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The medical management of intestinal failure: methods to reduce the severity

Proceedings of the Nutrition Society (2003), 62, 703–710
03ociety (2003)0029-6651 Nutrition Society 2003 623 The Annual Meeting of the Clinical Nutrition and Metabolism Group of the Nutrition Society with the British Association for Parenteral and Enteral Nutrition, in conjunction with the 24th Congress of the European Society for Parenteral and Enteral Nutrition, was held at the Scottish Exhibition and Conference Centre, Glasgow on 4 September 2002 Symposium on ‘Intestinal failure’
The medical management of intestinal failure:
methods to reduce the severity
Leicester Royal Infirmary, Leicester LE1 5WW, UK Dr Jeremy Nightingale, fax +44 116 2586985, email jnight@globalnet.co.uk A new definition of intestinal failure is of reduced intestinal absorption so that macronutrientand/or water and electrolyte supplements are needed to maintain health or growth. Severeintestinal failure is when parenteral nutrition and/or fluid are needed and mild intestinal failure iswhen oral supplements or dietary modification suffice. Treatment aims to reduce the severity ofintestinal failure. In the peri-operative period avoiding the administration of excessive amounts ofintravenous saline (9 g NaCl/l) may prevent a prolonged ileus. Patients with intermittent bowelobstruction may be managed with a liquid or low-residue diet. Patients with a distal bowel entero-cutaneous fistula may be managed with an enteral feed absorbed by the proximal small bowelwhile no oral intake may be needed for a proximal bowel enterocutaneous fistula. Patientsundergoing high-dose chemotherapy can usually tolerate jejunal feeding. Rotating antibioticcourses may reduce small bowel bacterial overgrowth in patients with chronic intestinal pseudo-obstruction. Restricting oral hypotonic fluids, sipping a glucose–saline solution (Na concentrationof 90–120 mmol/l) and taking anti-diarrhoeal or anti-secretory drugs, reduces the high output froma jejunostomy. This treatment allows most patients with a jejunostomy and > 1 m functioningjejunum remaining to manage without parenteral support. Patients with a short bowel and a colonshould consume a diet high in polysaccharides, as these compounds are fermented in the colon,and low in oxalate, as 25 % of the oxalate will develop as calcium oxalate renal stones. Growthfactors normally produced by the colon (e.g. glucagon-like peptide-2) to induce structural jejunaladaptation have been given in high doses to patients with a jejunostomy and do marginallyincrease the daily energy absorption.
Intestinal failure: Short bowel: Clinical management: Nutritional support: Water and
electrolyte status
The commonly quoted definition of intestinal failure is of Unfortunately, there is no simple clinical or biochemical ‘reduction in functioning gut mass below the minimum measurement to define and grade the severity of intestinal amount necessary for adequate digestion and absorption of failure (as serum creatinine in renal failure or blood gases in nutrients’ (Fleming & Remington, 1981). This definition respiratory failure), although xylose absorption or post- has often been interpreted as referring only to patients who prandial plasma citrulline (Crenn et al. 2000) measurements need parenteral nutrition. This interpretation would be similar to defining patients as having renal failure only when A new definition of intestinal failure is of reduced they needed dialysis. This definition makes no mention of intestinal absorption so that macronutrient and/or water and water and electrolyte losses and yet this issue dominates the electrolyte supplements are needed to maintain health and/or clinical management of most patients with intestinal failure.
growth (Nightingale, 2001a). Without such treatment or Corresponding author: Dr Jeremy Nightingale, fax +44 116 2586985, email jnight@globalnet.co.uk
compensatory mechanisms undernutrition and/or dehy- While methods for reducing the severity of intestinal failure dration will result. This definition allows the severity of include the judicial use of surgery, the present article only intestinal failure to be graded according to the type of nutri- addresses medical or dietary methods for reducing the tional support needed (Fig. 1) and a wide range of underlying severity of intestinal failure, with particular reference to diagnoses are included (Fig. 2). Acute (or temporary) intes- tinal failure is potentially reversible and most commonlyencountered, with > 90 % of patients with severe intestinal Methods for reducing the severity of acute intestinal
failure being in the peri-operative period (Kennedy et al.
2002). Chronic intestinal failure is less common and mostpatients have a short bowel.
Patients with acute intestinal failure as the result of a distal There are four aims in the management of patients with entero-cutaneous fistula can often be managed with an enteral feed (often a peptide feed) rather than parenteral nutrition,nil by mouth with or without octreotide (Carlson, 2001).
to provide the nutrition and/or water and electrolytes Intermittent small bowel obstruction can be managed with a necessary to maintain health and/or growth; to reduce the severity of intestinal failure; In a study of patients undergoing a colonic resection for to prevent and treat complications, including those cancer two groups each of ten patients were randomized to related to the underlying disease, intestinal failure itself receive either a ‘normal’ (more than 3 litres water and 154 mmol Na/24 h) or a ‘restricted’ (< 2 litres water and 77 mmol Na/24 h) peri-operative fluid management (Loboet al. 2002). On the second post-operative day patients inthe ‘normal’ group had gained 3 kg weight. Measurements of gut function (solid and liquid gastric emptying, time to pass flatus and stool, and time before eating solid food) weresignificantly slower in the ‘normal’ group (P < 0·03 in allcases). Complications were more frequent and hospital stayslonger in those having the normal regimen. This studydemonstrated that the administration of large amounts offluid, especially saline (9 g NaCl/l), to peri-operative Moderate
patients could cause and prolong the period of acute intes-tinal failure (ileus).
Patients undergoing high-dose chemotherapy, particularly as part of bone marrow transplantation, have traditionallybeen given parenteral nutrition. However, there is increasing evidence that enteral feeding may suffice (and be safer) if the nausea or vomiting is controlled. Jejunal feeding may be Fig. 1. Severity of intestinal failure. An aim of treatment is to reduce
given via a percutaneous endoscopic gastrostomy with a jejunal tube placed through it (Steward et al. 2001).
Fig. 2. Classification of intestinal failure.
Methods for reducing the severity of chronic intestinal
Net ‘secretors’ generally have < 1 m jejunum and have an failure: intestinal dysmotility
intestinal output that is greater than the oral intake, so thatthey are in negative intestinal water and Na balance, and These patients are relatively uncommon and have the thus need parenteral support (Fig. 4). Net ‘absorbers’, on the symptoms and signs of intestinal obstruction without a other hand, have 1–2 m jejunum remaining and have an mechanical blockage. This outcome can be due to an intestinal intestinal output that is less than the oral intake, so that they myopathy (e.g. systemic sclerosis or visceral myopathy) or achieve positive water and Na balance and can be managed neuropathy (e.g. diabetes or visceral neuropathy) or a combi- with oral therapy (Nightingale et al. 1990).
nation (e.g. amyloidosis). Treatment addresses the main Patients with a jejuno–colic anastomosis are often well problems of abdominal pain, vomiting, diarrhoea (consti- after surgery except for diarrhoea, which is worse with food.
pation in the early stages) and undernutrition. Abdominal pain They may feel well after the resection but present later with may be treated with antispasmodics, transcutaneous or severe weight loss due to malabsorption.
sublingual opiates, or octreotide. Vomiting may be helped byprokinetic agents (metoclopramide, domperidone, cisapride,ondansetron or erythromycin) or by antibiotics. Diarrhoea Assessment of a patient with a high-output stoma may be helped by drugs that delay gastrointestinal transit(loperamide or codeine phosphate) or by antibiotics (Powell- A patient with a high-output stoma (usually from the small bowel) is likely to feel thirsty. The patient may have suddenly Undernutrition, in addition to vomiting and diarrhoea, lost > 2 kg in weight and may have a low urine output. The may be considerably helped by using oral antibiotics urea and creatinine levels may be high if the patient is very (rotating every 6–8 weeks or short courses of 1–2 weeks) to dehydrated. A random urine Na concentration of < 10 mmol/l treat small-bowel bacterial overgrowth. Traditionally, metro- suggests Na depletion. Hypomagnesaemia (see p. 706) is nidazole, tetracycline and cephalosporins have been given, common. Measurement of the residual bowel length is useful although an amoxycillin–claevulinic acid combination or and can be performed using an opisometer in a small-bowel ciprofloxacin may be more effective.
Ba study if the length was not measured at the time of surgery(Nightingale et al. 1991a; Carbonnel et al. 1996).
Abdominal sepsis and partial small-bowel obstruction Methods for reducing the severity of chronic intestinal
can give rise to a high-output stoma and may be excluded failure: short bowel
clinically with the help of radiology (computerized tomog- Two types of patients with a short bowel are shown in Fig. 3, raphy scans and contrast studies). Occasionally, infective those with a jejunostomy and those with a jejuno–colic enteritis (e.g. by Clostridium difficile), recurrent disease or an internal entero-enteral fistula may cause a high-output Patients with a jejunostomy have a high-output stoma, stoma. Patients who have suddenly stopped corticosteroids which is apparent immediately after surgery, especially (e.g. after a colectomy for ulcerative colitis) can have acute when the patient starts to take food and drink. There are two adrenal insufficiency, which includes an increase in stomal types of patient with a short bowel and a high-output stoma.
08.00 10.00 12.00 14.0016.00 18.00 20.00 22.0024.00 02.00 04.00 06.00 08.00 Fig. 4. Oral intake (---) and stomal output (
in a patient who has 0·3 m residual jejunum. Note the large net Fig. 3. Types of patient with a short bowel: (a) a jejunostomy; (b) a
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a concentration gradient, it ferments carbohydrate, slows gastrointestinal transit and promotes adaptive changes.
precarious Mg balance mainly as a result of Na depletion A diet high in polysaccharides, although bulky, is and secondary hyperaldosteronism (Fig. 6). Initially, salt encouraged as the carbohydrate is fermented in the colon and water depletion (and thus secondary hyperaldos- to produce short-chain fatty acids, which when absorbed teronism) are treated, then an oral Mg compound (usually provide a source of energy (Nordgaard et al. 1994; Table 2).
three MgO (4 mmol) capsules at night) is given. If these A diet rich in polysaccharides needs to be of a considerable measures fail, 1-α-hydroxycholecalciferol may be given size (after the ‘malabsorption factor’ has also been taken into (Selby et al. 1984) in gradually-increasing doses, ensuring account). However, as these patients are often fastidious that hypercalcaemia does not occur. Regular Mg infusions, eaters who quickly feel satiated, such a diet is rarely practical.
usually with saline, may be necessary.
A diet rich in mono- and oligosaccharides can occasionally cause D(−)-lactic acidosis. Lactic acid produced by man is the through the stoma occurs only when < 0·50 m jejunum L(+)-isomer; however, abnormal bacterial or fungal coloni- remains (Nightingale et al. 1990). A low serum K level may zation of the colon may form the D(−)-isomer, which after be consequent upon secondary hyperaldosteronism (Night- absorption cannot be metabolized and can cause ataxia, ingale, 2001b) resulting from Na depletion and, thus, large blurred vision, ophthalmoplegia and nystagmus. D(−)-lactic urinary K losses. It may also occur secondary to Mg acidosis is suspected when these symptoms occur and a depletion. Thus, K does not usually need to be given, but Nadepletion and hypomagnesaemia should be corrected.
Table 2. Energy absorption in patients with a short bowel given three
diets, each for 3 d (Nordgaard et al. 1994) Dietary advice, oral or enteral nutritional support for These patients malabsorb 30–60 % of the oral or enteral nutrition given and this ‘malabsorption factor’ needs to betaken into account and more energy than normal consumed.
To keep up with these losses an enteral feed may be given at night to utilize the gut at a time when it is usually inactive.
A patient with a jejunostomy needs a diet or feed that is isosmolar (300 mOsm/kg) and has a Na concen- Mean value was significantly higher than that for the low-carbohydrate diet for tration of about 100 mmol/l. To achieve this requirement the jejunum–colon group: ***P < 0·001.
Fig. 6. Diagram showing the reasons for hypomagnesaemia in patients with a jejunostomy.
(↓), Decreased.
patient has a metabolic acidosis with a large anion gap.
twice daily was given subcutaneously to eight patients with Treatment consists of giving broad-spectrum antibiotics 0·30–1·7 m small bowel remaining (six with Crohn’s disease, (neomycin or vancomycin) and thiamine, and changing the four with home parenteral nutrition) for 35 d. Balance studies diet to one that is high in polysaccharides but low in mono- (3 d) using identical diets showed increases in mean daily and oligosaccharides (Editorial, 1990).
energy absorption of 0·44 MJ (106 kcal; P = 0·09), mean Unabsorbed non-esterified fatty acids resulting from daily wet weight absorption of 0·42 kg (P = 0·04) and solid triacylglycerol digestion cause problems within the colon, as gastric emptying time for 50 % of the meal of 30 min they reduce colonic water and Na absorption, increase the (P = 0·002; Jeppesen et al. 2001). Other growth factors colonic transit rate, are toxic to bacteria (so reducing the include epidermal growth factor, which has been used for amount of carbohydrate fermented) and bind divalent children with necrotising enterocolitis or microvillus atrophy cations (Ca and Mg), thus increasing their loss in the stools.
(Walker-Smith et al. 1985; Sullivan et al. 1991), and amino- A low-fat diet is theoretically ideal as it will reduce guanidine, an inhibitor of polyamine breakdown that has diarrhoea and malodorous steatorrhoea, but fat yields twice been used in animal studies (Rokkas et al. 1990).
as much energy as comparable weights of carbohydrate and makes food palatable, thus cannot be excessively restricted.
induce functional adaptation by giving peptide YY analogues Medium-chain triacylglycerols are an alternative source of energy that can be absorbed in the colon (Jeppesen &Mortensen, 1998).
Calcium oxalate renal stones occur in 25 % of patients with a retained colon (Nightingale et al. 1992a) because of A new definition of intestinal failure that includes reference increased colonic absorption of dietary oxalate. This situ- to water and electrolytes has been given and the severity of ation results in increased oxalate excretion in the urine intestinal failure graded according to the route by which where it may precipitate. The increased colonic absorption nutrients and fluid are given. An aim in the management of oxalate is partly the result of free unabsorbed fatty of patients with intestinal failure is to reduce its severity.
acids preferentially binding to Ca, which allows oxalate to Acute intestinal failure in the peri-operative period may be become soluble and hence absorbed. Other mechanisms prevented or its duration reduced by avoiding the adminis- include: unabsorbed bile salts directly increasing colonic tration of excessive intravenous saline. A patient with a high- permeability to oxalate; Oxalobacter formigenes, a species output small bowel stoma should restrict oral hypotonic of bacteria that normally metabolize oxalate within the fluids; serum Mg and random urinary Na concentrations colon, may be absent or present in small numbers; urinary should be monitored. The severities of intestinal failure can citrate, which prevents initial nucleation of calcium oxalate, be reduced in terms of water and electrolyte requirements by may be present in a reduced concentration. The formation of careful fluid balance management and the judicial use of calcium oxalate stones is prevented by advice about a low- drugs. The severity of intestinal failure in terms of macro- oxalate diet (avoid rhubarb, spinach, beetroot, peanuts and nutrient requirements is rarely markedly altered by dietary or excessive amounts of tea), reducing or avoiding excess fat in enteral feeding adjustments or the use of growth factors.
the diet, taking oral Ca supplements or a Ca-containingorganic marine hydrocolloid and/or cholestyramine (to bindbile salts; Tomson, 2001).
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