Practical issues in nutrition and supplementation in gastrointestinal disease

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Chapter 26 PRACTICAL ISSUES IN NUTRITION AND SUPPLEMENTATION IN GASTROINTESTINAL DISEASE

KEY POINTS

• In upper gastrointestinal obstruction, endoscopic techniques facilitate access to the normal functional bowel distal to the obstruction, and thus restore normal digestion and absorption. It is imperative to simultaneously decompress the stomach proximal to the obstruction when feeding distally in order to avoid secretion build-up in the stomach.
• In lower gastrointestinal obstruction, the treatment is early surgery or total parenteral nutrition (TPN).
• Intestinal adaptation to intestinal loss may take up to 2 years. Thus, strong initial support is needed to optimise conditions for adaptation.
• The secret of adaptation is to make the remaining intestine work overtime.
• Tailoring TPN for the individual patient is essential.
• If less than 200 cm of small intestine without colon is present and IV supplementation becomes necessary, the condition is regarded as ‘small bowel intestinal failure’. This is also the case if less than 50 cm of small intestine remains with colon, and TPN or home TPN becomes essential for survival.
• In intestinal fistulae the volume of output provides a good index of the site of the fistula.
• Treatment for low output fistulae is not TPN. Oral feeding should continue.
• Be wary of bowel rest in sick patients.

INTRODUCTION

The function of the bowel is to digest and absorb food. Consequently, it is no surprise that disorders of the gastrointestinal tract are associated with nutritional problems. In chronic gastrointestinal disorders, the situation becomes complicated by the secondary effects of malnutrition on digestive function. The mucosa has one of the highest protein turnover rates of any organ within the body, and the synthesis of pancreatic enzymes is directly dependent on an abundant supply of amino acids. Thus, in chronic malnutrition, digestive and absorptive function becomes impaired, leading to a vicious cycle of malabsorption, maldigestion, malabsorption, etc.

Equally important to realise is the tremendous depth of reserves in digestive and absorptive function. For example, we can survive following the loss of >90% of the small intestine if the colon remains intact. Similarly, maldigestion and fat malabsorption only occurs after we have lost >90% of our pancreatic enzyme secretion. However, it must be remembered that adaptation to loss takes time; in the situation of the small intestine up to 2 years. Consequently, strong initial support will be needed to optimise conditions for adaptation to occur.

NUTRITIONAL PROBLEMS

Management options for various nutritional problems are summarised in Figure 26.1.

image

FIGURE 26.1 Nutritional problems.

NPO = non per os; PEG = percutaneous endoscopic gastrostomy; PEG-J = percutaneous endoscopic gastrostomy with post-pyloric J extension; PEJ = direct endoscopic jejunostomy; TPN = total parenteral nutrition.

Intestinal obstruction

In the days prior to total parenteral nutrition (TPN), intestinal obstruction was a fatal condition unless early surgery could correct the cause. In the 1970s and ’80s, TPN was exclusively used to stabilise the patients before surgery could be performed. In the short term, this was usually successful, but when continued >2 weeks, complications began to outweigh benefits.

TPN therapy

• Benefits

– Prevents fluid and electrolyte deficiencies
– Maintains nitrogen balance
– Prevents weight loss
– Maintains life

• Risks:

– It is unphysiological to feed directly into the right side of the heart
– Catheter sepsis
– Central vein thrombosis
– Hyperglycaemia
– Intestinal stasis:

• Small intestine bacterial overgrowth
• Mucosal atrophy and bacterial translocation
• Endotoxaemia
• Cholestasis
• Pro-inflammatory cytokine over expression

– Liver disease

Upper gastrointestinal obstruction

Because of concerns about TPN, endoscopic techniques have been developed to gain access to the normal functional intestine distal to the obstruction, and thus restore normal digestion and absorption.

• Oesophageal obstruction (e.g. cancer, stenosis, dysmotility):

– Endoscopic dilation
– Stenting
– Percutaneous endoscopic gastrostomy (PEG).

• Gastric, duodenal and proximal jejunal obstruction:

– Endoscopic dilation
– Stenting
– Percutaneous endoscopic gastrostomy with post-pyloric J extension (PEG-J)
– Direct endoscopic jejunostomy (PEJ)
– Double-lumen nasogastric decompression—jejunal feeding tube.

Note: It is imperative to simultaneously decompress the stomach proximal to the obstruction when feeding distally, as secretion will build up in the stomach leading to vomiting and possible aspiration.

Lower gastrointestinal obstruction

It is impossible to feed proximally with an intestinal obstruction because motility will be impaired and feed and secretions will build up without a chance for absorption to occur, producing vomiting. Consequently, the only alternatives are early surgery or TPN.

Short bowel

Short bowel syndrome 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.

Traditionally, the short bowel syndrome has been defined by the loss of all but 200 cm of small intestine, bearing in mind that the average length of the small intestine is 4 metres. However, this is imprecise as function will be influenced by whether the colon is remaining or not, and whether the residual small intestine is healthy. It has been estimated that the colon represents another 100 cm of small intestine after adaptation (which can take up to 2 years), and colonic salvage of maldigested food can result in the absorption of a further 1000 kcal/day. Clearly, 200 cm of residual intestine with active Crohn’s disease will not be equivalent to 200 cm of previously healthy mucosa. The most sensitive measure of remaining intestinal absorptive capacity is citrulline synthesis. Citrulline synthesis, and hence the functional bowel length, can be estimated from the fasting plasma citrulline concentration, which helps overcome errors in measurement of diseased bowel at surgery.

Management

The loss of small intestine, particularly the distal portion (which is usually the region removed, for example in Crohn’s disease), results in a loss of the ability of the intestine to conserve fluids. The proximal small intestine characteristically has leaky junctions between the mucosal cells, which means that the presence of hypertonic or hypotonic fluid in the lumen results in the passive loss of either water or salt from the body. As there is no distal intestine to reabsorb this fluid or the intestinal and pancreatic secretions stimulated by eating, there is net loss of fluid and electrolytes from the body after eating. In order to maximise residual intestinal function it is important that patients:

• Avoid drinking water
• Increase the consumption of isotonic fluids containing a carbohydrate source and electrolytes; e.g. WHO solutions containing 100 g carbohydrates/litre and 70 mEq sodium
• Increase consumption of soups containing salt and carbohydrates
• Avoid large infrequent meals: ‘nibble like a rabbit’ all day long
• Consider nutritional supplementation with nutrient-dense liquid formula diets
• Supplement diet with nocturnal tube feeding 1000 kcal/8 h to make the gut work 24 hours a day.

Intestinal failure

Intestinal failure 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.

The first loss of function is the capacity to reabsorb secretions, resulting in fluid and electrolyte depletion, or ‘dehydration’. It is only if <200 cm of small intestine and no colon remains that intravenous (IV) supplementation becomes necessary, and a state of ‘small bowel intestinal failure’ is said to exist. The same is true if <50 cm of small intestine remains with an intact colon, and TPN or home TPN then becomes essential for survival.

Measurement

The patient excretes less that 1000 mL urine and <5 mmol of sodium when on a normal diet.

Management: home TPN

It must be remembered that intestinal failure due to short bowel may recover through the process of adaptation. This process takes up to 2 years, and so intravenous (IV) nutritional requirements can be expected to decrease throughout this period. Adaptation occurs due to:

• Villous hyperplasia
• Dilation and hypertrophy of the residual bowel and slower motility
• Hypersecretion of digestive enzymes
• Hyperphagia
• Enhanced absorption
• Increased blood flow.

In order to maximise adaptation, food intake must be liberalised, as luminal nutrients are the chief stimulatory factors. Although this will increase stomal losses or diarrhoea, this must be accepted, as the quantity of absorbed nutrients will be maximised. The secret is to make the remaining bowel work overtime. Thus patients should be instructed to eat small frequent meals (‘eat like rabbits’). In borderline patients, nocturnal tube feeding may well tip the balance in favour of nutritional autonomy. The longer food is in contact with the absorptive epithelium, the greater the chance for absorption, so the liberal use of antimotility drugs is encouraged, bearing in mind that much will be malabsorbed, so usual maximum doses can be exceeded (e.g. loperamide three tablets [6 mg] four times daily).

Tailoring TPN

1. Start with IV fluids and adjust to maintain a urine output of 1.5 L/day, and a sodium excretion of 20–80 mEq/d and potassium excretion 40–60 mEq/d.
2. Start with 80 g amino acids and 1000 kcal/day. Increase slowly to 1.5 g amino acids and 25 kcal/kg ideal body weight/day over 5 days.
3. Monitor urea and creatinine. If urea increases and creatinine stays stable, cut back on amino acids. If both increase, the patient is dehydrated and IV fluids need to be increased and urine volume monitored.
4. Long term, monitor body weight and adjust calories to maintain an ideal body weight, i.e. BMI of 23.5 kg/m2.

Intestinal fistulae

Not all intestinal fistulae are treated the same. This stands to reason, as a fistula originating from the distal bowel will have little nutritional consequence, while a proximal fistula will result in major malabsorption of food, particularly if the leak is large. Consequently, it is important to first measure the fistula output. In an ideal world, the measurement of the contents of the fistulous fluid will provide even more specific guidelines for management, but this is costly and rarely done short of research studies. In general terms, the volume of output provides a good index of the site of the fistula: if output is >500 mL/day, it is likely to be proximal and associated with nutrient malabsorption, if it is <500 mL/day it is likely ileocolonic and therefore not associated with much malabsorption, as >90% of digestion and absorption occurs in the proximal gut. In a way, management is similar to that for short bowel syndrome discussed above, with the exception that high output fistulae may close spontaneously, and therefore TPN with bowel rest to reduce aggravating pancreaticobiliary secretions is recommended for up to 6 weeks. Low-output fistulae are not treated with TPN. Luminal nutrition helps the intestine recover, and oral feeding should continue in the form of small frequent meals, with IV supplementation of electrolytes and fluid as needed.

Malabsorption

Malabsorption is conventionally divided into conditions that interfere with:

• Mucosal absorption
• Food digestion.

Classic examples of diseases that interfere with mucosal function are coeliac disease and inflammatory and infiltrative disorders. Because such disorders are often patchy and because there is a redundancy of absorptive area, these diseases result in lower grades of malabsorption than diseases that impair digestive function, such as pancreatic diseases. It is therefore useful to measure the degree of fat malabsorption: in general mucosal disease results in fat malabsorption of <20 g/day, while pancreatic malabsorption usually causes losses >20 g/day. It is, however, extremely important to measure fat malabsorption accurately: it is amazing how frequently stool fats are measured in patients who are on restricted diets or even TPN, in which case such cut-off numbers are meaningless.

Measurement of fat malabsorption

• Patients must consume a ‘normal’ diet containing 100 g fat for 72 h.
• All stools must be collected from commencement of the diet after stools have been passed and discarded, to 72 h later when all stools must be collected, weighed and the fat content measured.

Management

Mucosal malabsorption can often be controlled by simply increasing the oral intake. Although this will inevitably increase stool losses initially, the proportion absorbed remains the same and so the quantity retained will increase. This is even true for vitamin B12 malabsorption in pernicious anaemia, as there is also a less efficient passive absorption mechanism. The ways of increasing nutrient intake is the same as those outlined above for the management of short bowel syndrome. For pancreatic malabsorption, commercial pancreatic enzyme supplements should be used. It must be remembered that the output of proteinaceous enzymes by the healthy pancreas is extremely large particularly during eating, approximately 20 g/day, and so enzyme supplementation has to follow a similar pattern and frequency (e.g. four capsules with meals and two with snacks). Much effort has been put into designing effective preparations that are not inactivated by gastric acid, that migrate with food through the pylorus and are only released on entering the duodenum. Despite this, it is rare to completely reverse steatorrhoea, but the improvement is usually sufficient to prevent further weight loss.

Bowel rest and pancreatic rest

Increasing knowledge about intestinal function and health has led to more cautious use of bowel rest, with or without TPN. This is because:

• the intestine depends upon luminal nutrients for the high turnover rate of mucosal proteins and maintenance of barrier function
• gut function and motility is stimulated by food
• the absence of feeding results in mucosal atrophy and disturbance of the bacterial flora with potential overgrowth with pathogens.

In contrast, bowel rest is advisable in the management of acute pancreatitis and in chronic pancreatic secretory disorders, such as fistulae and pseudocysts. If enteral feeding is delivered >40 cm past the ligament of Treitz, pancreatic stimulation is avoided, so that TPN is not the only way of feeding without stimulating the pancreas.

SUMMARY

There is a tremendous depth of reserves in digestive and absorptive function in the intestine. Adaptation is an important function but it can take up to 2 years, necessitating strong initial support.

TPN therapy is a vital component of the therapeutic armamentarium but it has both risks and benefits. Endoscopic techniques have facilitated access to the normal functional bowel distal to the obstruction. In lower gastrointestinal obstruction, the treatment is early surgery or TPN.

Short bowel syndrome is characterised by the inability to maintain protein–energy, fluid, electrolyte or micronutrient balances when on a conventionally accepted normal diet. The most sensitive measure of remaining bowel absorptive function is its citrulline synthesis capacity.

Intestinal failure is characterised by the inability to maintain protein–energy, fluid, electrolyte or micronutrient balance. Home TPN is an essential component of management but, in order to maximise adaptation, the remaining bowel should be made to ‘work overtime’ with oral intake. As part of the process, TPN should be tailored to the individual patient.

In the management of intestinal fistulae the volume of output provides a good index of the site of the fistulae. Treatment for low output fistulae (ileocolonic) is not TPN, as luminal nutrition helps the bowel to recover, and oral feeding should continue with IV supplementation.

Bowel rest is advisable in the management of acute pancreatitis and in chronic pancreatic secretory disorders, but, otherwise, caution is advised with regard to bowel rest.

FURTHER READING

Kaushik N, Pietraszewski M, Holst JJ, et al. Enteral feeding without pancreatic stimulation. Pancreas. 2005;31:353-359.

Matarese LE, O’Keefe SJ, Kandil HM, et al. Short bowel syndrome: clinical guidelines for nutrition management. Nutr Clin Pract. 2005;20:493-502.

Mullady DK, O’Keefe SJ. Treatment of intestinal failure: home parenteral nutrition. Nat Clin Pract Gastroenterol Hepatol. 2006;3:492-504.

O’Keefe SJ, Buchman AL, Fishbein TM, et al. Short bowel syndrome and intestinal failure: consensus definitions and overview. Clin Gastroenterol Hepatol. 2006;4:6-10.

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