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Update on the management of intestinal failure

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ABSTRACTIntestinal failure is a serious complication of conditions such as inflammatory bowel disease, mesenteric ischemia, and radiation enteritis—and of extensive bowel resection performed because of these diseases. Imbalances of fluids and electrolytes and poor nutritional status manifest as chronic diarrhea or increased ostomy output. Prompt referral to a center specializing in intestinal rehabilitation is key to achieving nutritional homeostasis and, in some cases, can help the patient return to oral food intake. We review the intestinal sequelae of bowel resection and provide an update on intestinal rehabilitation with dietary modification, drug therapy, and parenteral nutrition. We also review current experience with intestinal transplant, a potentially lifesaving option in select patients when intestinal rehabilitation fails or parenteral nutrition causes severe complications.

KEY POINTS

  • Some patients with intestinal failure require lifelong parenteral nutrition, which increases the risk of complications such as infection and liver disease. For these patients, intestinal transplant has emerged as a therapeutic option toward the goal of restoring nutritional autonomy.
  • The complexities of intestinal failure require collaboration of multiple specialists—gastroenterologists, surgeons, dietitians, nurses, psychiatrists or psychologists, pharmacists, and social workers. This multidisciplinary team is essential to intestinal rehabilitation.
  • Dietary modification is the single most effective means of weaning patients safely from parenteral nutrition.


 

References

Intestinal failure, the inability of the gut to maintain nutritional homeostasis,1 is a complication of vascular thrombosis, inflammatory bowel disease, radiation enteritis, obstruction, and other conditions, and of removing segments of the small and large intestines in response to these diseases.1,2 Imbalances of fluids and electrolytes, dehydration, malabsorption, vitamin and mineral deficiencies, chronic diarrhea, and increased ostomy output contribute to a decline in the quality of life and in the survival rate in these patients.2,3

Referral to an intestinal rehabilitation program that combines gastroenterology, nutrition, pharmacy, nursing, and social work can improve nutritional status and quality of life.4 Whenever possible, the goal of rehabilitation is nutritional autonomy, helping the patient make the transition to an independent oral diet.4 In selected patients in whom rehabilitation is not effective, intestinal transplant may be an option.

In this article, we review the intestinal adaptations that follow surgical resection and provide an update on intestinal rehabilitation techniques such as dietary modification, drug therapy, and parenteral nutrition. We also review experience with intestinal transplant in patients with intestinal failure.

INTESTINAL FAILURE

Intestinal failure results from reduction in enterocyte cell mass, obstruction, dysmotility, surgical resection, congenital defects, or disease-associated loss of absorption with suboptimal nutritional autonomy.5 Patients often suffer from extensive nutrient, electrolyte, and fluid abnormalities proportional to the remnant length and part of the intestine removed.5

Epidemiologic studies have demonstrated that short-bowel syndrome is the most common cause of intestinal failure in adults and children.6,7 Short-bowel syndrome is defined as a small-bowel length less than 200 cm, most commonly from extensive resections for inflammatory bowel disease.6 In children, the syndrome is also defined by a residual small-bowel length of less than 25% expected for gestational age.7

Table 1 lists the frequencies of the underlying disorders leading to intestinal failure or short-bowel syndrome in one series.8

INTESTINAL ADAPTATION

The gastrointestinal tract is the only organ for nutrient, fluid, and electrolyte absorption.9 Every day, 8 to 9 L of fluids and secretions reach the small intestine, comprising about 2 to 3 L of oral fluids, 1 L of saliva, 2 L of gastric juices, 1 L of bile, and 2 L of pancreatic juices.9 Approximately 7 to 8 L are reabsorbed by the small intestine and 1 to 2 L by the colon.9

Although carbohydrates, lipids, and proteins are absorbed through the entire small intestine and colon, site-specific digestion and absorption of different nutrients occur in different parts of the gastrointestinal tract.10 Also, certain nutrients may need site-specific receptors or transporters for their absorption,10 for example:

  • Iron in the duodenum and proximal jejunum1
  • Lactose in the brush border membrane of the jejunum and proximal ileum, where most of the enzyme lactase is present
  • Vitamin B12 and bile salts in the distal ileum.

Hence, resection of a specific part of the intestine may predict deficiencies the patient may encounter after surgery.

The diarrhea that occurs in short-bowel syndrome may be due partly to loss of neurohumoral mediators that govern gastrointestinal transit time, most importantly cholecystokinin, peptide YY, and glucagon-like peptide 1.11 After contact with lipid- or protein-rich nutrients, cholecystokinin is released from the proximal small intestine, which decreases the gastric emptying to maximize nutrient digestion.12 Additionally, release of peptide YY and glucagon-like peptide 1 from the ileal L cells decreases gastric and intestinal motility. These mediators prolong gastrointestinal transit, increase nutrient processing time, and enhance absorption.12

After massive intestinal resection, the remnant bowel undergoes physiologic and functional adaptation to maintain nutritional homeostasis.13 Enterocytes express membrane-bound transporters and undergo accelerated cell division to enhance the absorptive surface area.13 Intestinal hypertrophy, which includes an increase in villous diameter and crypt height, continues for 2 years or more after intestinal resection, leading to greater absorptive surface area.14 It is estimated that villous height may increase by as much as 80%, illustrating a dynamic process in response to intestinal stress.15

Luminal nutrients are essential to the stimulation of enterocyte cells through paracrine mechanisms as well as through the up-regulation of colonic peptide transporter PepT1.15 Furthermore, gut motility is initially decreased in order to increase the concentration of local luminal growth factors.16

Other factors that may affect intestinal adaptation are the length of the residual colon and small intestine, enteral growth, and enterotropic factors.16 And especially in patients with short-bowel syndrome, complications such as malabsorption secondary to pancreatic insufficiency or rapid transit, excessive gastric acid secretion, bile acid wasting due to terminal ileum resection, and bacterial overgrowth in the small intestine result in worsened nutritional status and poor quality of life.16

Key factors that affect the degree of nutritional deficiencies

The degree of nutritional deficiencies and fluid and electrolyte imbalances depends on the length and location of resection and whether the colon is still continuous with the small intestine.17 Normal small-bowel length in adults is highly variable and can be up to 600 cm. Malnutrition after surgical resection usually occurs when more than three-fourths of intestinal tissue is removed.17 However, because of intestinal adaptation, patients with 50% of remnant small bowel may be able to achieve nutritional autonomy.18 Furthermore, because absorption of nutrients occurs primarily in the first 150 cm of the small intestine, resections of this anatomic region have the highest probability of resulting in malnutrition.18

After extensive intestinal resection, absorption of water and electrolytes is better and intestinal transit time is longer if the colon is still continuous with the rest of the gastrointestinal system.19 Approximately 100 cm of remnant intestinal tissue without colonic continuity or 60 cm with colonic continuity is needed to ensure the possibility of nutritional autonomy and independence from parenteral nutrition.19 Severe malnutrition and fluid and electrolyte imbalances can be prevented by appropriate and timely multidisciplinary care and early referral for intestinal rehabilitation.

INTESTINAL REHABILITATION AND NUTRITIONAL AUTONOMY

The aim of intestinal rehabilitation is to improve quality of life by reversing malnutrition and promoting nutritional autonomy, ie, independence from parenteral nutrition (Table 2).20 The complex nature of intestinal failure necessitates collaboration of multiple specialists—gastroenterologists, surgeons, dietitians, nurses, psychiatrists or psychologists, pharmacists, and social workers.20

Although most patients with intestinal failure initially require parenteral nutrition to maintain nutritional homeostasis, progressive adaptation of the remnant intestine enables a transition to enteral nutrition.21 Stimulation of the remnant intestine by enteral feeding reduces the complications of parenteral nutrition and encourages intestinal adaptation.21

Outpatient participation in an intestinal rehabilitation program can facilitate weaning from parenteral nutrition. Patients are monitored and supported during dietary modification, pharmacologic interventions, and reconstructive surgeries.21 A study of 61 patients with short-bowel syndrome undergoing a 3-week program of intestinal rehabilitation (recombinant human growth hormone, glutamine, enteral nutrition, and parenteral nutrition) reported an overall survival rate of 95% with an 85% success rate in weaning from parenteral nutrition during a mean follow-up of 50 (± 24) months.22 Permanent dependence on parenteral nutrition despite rehabilitation was predicted by length of the small bowel less than 100 cm and by the absence of terminal ileum and colon.22

Permanent intestinal failure, defined by the inability to wean from parenteral nutrition and restore nutrition autonomy, may require early referral for evaluation for intestinal and multivisceral transplant. Early referral improves survival rates, possibly because of fewer complications from parenteral nutrition.4

DIETARY MODIFICATION

Dietary modification is the single most effective means of weaning patients safely from parenteral nutrition (Table 3).23,24 Small, frequent feedings help reduce symptoms associated with rapid intestinal transit and increase the activity of luminal growth factors.23 Likewise, limits on intake of simple sugars, stimulants such as caffeine or insoluble fiber, and hypo- or hypertonic fluids decrease intestinal losses and the risk of dehydration.23 Low sugar loads also aim to reduce the occurrence of d-lactic acidosis and bacterial overgrowth in the small intestine.23 Patients who cannot maintain positive fluid balance may require standardized oral rehydration (Table 4) to improve absorption by way of the sodium-glucose coupled transporters at the brush border membrane, or they may require intravenous fluid supplementation.25

Colonic continuity

Other dietary recommendations depend on colonic continuity. In 1994, Nordgaard et al26 compared the effects of high-carbohydrate and high-fat diets in eight patients with colonic continuity and six patients with jejunostomies. The authors noted that a high-carbohydrate diet (60% carbohydrate, 20% fat) reduced fecal loss of energy and increased energy absorption in patients with colonic continuity. However, patients with an end-jejunostomy experienced equal fecal losses of carbohydrates and fat proportional to the amount consumed. The authors concluded that the presence of colonic bacteria promoted carbohydrate salvage, ie, the fermentation of malabsorbed carbohydrates to easily absorbed short-chain fatty acids.26

The colon can salvage as much as 1,000 kcal/day in patients with less than 200 cm of small bowel, and the presence of at least 50% of colon in continuity has been shown to reduce parenteral nutrition requirements by half in patients with less than 100 cm of small bowel.27 As a result, a diet high in complex carbohydrates and soluble fiber supplements is recommended in cases of preserved colon to promote adaptation and nutritional autonomy.27

Another aim of a high-carbohydrate, low- fat diet is to prevent calcium oxalate-related nephrolithiasis and choleretic diarrhea.26

In summary, patients with short-bowel syndrome with or without colonic continuity need different dietary regimens to attain nutritional autonomy.

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