium and water into the proximal small bowel lumen, which leads to sodium and water depletion.¹⁹ This depletion manifests itself clinically as significant thirst. The belief, therefore, that drinking more will lead to increased water absorption is incorrect. This concept is difficult for patients to accept as it is only natural to want to drink more when thirsty. The correct management of sodium and water depletion and the accompanying thirst is to drink less and to drink an electrolyte mix with a sodium concentration of ≥90 mmol/L. 

We suggest the following regimen:

• Patients should restrict the amount of hypotonic and commercial isotonic fluids that they drink to less than 1 L per day. This includes all beverages—tea, coffee, juices, “isotonic” sports drinks and alcoholic beverages etc.
• Patients should drink 1 L per day of a glucose/saline solution with a sodium content of >90 mmol/L.^20–22 Examples include an electrolyte mix (e.g. St Mark’s electrolyte mix [figure 3]) or other commercial preparations. It is important for the clinician to remember that the palatability of these solutions is a significant issue. To try and overcome this, patients should add concentrated flavourings (e.g. neat fruit-flavoured cordials) when making up the solution. Pre-constituted glucose/saline solution should not be further diluted as this renders the electrolyte mix less effective.
• Patients should be advised to add salt to their meals to the limits of palatability. 
• If the stomal output is >5 L/24 h and the above measures have not worked, patients should consider a period of 24–48 h of “nil-by-mouth”.

Figure 3 | St Mark’s electrolyte mix.

As already mentioned, short bowel is characterised by a high stomal output. To reduce the loss of water, electrolytes, minerals and nutrition, a short bowel regimen can be effective. This regimen comprises restricting oral hypotonic fluids to <1 L per day, drinking ≥1 L of a glucose/saline solution per day, taking antimotility agents before food, taking antisecretory medications, involving a dietitian to give tailored dietary advice, and separating food and fluid at mealtimes. 

In terms of antimotility agents, loperamide is an opioid receptor agonist ^23,24 that is not readily absorbed from the bowel and, thereby, has no addictive or sedative side effects, and in this regard should be considered the first-line treatment.¹⁶ Higher than standard dosages of loperamide are often required as transit through the small bowel in patients with short bowel is often very rapid. These dosages are up to 24 mg four times a day.^15,16,24,25 Loperamide capsules can be opened if they are found to pass into the effluent unchanged. Of note, there has been a safety warning regarding ECG abnormalities and mortality with very-high-dose loperamide in patients taking it for nonlicenced usages.^26,27 We therefore suggest that it would be prudent to check an ECG and measure the QT interval in all patients who require regular loperamide.  Codeine (30–60 mg four times a day) can be used for a similar effect to loperamide,^15,25 but should be considered as a second-line treatment, ideally in combination with loperamide. This preference is due to the systemic side effects of codeine, which include drowsiness and dependence. 

For the antisecretory medications, PPIs (e.g. omeprazole) and H2 antagonists (e.g. ranitidine) reduce gastric secretions and are effective at reducing stomal output with no effect on energy or micronutrient absorption.²⁸ Ranitidine should be given at a dosage of 300 mg orally twice a day, whereas omeprazole should be given at a doseage of 40 mg orally once or twice a day, or 40mg intravenously twice a day (if small bowel length is less than 50 cm).¹⁵ The side effects of these classes of drugs include hypomagnesaemia in patients on a PPI and CNS side effects for H2 antagonists, in particular in elderly patients.¹⁵ 

Somatostatin analogues are also antisecretory medications that can reduce intestinal output while maintaining micronutrient and energy absorption.²⁹ In practice they should only be tried in patients who have a resistant high output, starting at a dose of 50 µg of octreotide twice a day, administered subcutaneously, and titrated up to a dose of 100 µg three times a day. There are several disadvantages to octreotide: the clinical response is unpredictable; it is suggested that it affects postresectional intestinal adaptation; it predisposes patients to cholelithiasis;³⁰ it is expensive, and injections are uncomfortable for patients. For these reasons, octreotide is best reserved for patients in whom other attempts to reduce stoma output have been unsuccessful. In patients for whom octreotide is effective, long-acting depot preparations of octreotide can be used. Note that PPIs and somatostatin analogues have only been shown to reduce secretion in patients who are net ‘secretors’.¹⁵

Other management options such as intestinal lengthening, transplantation and growth factors (e.g. Teduglutide®) may be considered in patients who are atable, in a tertiary setting, but the focus is always ensuring that patients are on an optimal short bowel regimen.