Intestinal failure and nutrition

Chapter 3.16
Intestinal failure and nutrition

Alison Culkin

St Mark’s Hospital, Harrow, UK

Intestinal failure (IF) results from obstruction, dysmotility, surgical resection, congenital defect or disease-associated loss of absorption and is characterised by the inability to maintain protein-energy, fluid, electrolyte or micronutrient balance [1]. It is classified using a combination of severity, type and length of nutrition support required [2,3].

Type 1 – self-limiting, usually <28 days duration and includes postoperative ileus or small bowel obstruction requiring short-term parenteral nutrition (PN).
Type 2 – lasting >28 days and includes complex Crohn’s disease, trauma, intestinal fistula or abdominal sepsis. These patients are severely ill with major GI resections plus septic, metabolic and nutritional complications requiring multidisciplinary intervention with metabolic and nutritional support to permit recovery.

Types 1 and 2 are often referred to as acute intestinal failure. The prevalence is currently unknown but estimates range from 10% to 15% of patients undergoing intestinal surgery [3]. The introduction of enhanced recovery after surgery (ERAS) programmes may minimise the likelihood of developing type 1 in the future. The Association of Surgeons of Great Britain and Ireland has published good principles on the management of patients with acute IF which includes information on prevention and treatment. The detection and management of abdominal sepsis are a priority for patients as this is the most common cause of death if left untreated [4].

The judgement on whether to instigate nutritional support in type 1 IF is often fraught with indecision. The ‘wait and see’ approach or the assessment of ‘bowel sounds’ is misleading and can result in significant periods without adequate nutrition in those who are likely to benefit from PN. In a pragmatic study, patients with inadequate GI function were allocated to PN (n=267) and those with adequate GI function to enteral nutrition (EN) (n=231). Where genuine uncertainty existed, patients were randomised to either PN (n=32) or EN (n=32). In the non-randomised arm, patients receiving EN had a significantly higher mortality and were more likely to receive <80% of their target nutrition compared to PN. In the randomised group there was no difference in mortality between the two routes of nutrition and the authors concluded that if in doubt, PN is superior [4].

Type 3 – generally irreversible and therefore known as chronic intestinal failure, resulting from massive GI resection, leading to short bowel (e.g. mesenteric infarct/thrombosis, intestinal volvulus, inflammatory bowel disease, chronic radiation enteritis). Patients with failure of intestinal motility (e.g. chronic idiopathic intestinal pseudo-obstruction, visceral myopathy/neuropathy and scleroderma) are included in this group and usually require long-term home parenteral nutrition (HPN).

The incidence of type 3 is unknown but estimations can be made based on the number of patients requiring HPN. A recent UK survey reported a prevalence of 7 per million although it is recognised that this may be an underestimate [5]. The reasons for dependency on HPN are short bowel (55.4%), malabsorption (14.8%), fistula (10.1%) and obstruction (7.5%). Crohn’s disease (30.4%), mesenteric ischaemia (18.8%), chronic intestinal pseudo-obstruction (12.8%) and surgical complications (14.2%) represent the major diagnoses responsible for HPN [5].

3.16.1 Consequences of intestinal failure and short bowel

Short bowel is a subcategory of IF and is defined as short bowel syndrome-intestinal failure which results from surgical resection, congenital defect or disease-associated loss of absorption and is characterised by the inability to maintain protein-energy, fluid, electrolyte or micronutrient balances when on a conventionally accepted, normal diet [1]. All patients with short bowel will have problems with fluid and electrolyte balance, particularly in the immediate postoperative period, with nutritional requirements increased as a result of malabsorption.

The consequences of intestinal resection are dependent on four factors:

extent of resection
site of resection
integrity of the remaining bowel
adaptation in the remaining bowel.

Due to the variability in length of the small intestine, the outcome post resection depends on the length of bowel remaining rather than the length resected. A residual small intestine length of <200 cm is deemed short bowel and can lead to nutritional, fluid and electrolyte depletion if not adequately managed. The loss of the ileum and some of the jejunum considerably impairs digestive and absorptive function. When the absorptive function of the colon is no longer available, more fluid and electrolytes will be lost [6]. It has been shown that the following lengths of small intestine are inadequate to be managed on diet alone, and parenteral support of some form is required [7].

<100 cm jejunum will need long-term parenteral fluid and electrolyte replacement.
<75 cm jejunum will need long-term PN, fluid and electrolytes.
<50 cm jejunum plus colon will need long-term PN, fluid and electrolytes.

Citrulline is an intermediary product of glutamine metabolism, mainly occurring in the enterocytes of the small intestine, and therefore citrulline production reflects enterocyte mass. A study of 82 patients with <200 cm of small intestine 2 years post resection found that plasma citrulline concentration correlated with length of small intestine (r = 0.83, P<0.0001) with plasma concentration of <20 µmol/L being prognostic of patients with IF who continued to require HPN [8].

Studies in healthy volunteers have shown that approximately 4 litres of fluid pass the duodenojejunal flexure daily, including saliva, gastric and pancreatic secretions and bile. The upper jejunum secretes fluid as part of normal digestion. This process contributes to the high intestinal losses experienced by patients with short bowel, especially those with a jejunostomy. The ingestion of food and fluid further dilutes these secretions [9], exacerbating losses. Balance studies undertaken on 15 jejunostomy patients demonstrated that in patients with <100 cm of jejunum, the intestinal output exceeded the oral intake. These patients, known as ‘secretors’, are in a constant negative fluid and sodium balance and thus parenteral support is required. Conversely, in patients with >100 cm of jejunum, the intestinal output was less than oral intake. These patients, known as ‘absorbers’, were able to avoid parenteral support using oral electrolyte supplements (glucose-saline solution or sodium chloride tablets) to maintain fluid and sodium balance. However, these lengths were based on healthy bowel and longer lengths are required if disease is present [10]. In patients with a jejunocolic anastomosis (JCA), the problems of fluid and sodium depletion are reduced as the colon is able to reabsorb fluid and sodium efficiently and intestinal transit time is usually unaffected as the colon acts as a ‘brake’, increasing transit time [11].

3.16.2 Fluid and electrolyte management in short bowel

The focus of treatment is to reduce intestinal losses, thereby preventing dehydration and electrolyte disturbances. Restricting oral fluids to <1500 mL per day reduced intestinal losses by 23% [12]. The sodium content of jejunostomy effluent averages 88 mmol/L (range 60–118) and when fluids containing <90 mmol/L of sodium are consumed, the jejunum secretes fluid and sodium from the plasma into the lumen of the intestine which is then lost from the body, resulting in dehydration and sodium depletion [10]. The ingestion of 500 mL of water or tea resulted in negative sodium and fluid balance whereas 500 mL of an oral rehydration solution containing 90 mmol/L led to positive sodium and fluid balance [13]. Jejunal absorption of sodium occurs against a small concentration gradient, dependent on water movement and coupled to glucose and amino acids. Therefore, to optimise sodium and fluid absorption in the jejunum, patients are encouraged to consume an oral rehydration solution which has a sodium content of 90 mmol/L (20 g of glucose, 3.5 g of sodium chloride and 2.5 g of sodium bicarbonate). Compliance can be poor due to palatability and the use of overnight infusions via a gastrostomy tube has enabled patients to become independent from HPN.

3.16.3 Pharmaceutical management

The aim of pharmaceutical intervention is to reduce intestinal losses and increase intestinal transit, allowing an increase in the time that nutrients and fluid are in contact with the GI lumen. Post resection, increased gastric acid production and reduced intestinal transit time exacerbate the problems of dehydration and sodium depletion. Gastric antisecretory drugs, such as proton pump inhibitors and H₂ antagonists, have been shown to reduce intestinal losses by 1.5 kg /day [14]. Patients who fail to absorb oral proton pump inhibitors may benefit from parenteral administration [15].

The somatostatin analogue octreotide reduces gastric, pancreatic and biliary secretions but research using a long-acting somatostatin in short bowel confirmed a lack of efficacy [16]. Others have demonstrated that while the treatment can reduce jejunostomy output, its use is associated with the suppression of serum concentrations of gut hormones including insulin, gastrin, glucagon and peptide tyrosine tyrosine (PYY) and could therefore interfere with intestinal adaptation [17]. In practice, octreotide is usually reserved for patients with uncontrollable intestinal losses which are refractory to conventional treatment.

Antimotility agents such as loperamide and codeine phosphate increase GI transit time, decrease intestinal output and reduce electrolyte losses [18]. High doses are normally required in order to achieve the desired outcome. Clonidine, an alpha-2 adrenergic agonist, has been investigated as an antimotility agent. The benefit of this treatment is transdermal application, removing the potential for malabsorption via the GI tract. Clinically significant reductions in intestinal volume, weight and sodium and increased urine production equating to improved hydration were demonstrated in eight jejunostomy patients [19].

Removal of the terminal ileum may cause bile acid depletion, resulting in high intestinal losses. Cholylsarcosine, a synthetic bile acid, has been shown to improve fat absorption in patients with and without a colon although the overall energy gain was poor (6%) with no other benefits demonstrated [20].

Magnesium deficiency is common and can usually be corrected with an oral magnesium preparation. Most magnesium salts result in an increased intestinal output and therefore high doses are required. If oral supplements are ineffective then magnesium sulphate can be added to normal saline and given subcutaneously or intravenously to maintain plasma concentrations [21]. Vitamin D increases intestinal and renal absorption of magnesium so concentrations should be monitored.

Further research is required to establish efficacy and optimum dosage of all medications used in the management of short bowel.

3.16.4 Adaptation

In the postoperative period, spontaneous intestinal adaptation occurs in an attempt to minimise the consequences of intestinal resection. The presence of nutrients in the GI lumen is essential to take advantage of this process so patients should not remain nil by mouth for prolonged periods. Adaptation reaches a plateau 2 years post resection and the optimum diet to stimulate human intestinal adaptation is not yet known as most data come from animal models. Complex diets were found to exert a more potent effect than elemental diets in pigs, suggesting that a polymeric formula is superior [22]. The soluble fibre pectin is fermented by colonic bacteria into short-chain fatty acids which are known to contribute significantly to energy balance in patients with a JCA. A recent study in humans failed to demonstrate improvements in macronutrient or fluid absorption [23].

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