Artificial nutrition support - technical
- Nutritional screening and assessment of nutritional status
- Indications for artificial nutrition support
- Estimating nutrition requirements
- Complications of artificial nutrition support
- Ethics of artificial nutrition support
- Special situations in nutrition support
- Perioperative nutrition
- The hospital nutrition support team
- Cost-effectiveness of nutrition support
- Future developments
The prevalence and importance of malnutrition in affluent societies is under-recognized, and nutritional status is a major predictor of outcome for most diseases.
Nutrition screening identifies patients at risk of malnutrition and should be performed in all clinical areas: this requires evaluation of events in the past (recent weight loss); present (current body mass index (BMI) and clinical signs of malnutrition); and future (current nutrient intake and foreseeable likely causes of reduced intake). A BMI of less than 18.5 kg/m2, or weight loss of more than 10% over 3 to 6 months, or BMI of less than 20 kg/m2 with weight loss of more than 5% over 3 to 6 months, is indicative of malnutrition.
Nutrition support is indicated for malnourished patients or those at risk of malnutrition in view of inadequate oral intake or malabsorption. Timing of intervention depends on the pre-existing nutritional status and the likelihood of restoring adequate intake. Nutrient requirements are calculated using weight-based formulae for basal energy and protein requirements, with additional factors for physical activity, severity of illness, or desired weight gain. Increased requirements due to disease are often counterbalanced by reduced activity.
Proper provision of appetizing food of appropriate quantity, texture, temperature, and variety in a conducive environment, with facilities for assistance and encouragement, can obviate the need for artificial nutrition support. Artificial nutrition support can be provided by oral (supplements), enteral, or parenteral routes, but enteral is preferable to parenteral feeding when possible—it maintains gut integrity, appropriately stimulates hormonal regulation of metabolism and gastrointestinal functions, and delivers nutrients to the liver via the portal circulation. Enteral feeding is also cheaper and safer than intravenous nutrition.
Both enteral and parenteral nutrition can be associated with significant complications relating to the means of access or the delivery of nutrients. Catabolic patients are unable to utilize excess protein or energy, and overfeeding results in an increased rate of complications. Oral nutrition support is associated with improved outcomes and significant reductions in mortality in selected patient groups. A multiprofessional team is essential to coordinate and monitor artificial nutrition in the hospital environment, and to provide support for patients fed long-term in the community, most of whom now die from their underlying disease, rather than complications of nutrition support.
Undernutrition in societies where food is plentiful is predominantly disease-related and the extent of the problem is underestimated. More than 10% of adults over the age of 65 years in the community are affected, and this figure rises to around 40% of all hospital inpatients and elderly care-home residents. Surveys suggest little change to these proportions over the last 25 years in the United Kingdom. Malnutrition profoundly affects the outcome of all disease states and their treatment, by altering physiological responses and effects on immunity and healing as well as psychology and motivation. Although nutritional requirements are undoubtedly increased by chronic illness, associated anorexia or inability to feed orally contributes more significantly to the malnutrition and is directly amenable to intervention by nutrition support.
Nutritional screening and assessment of nutritional status
Weight loss is easier to prevent than to reverse, and early weight gain after illness or starvation comprises significant components of fluid and fat rather than muscle mass. Therefore, although assessment of a patient’s immediate nutritional status is important, it is also crucial to determine the nutrition trajectory—the rate of weight loss and the likelihood of future weight loss due to increased requirements or inadequate intakes—in order to determine a nutrition ‘risk score’. Such scores are routinely used to screen for malnutrition in all clinical settings and provide a valuable tool for the prioritization of intervention, for prevention as well as treatment (Fig. 1).
Fig. 1 The ‘Malnutrition Universal Screening Tool’ (MUST)—an example of an algorithm for the screening and identification of malnutrition and the appropriate actions to be taken based on risk score.
A good nutrition history will include the nature of the baseline diet—not only for vegans or vegetarians (low in vitamin B12 and haem iron), but also for poor fresh fruit and vegetable intake (vitamin C, folic acid), and dairy avoidance (calcium) or other dietary restrictions due to intolerances or dislikes. Excessive alcohol intake can result in thiamine and folic acid deficiency. Oral conditions may make ingestion painful, and abdominal symptoms such as nausea, bloating, or pain can affect dietary intake, but changes in appetite might not be volunteered. Medications can affect nutrition by reducing appetite or inducing nausea. Intake can be significantly affected by psychosocial circumstances such as depression, bereavement, social isolation, impaired mobility, or poverty.
Patients may not be able to quantify weight loss, but this is often clear on clinical examination—e.g. prominent cheekbones, muscle wasting, redundant skin folds, and a concave abdomen. Ill-fitting clothing, belt notches, and loose finger rings provide clues in the clinic. Certain of these signs can be present with recent weight loss even in patients who remain obese. Signs suggestive of specific nutritional deficiencies can be apparent on examination (see: Vitamins and trace elements), particularly of the hair, eyes, skin, nails, teeth, and tongue.
The ratio of weight (in kg) to the square of the height (in m2) is known as the body mass index (BMI). This provides a useful indication of nutritional status, but is difficult to apply in some cases such as young adults with cerebral palsy or elderly patients with osteoporosis. A BMI of less than 18.5 kg/m2 is considered indicative of malnutrition, as is weight loss of more than 10% in the preceding 3 to 6 months, or a BMI of less than 20 kg/m2 in the setting of recent or ongoing weight loss (>5%). The use of centile charts in children is valuable, as sustained undernutrition results in reduced height velocity and failure to meet expected height. Weight-for-age charts will reflect the current nutritional status more accurately.
Clinically important changes in lean body mass can be masked by shifts in fluid distribution and adipose tissue, reducing the value of weight measurements in assessing and monitoring nutritional status. Modern bio-impedance scales provide measurements of extracellular water and estimates of fat-free mass from which lean body mass can be calculated, but validation in disease settings is still required. A reasonable estimate of changes in lean mass can be derived from sequential measurements of the mid upper-arm circumference and the triceps skinfold thickness using a tape measure and calipers, respectively. Simple hand-grip dynamometry can similarly provide an objective sequential indication of functional muscle mass. However, wide reference ranges make single measurements of these anthropometric parameters unreliable for nutritional assessment.
Indications for artificial nutrition support
Malnutrition can often be prevented in patients at risk by simple measures to optimize appetite and reduce symptoms such as pain and nausea that can lead to anorexia. In institutions such as hospitals, the range of menus and the presentation and temperature of meals clearly affect the amount consumed. ‘Nil by mouth’ orders for investigations or procedures, or mealtimes disturbed by interventions, also reduce food intake. Hospital catering needs to accommodate the requirements of patients with altered feeding patterns—e.g. after upper gastrointestinal surgery or with gastrointestinal dysmotility—and older people often prefer to snack rather than take large meals.
Patients with disabilities frequently require assistance with feeding, and sufficient staff and time dedicated to helping such patients can maintain nutrition. Altering the food texture may be required in some conditions—puréed or liquid diets benefit patients with oesophageal strictures or gastroparesis, whereas thickening fluids with starch reduces the risk of pulmonary aspiration in neurological causes of dysphagia.
If despite such measures, patients are unable to take sufficient oral food to meet requirements, then artificial nutrition support is required. If swallowing remains intact and palatability is acceptable, this can be in the form of liquid oral nutrition supplements. Unconscious patients, and those unable to swallow or with upper gastrointestinal obstruction, can receive enteral nutrition support if intestinal function is preserved. Access can be achieved by pernasal or transabdominal feeding tube to the stomach or intestine. Patients without adequate intestinal function require total or partial parenteral nutrition support via an intravenous catheter. Common indications for enteral and parenteral artificial nutrition support are given in Table 1.
The timing of nutrition support intervention depends on the pre-existing nutritional status of the patient. A young well-nourished patient undergoing gastrointestinal surgery may tolerate starvation for up to a week, but a malnourished patient will require nutrition support from the onset of being ‘nil by mouth’.
|Table 1 Common indications for enteral and parenteral artificial nutrition support|
|Coma||Intestinal failure: inability of the gastrointestinal tract to absorb sufficient fluid and/or nutrients to maintain life|
|Ventilated, sedated patients in critical care setting||Anatomical short gut secondary to:|
|Cerebrovascular disease||Infarction (superior mesenteric artery or vein thrombosis)|
|Motor neuron disease||Volvulus|
|Multiple sclerosis||Desmoid tumour|
|Bulbar palsy||Surgical resections for:|
|Cerebral palsy||Crohn’s disease|
|Head and neck cancer||Vasculitis|
|Mucositis due to chemo/radiotherapy||Radiation enteritis|
|Oesophagogastric malignancy||Necrotizing enterocolitis|
|Acute pancreatitis||Long segment Hirschprung’s disease (children)|
|Oesophageal dysmotility||Microvillous inclusion body disease|
|Gastroparesis||Protracted diarrhoea of infancy|
|Liver transplantation||Visceral myopathy|
|Inability to meet requirements due to malabsorption, increased requirements or anorexia secondary to chronic illness: overnight feeding to maximize gastrointestinal tract use||Peritoneal disease|
|Cystic fibrosis||Sclerosing peritonitis due to peritoneal dialysis|
|Severe pulmonary or cardiac disease (particularly children)||Ovarian or metastatic lobular breast cancer undergoing chemotherapy|
|Borderline short gut||Postoperative/critical illness|
|High-output enterocutaneous fistula|
Estimating nutrition requirements
Energy expenditure under basal conditions reflects physiological cellular metabolic functions and hence correlates with body mass. Derivative equations based on weight alone provide estimates of energy consumption that adequately match measurements based on oxygen uptake and CO2 production (indirect calorimetry) for most clinical purposes. To this basal rate, additions are required for activity and the thermal effect of food. Energy expenditure is increased by disease states such as burns, sepsis, or trauma—however, it is easy to overestimate such contributions, which are often negated by reduced physical activity in illness and may amount to only 10 to 20% of resting energy expenditure. Difficulties arise in estimating the requirements for patients with oedema or obesity based on weight alone, and adjustments based on ideal body weight or a proportion of current weight can be used. Most hospital patients’ requirements lie within the range of 25 to 40 kcal/kg per day (105–168 kJ/kg per day).
Fluid balance must be factored into estimating nutrition requirements. Most hospitalized adults require 30 to 35 ml/kg per day with additions for replacement. Losses can be high from the kidneys due to diabetes insipidus or recovering from acute tubular necrosis, and can exceed 8 litres a day from the gastrointestinal tract via a proximal jejunostomy or enterocutaneous fistula (Table 2). Fluid restriction is indicated in overloaded states or in renal or cardiac failure, and diluents for intravenous drugs and line flushes can reduce the fluid allowance available for the feed in ill patients. Most enteral feeds provide 1 kcal/ml but specialized feeds with up to 2 kcal/ml are available for such circumstances.
Average requirements for sodium and potassium are of the order of 1 mmol/kg per day for most adults. However, significant sodium losses can occur through the gastrointestinal tract and require replacement. Potassium deficits may be large in patients receiving thiazide diuretics, with secretory diarrhoea, during recovery of metabolic acidosis, and during refeeding of malnourished patients. Similarly, phosphate requirements increase greatly during refeeding from a baseline of approximately 0.3 mmol/kg per day. Feeds with minimal electrolyte content are required in renal impairment where solute clearance is reduced. However, the commonest cause of excessive electrolyte administration in hospitals is the use of normal saline and salt-rich colloid solutions for maintenance fluid requirements.
|Table 2 Electrolyte composition of gastrointestinal fluids (in order to calculate replacement of losses)|
|Fluid||Na+ (mmol/litre)||K+ (mmol/litre)||HCO3− (mmol/litre)||Cl− (mmol/litre)||Approximate volume secreted in 24 h (ml)|
|Small intestinal contents||100||10||25||100||1000 (succus entericus)|
Protein is required to meet obligatory catabolic losses (minimal requirement) and to stimulate protein synthesis (optimal requirement). The World Health Organization (WHO) recommendation of minimal requirement is 0.75 g protein/kg per day (0.12 g N/kg per day) based on nitrogen balance studies on a protein-free diet . Increasing the dietary protein intake will increase protein synthesis in depleted patients as long as sufficient calories are taken, and the optimal calorie:nitrogen ratio may vary on the disease state. Although net protein synthesis can be achieved by increasing dietary protein in malnourished patients, the same is not true in the catabolic state induced by sepsis, burns, or trauma where excess amino acids can exert detrimental effects. Intakes of above 1.5 g protein/kg per day (>0.24 g N/kg per day) are not generally recommended.
Amino acids have physiological roles beyond protein synthesis, and individual amino acid levels vary significantly between different disease states. Most artificial feeds provide standard amino acid solutions that do not cater for such differences and may result in relative imbalances of amino acids that could compromise nitrogen utilization. Histidine levels are low in renal impairment, and branched chain amino acids (valine, leucine, isoleucine) are reduced in chronic liver disease. Glutamine is significantly depleted in critical illness, and improvement in nitrogen balance has been demonstrated with supplementation.
Carbohydrates should make up 50 to 65% of calories in a healthy diet. In excess of 5 g/kg per day, glucose is stored as glycogen up to a maximum storage capacity of about 15 g/kg. Continued administration of glucose results in lipid synthesis. In disease states, however, maximal glucose oxidation rates are frequently lower due to insulin resistance, and excessive glucose administration results in hyperglycaemia.
The lower limit constraint on lipid provision is the need for essential fatty acids (linoleic and α-linoleic acids), which can be provided in 3 to 4.5% of the total energy requirements as fat. Lipid is used in artificial nutrition to provide the energy that cannot be supplied as carbohydrate due to the limit of glucose oxidation. The amount of CO2 produced by oxidation of lipid is 30% less than that of glucose, and could theoretically help patients with respiratory failure or weaning from a ventilator; however, clinical benefits are small in practice.
Vitamin requirements differ between health and disease, and patients may have pre-existing deficiencies, particularly of the water-soluble vitamins for which there are no body stores. As deficiencies can have profound effects on cellular metabolism and few vitamins are toxic in excess, levels of vitamins in commercial feed preparations are often above estimated requirements. This also helps to compensate for the degradation that occurs in solution—vitamin A and riboflavin are photosensitive (hence parenteral nutrition at the bedside is light-protected), thiamine reacts with preservatives required to maintain shelf life, and vitamin C and vitamin E are ineffective when oxidized. The latter is used in parenteral nutrition solutions in excess to prevent lipid peroxidation. Vitamin K is normally not required in artificial nutrition, due to enteric bacterial synthesis, and its addition could affect therapeutic anticoagulation. Other fat-soluble vitamins—vitamin A, vitamin D, and vitamin E—can be provided in a water-miscible solution in parenteral nutrition.
Minerals and trace elements
In contrast to vitamins, toxicity is associated with excessive delivery of some trace elements. The enterocyte regulates iron uptake, and relatively small amounts of trace elements are absorbed from the intestine. Overadministration is therefore easier in parenteral than enteral nutrition delivery. Manganese and copper undergo biliary excretion, and accumulation can occur in parenterally fed patients with cholestasis—basal ganglia deposition can be detected on brain MRI scanning, but neurological effects are rarely reported. Chromium is excreted in the urine and can accumulate in renal failure.
Zinc is lost through the intestine in high output states and in wound exudates; additional replacement may be required. Selenium as a cofactor in glutathione peroxidase plays a key role in cellular redox maintenance, and some authorities recommend supplementation in critical illness. Unfortunately, trace elements are difficult to measure accurately, levels are affected by acute-phase response, and serum albumin concentration and interpretation of low levels is complicated by the possibility that it reflects a physiological response to acute illness, as in the case of iron sequestration.
Complications of artificial nutrition support
The ease with which full nutritional requirements can be delivered by artificial means results in a risk of ‘refeeding syndrome’ on initiating feeding in chronically malnourished patients. Features include electrolyte imbalance (hypokalaemia, hypophosphataemia, hypomagnesaemia) and an associated risk of cardiac arrhythmia and sudden death, hyperglycaemia, and fluid shifts that can precipitate heart failure. Rapid depletion of available thiamine, an essential cofactor of pyruvate decarboxylase, results in inhibition of glycolysis on refeeding and damage to glucose dependent cells such as neurons—the clinical presentation of Wernicke–Korsakoff syndrome. This is preventable by the administration of high-dose intravenous thiamine prior to refeeding (or glucose administration) in patients considered at risk. Other complications of artificial nutrition support are specific to the route of delivery. Access devices in common use, with their advantages and disadvantages, are listed in Table 3.
Complications of access
Nasogastric tubes Incorrectly placed nasogastric tubes can result in fatality. Inadvertent pulmonary placement is the most common, but insertion into cranial, pleural, and peritoneal cavities has occurred. Feeding should only be initiated after confirmation of gastric placement by pH measurement of aspirated stomach contents, or radiography. Interruptions due to frequent tube displacement cause a significant reduction in feed delivery—as little as 55% of prescribed feed in one study. This can be prevented by the use of a loop of tape that can be safely and simply passed around the nasal septum to secure the tube. Modern tube materials do not cause significant erosion or irritation of the face, nares, or mucosal surfaces, even with long-term use. However, the difficulty of managing these tubes in the community makes them undesirable for long-term use.
Gastrostomy tubes are used for the majority of enterally fed patients in the community. Percutaneous endoscopically guided gastrostomy (PEG) and radiologically inserted gastrostomy (RIG) are now the commonest techniques used for placement (Fig. 11.6.3). A high fatality rate early after PEG insertion may be due to cardiorespiratory complications in patients sedated for endoscopy who are already at risk of pulmonary aspiration. Asymptomatic pneumoperitoneum is common after PEG insertion, but feed leakage into the peritoneal cavity can result in a chemical peritonitis. Superficial infections at the PEG site are commonly due to methicillin-resistant Staphylococcus aureus (MRSA) and are usually easily treated. Growth of gastric mucosa over the internal bolster of the device (the ‘buried bumper’) can result in blockage, external feed leakage, and infection, but may only be detected at the time of attempted PEG removal.
Complications of feeding
The role of the intestine in regulating nutrient uptake is demonstrated by the reduced metabolic complications of enteral compared to parenteral feeding, and nutritional deficiencies in patients fed appropriately with commercial preparations are highly unusual.
Patients who require enteral feeding often have impaired conscious level or swallowing and are therefore at risk of pulmonary aspiration. Delayed gastric emptying—as frequently occurs in the critically ill—increases the likelihood of aspiration of stomach contents and pneumonia, but this can occur due to gastro-oesophageal reflux even with normal gastric emptying. Reflux may be exacerbated, rather than reduced, by PEG feeding compared to nasogastric delivery. Patients should be fed continuously by infusion pump rather than feed bolus and at a 30° tilt to reduce this risk. Those with high gastric aspirate volumes and no evidence of intestinal ileus or obstruction should be fed by a tube passed beyond the pylorus.
|Table 3 Types of enteral and parenteral access devices in common use|
|Type of tube||Description||Use||Advantages||Disadvantages|
|Nasogastric||Fine bore (6–8F) polyurethane tube; can be secured with a ‘nasal bridle’ (loop of tape around the nasal septum)||Short- to medium-term intragastric feeding due to inability to swallow; nutritional supplementation: bolus or drip feed||Bedside placement without sedation; well tolerated||Risk of malposition; easily displaced; difficult to manage in community|
|Nasojejunal||Fine-bore polyurethane tube with tip passed into distal duodenum/proximal jejunum||Inability to swallow complicated by gastro-oesophageal reflux or gastroparesis; gastric outlet obstruction; acute severe pancreatitis||Can be placed noninvasively at bedside; accurate delivery into proximal intestine; drip feed only.||May require endoscopic or fluoroscopic placement; easily displaced;|
|PEG (percutaneous endoscopically placed gastrostomy)||Tube passed into stomach through abdominal wall using endoscopic technique, retained by internal bumper or balloon; available in lumen sizes up to 24F||Long term intragastric feeding; mucositis due to head and neck cancer therapy; palliative venting use in terminal intestinal obstruction||Difficult to displace; reliable in long term use; can be exchanged for skin-level (‘button’) device, ideal for younger or ambulant patients||Requires endoscopy for placement; local complications (infection/leakage/granulation tissue) balloon - retained tubes require regular replacement (3–6 monthly); endoscopy is required to change bumper retained PEGs: every 2–3 years|
|RIG (radiologically placed gastrostomy)||Radiologically placed trans-abdominal gastrostomy tube||Intragastric feeding where endoscopic placement is not possible due to risks of endoscopy or anatomical considerations||Safer than PEG in high-risk patients||Require gastric insufflation via nasogastric tube; some centres report higher rates of local complications than with PEG|
|PEG-J (PEG with jejunal extension)||Transgastric tube positioned with tip in distal duodenum/proximal jejunum through existing gastostomy||Long-term intestinal feeding where gastric feeding is not available due to gastric dysfunction or outlet obstruction||Minimally invasive route for long-term postpyloric feeding||Jejunal tube can be easily refluxed back into stomach; inner jejunal tube can be displaced from PEG tube|
|DPEJ (direct percutaneous enteroscopic jejunostomy tube)||PEG tube placed directly into the proximal small intestine rather than stomach||Long-term intestinal feeding||Reliable intrajejunal feeding||May require prolonged endoscopic procedure under deep sedation or general anaesthetic High risk of complications including intestinal volvulus and intractable pain|
|Surgical jejunostomy||Feeding tube placed surgically into the jejunum and retained by external sutures||Postoperative feeding in upper gastrointestinal surgery and liver transplantation||Permits early enteral feeding in postoperative setting||Not designed for long term use;can be displaced; can result in adhesional intestinal obstruction|
|Midline catheter||Short peripheral (22G) cannula placed into antecubital vein||Short-term parenteral nutrition support||May allow effective parenteral nutrition support or supplementation without risks and delays of central venous access||Limited range of available feeds due to osmolality and pH considerations;thrombosis or thrombophlebitis usually limits use to 7–14 days|
|PICC (peripherally inserted central venous catheter)||‘Long-line’: tube placed via the cephalic vein into large central veins||Short- to medium-term parenteral nutrition support (suitable for majority of inpatient PN episodes)||Reduced risk of infection;preserves central venous access points||Thrombophlebitis and thrombosis (avoided with low-dose anticoagulation); not practical for long-term use in ambulant patients or for patients to manage at home|
|Triple lumen venous catheter||Multilumen direct-puncture central venous access tube||Fluid and drug delivery; central venous pressure monitoring (severely ill patients)||Ease of access in critically ill patients with pre-existing central access||High risk of infection and local complications; In view of this, usage for PN should be discouraged except via a dedicated lumen for limited periods of time|
|Tunnelled Hickman catheter||Single or double lumen line tunnelled subcutaneously to the skin surface with a Dacron cuff for retention||Medium–long-term parenteral nutrition support||Low risk of infection if properly maintained; low risk of displacement once cuff is ‘enmeshed’||Care needs to be taken with the external tube to prevent damage and maintain asepsis, and with the exit site to prevent infection|
|Implantable subcutaneous port device||Line accessed via a hub placed in a subcutaneous pocket||Long-term parenteral nutrition||Invisible from exterior with no external parts: ideal for active patients requiring long-term parenteral access||Skin puncture required for access: not ideal for frequent/daily use; more difficult than a tunnelled line to reposition; risk of blockage with lipid-containing feeds|
Diarrhoea is common in enterally fed hospital patients, and is often due to the concomitant use of antibiotics. Liquid feed empties rapidly from the stomach compared to solids and can result in an osmolar load that precipitates fluid influx and intestinal hurry, and neuroendocrine mechanisms have been described that result in right colonic fluid secretion with intragastric feeding.
Constipation is a more frequent accompaniment of enteral feeding in the community and is helped by the use of fibre-containing feeds, but may require osmotic laxatives.
Complications of access
Intravenous delivery via peripheral cannulae is limited by the propensity for thrombosis and thrombophlebitis and available preparations are constrained by pH and osmolality requirements. Central venous access is required for longer-term parenteral nutrition with attendant risks of pneumothorax and haemothorax that can be reduced but not eliminated by insertion under ultrasound guidance. Peripherally inserted central lines are convenient for parenteral nutrition in hospital. Infection is the major hazard of intravenous feeding catheters in hospital patients and is reduced by strict asepsis and using a single dedicated line or lumen for feed. Patients predicted to require more than a few days of intravenous feeding should have a peripherally inserted central line or a subcutaneous tunnelled line placed. Staphylococci (coagulase negative and positive strains), Gram-negative bacilli, and candida are common infecting organisms. Infection can present insidiously with low-grade fever, and be complicated by dissemination resulting in bacterial endocarditis, discitis, osteomyelitis, or fungal endophthalmitis.
With longer-term parenteral feeding in the community, catheter-related infections average one every 2 years. Venous thrombosis can occur despite anticoagulation and may limit available venous access for feeding. Creative solutions such as transhepatic caval cannulae or intracardiac lines may be required.
Complications of feeding
Metabolic complications are more likely to occur with parenteral than enteral feeding for a number of reasons:
- Parenteral feeding bypasses the enterocyte, which actively regulates uptake, metabolizes nutrients, and re-exports them via the portal circulation to the liver.
- Insulin and glucagon secretion and other enteroendocrine hormones are controlled by the presence or absence of nutrients in the gut.
- Parenteral feeds cannot replicate the complexity of circulating nutrient molecules, being constrained by requirements of chemical stability.
The metabolic risks of parenteral nutrition have previously been overestimated as a result of ‘hyperalimentation’, reflecting the ease of nutrient delivery by this route. Hyperglycaemia is especially common, due to insulin resistance associated with critical illness, and results in increased risk of infection and adverse outcomes if not treated with exogenous insulin. Imbalances of other nutrients may occur as a result of variable losses associated with the underlying condition and require regular monitoring and replacement.
The gut derives a proportion of its nutrient requirements from the lumen rather than the bloodstream, therefore parenteral nutrition may result in intestinal mucosal atrophy and impaired barrier function. Physiological and anatomical changes have been described, but sepsis due to bacterial translocation appears to be rare from this cause in humans.
Intestinal failure-associated liver disease (IFALD)
Patients requiring parenteral nutrition are at risk of liver complications. Asymptomatic elevation of liver enzymes is common, but can progress rapidly to cholestasis and cirrhosis in children. Cholestasis also occurs in adults but liver disease normally progresses more insidiously through steatohepatitis to cirrhosis. The underlying disease is responsible for reduced portal inflow in patients with short bowel, and lack of enteral stimulation of cholecystokinin production results in impaired choleresis, gallbladder stasis, and calculi formation. A number of factors associated with the feed—in both excess and deficiency—have been implicated in the aetiology of IFALD (Table 4). Maintaining oral intake, cyclical rather than continuous feeding, and keeping average exogenous lipid delivery under 1 g/kg per day appears to reduce the risk of advanced liver disease in adults during long-term feeding.
Intestinal failure-associated bone disease
Metabolic osteopenia is common in intestinal failure requiring long-term parenteral nutrition. Prolonged bed rest and immobilization, and vitamin D malabsorption and intestinal loss contribute prior to initiation of parenteral nutrition; however, a low bone turnover state is reported, resembling osteoporosis. Maintenance treatment with intravenous bisphosphonates and in the most severe cases, teriparatide is indicated.
|Table 4 Aetiological factors implicated in intestinal failure-associated liver disease (IFALD)|
|Reduced enteral stimulation||Excess provision of calories as carbohydrate or lipid|
|Phytosterols present in soy-based formulae||Choline deficiency|
|Bacterial translocation||Reduced VLDL synthesis|
|Taurine deficiency||Inadequate glucagon secretion|
Long-term artificial nutrition support
Patients can receive oral, enteral, or parenteral nutrition support in the community. In the United Kingdom, the British Artificial Nutrition Survey (BANS) carries out an annual survey of the number of tube-fed patients. Approximately 25 000 British adults receive enteral feeding in the community, but only about 600 are fed parenterally (2005 data). Quality of life is often significantly impaired by the underlying disease rather than the nature of the maintenance therapy, and infusing feed overnight helps to minimize disruption to lifestyle. Life expectancy is similarly dictated by the underlying disease with few deaths being attributable to complications of feeding. Recent surveys suggest 10-year survival rates on parenteral feed of 71% in adults, 81% in children. Patients receiving enteral feed at home are generally older and more infirm than parenterally fed patients, with a 5-year survival rate as low as 25%.
Patients with irreversible intestinal failure who experience life-threatening complications of parenteral nutrition—recurrent catheter-associated infections, IFALD, or loss of venous access through thrombosis—can be considered for intestinal transplantation, which can include other organs such as liver, stomach, pancreas, and kidney (‘multivisceral’ transplantation). Recent advances in immunosuppression using anti-CD25 or antilymphocyte induction therapy followed by tacrolimus-based protocols have resulted in 5-year survival rates of over 50% and independence from parenteral nutrition in the majority of successful cases.
Ethics of artificial nutrition support
Nutrition and starvation are understandably emotive topics. Although it is a basic human right not to be deprived of food and fluid, the same is not true of artificial nutrition support, which involves the invasive placement of tubes for feeding that are associated with risk of morbidity and mortality in their own right. Ethically and legally, withdrawing and withholding nutrition are considered equivalent in view of the ultimate outcome. However, in practice, cessation of feeding through an established feeding tube is rarely practicable, and the natural history of a condition can be significantly altered by nutrition support. This may prolong the process of dying or maintain an intolerable quality of life. The placement of tubes such as PEGs to facilitate nutrition support must be carefully considered in all cases, preferably by a multidisciplinary approach involving clinicians, nutrition nurse specialists, dietitians, speech and language specialists, and carers and relatives or appointed surrogate, taking into the account the patient’s wishes or advance directives when stated. The United Kingdom General Medical Council’s advice for clinicians on withholding or withdrawing nutrition support has been tested in court.
Special situations in nutrition support
Critical illness—burns, trauma, and sepsis
The metabolic response to stress is characterized by hypermetabolism and rapid tissue catabolism with resulting insulin resistance and hyperglycaemia. Direct effects of inflammatory mediators and cytokines such as tumour necrosis factor α(TNFα) and interleukins IL-1 and IL-6 are responsible. Protein loss can be rapid, particularly in the case of burns, where exudates add to catabolic loss. Feeding during acute metabolic decompensation can be detrimental and should be withheld for 24 h; otherwise, early initiation of feeding is likely to be beneficial in the majority of settings. Gastric stasis occurs for 2 to 4 days in severe burns, but longer with head injury, and intestinal ileus is also common in circulatory failure requiring inotropic support.
The use of prokinetics such as metoclopramide may maintain gastric emptying in mild cases, but where gastric aspirate volumes remain high or increase during intragastric feeding, postpyloric or parenteral feeding avoids the risks of pulmonary aspiration and ensures nutrient delivery. Adverse outcomes are associated with overfeeding in the acute stages, despite control of hyperglycaemia with insulin infusion, but requirements can be increased for weight gain during recovery—appropriate recognition of the transition from catabolic to anabolic phases remains a challenge. Unfortunately, attempts at reversing catabolism by the use of inflammatory cytokine inhibitors, or anabolic agents such as growth hormone have been unsuccessful. However, nutrients themselves can modulate inflammatory and immune functions. For instance, the use of feeds enriched with n – 3 fatty acids can reduce the production of pro-inflammatory eicosanoids by competing with arachidonic acid, and early studies have demonstrated encouraging benefits in septic and surgical patients.
Renal failure results in wasting, electrolyte and fluid imbalances, and anorexia with resultant malnutrition. Patients undergoing dialysis lose protein into the dialysate—up to 10 g/day on haemodialysis and up to 15 g/day on peritoneal dialysis. Water-soluble vitamins—folic acid, pyridoxine, and vitamin C—are lost in dialysis and require supplementary replacement. Adequate energy intake is essential to minimize catabolism of endogenous protein, and appropriate protein sources are required to replace losses. Specialized artificial feeds are available to meet these requirements with minimal electrolytes and in reduced fluid volumes for renal patients. Parenteral nutrients are often given at the time of dialysis to replenish some of the losses. The use of a reduced (but high-quality) protein diet in predialysis chronic renal failure may delay the requirement for dialysis but this should not be at the cost of inadequate nutrition.
Malnutrition is common in patients with established liver disease due to reduced appetite, altered carbohydrate and lipid metabolism, and in severe cases, impaired urea synthesis from ammonia leading to increased muscle catabolism. In addition, cholestasis results in fat malabsorption. Glucose intolerance may limit glucose intake, and complex polysaccharides may provide the regular supply of glucose required as a result of diminished glycogen stores. Both oral and enteral nutrition support have been shown to improve outcomes in cirrhosis and in alcoholic hepatitis. High-protein feeds may precipitate encephalopathy in cirrhotic patients, but restricting protein is nutritionally undesirable, and an intake of 1.2 to 1.5 g protein/kg per day is recommended. An alternative to restricting protein intake is to optimize the amino acid composition of the feed, as patients with severe cirrhosis have a relative deficiency of branched chain amino acids. Specially enriched formulae exist and are indicated for patients developing encephalopathy while receiving enteral nutrition.
Nutrition support is required in a variety of gastrointestinal conditions where access to the gut is impaired as a result of proximal gastrointestinal obstruction or dysmotility, or intestinal failure due to short-bowel syndrome or malabsorption. Liquid, oral, or enteral feeds can be used to induce remission in active Crohn’s disease with a slightly lower efficacy than oral steroids—the mechanism of action may relate to altered bacterial flora rather than improvement of nutritional status.
Patients with enterocutaneous fistulae are often malnourished due to sepsis and increased losses (see Table 2 above). A high fistula output in the absence of distal obstruction usually indicates a proximal fistula, and parenteral nutrition may be required to provide sufficient nutritional intake and reduce effluent that may compromise wound healing or complicate stoma management. However, in patients who are able to maintain their requirements through enteral intake with a manageable fistula output, there is no evidence that parenteral nutrition and ‘bowel rest’ results in higher fistula closure rates.
|Table 5 Examples of disease-specific and therapeutic feeds designed to have disease-modifying activity (‘nutraceuticals’)|
|Feed composition||Intended use||Rationale|
|Low protein, high in essential amino acids and histidine, low electrolytes, high calorie density (2 kcal/ml)||Renal impairment||Appropriate matching of amino acid composition to requirements may improve protein metabolism; low protein reduces urea synthesis; high calorie density allows lower volumes|
|Low protein, reduced aromatic and increased branched chain amino acids, low sodium||Hepatic impairment||Reduced risk of encephalopathy with low protein: appropriate amino acid mix to allow optimal protein metabolism|
|High lipid, low carbohydrate||Pulmonary disease, weaning from artificial ventilation||Reduced CO2 production|
|High lipid (especially monounsaturated fatty acids), low carbohydrate, high fructose||Diabetes||Reduced glycaemia, improved diabetic control|
|Oligopeptides, medium chain triglycerides||Severe pancreatic exocrine deficiency||Reduced dependence on luminal digestion for absorption|
|Arginine, n − 3 fatty acids, nucleotides||‘Immune enhancing’: critical illness/perioperative nutrition||Substrates for rapidly dividing cells such as lymphocytes and competitive inhibition of pro-inflammatory eicosanoid production may enhance immune response and reduce inflammatory response|
|Glutamine||Critical illness||Glutamine levels severely depleted in critical illness: supplementation may improve nitrogen balance, and act as a fuel to rapidly dividing cells such as lymphocytes and enterocytes: maintaining immune responses and gut mucosal integrity|
In severe acute pancreatitis, nutrition requirements are increased by the systemic inflammatory response, and there are theoretical concerns of stimulation of pancreatic secretion by enteral feeding. In practice, enteral feed tolerance is limited by gastric stasis that occurs in severe cases, and intrajejunal enteral feeding is often required and preferred to parenteral feeding, which is associated with higher complication rates.
Malnourished patients undergoing surgery experience up to three times as many complications and a fourfold increase in mortality rate compared to well-nourished individuals. Patients may be at risk of malnutrition as a result of prolonged starvation due to obstruction or postoperative ileus. Surgery should be delayed where feasible in severely malnourished patients, in order to provide a minimum of 10 to 14 days of adequate preoperative nutrition. Recent findings have challenged traditional surgical dogma with regard to perioperative nutrition. Starvation immediately before surgery results in increased insulin resistance and increased complications postoperatively. The simple expedient of providing a 50 g oral carbohydrate load 2 h before surgery can speed postoperative recovery. Similarly, early reintroduction of feeding after routine abdominal surgery is feasible and results in more rapid rehabilitation than waiting for (unreliable) clinical signs of gastrointestinal function.
The hospital nutrition support team
A multiprofessional team comprising clinician, specialist nurse, dietitian, and pharmacist as its core members is required to provide the full range of nutrition support services. By appropriate use of nutrition support, reducing catheter-related complications, and monitoring patients receiving parenteral nutrition, such teams have also been shown to provide significant cost savings.
Cost-effectiveness of nutrition support
The estimated additional annual cost of treating patients with moderate and high risk of malnutrition compared to those with low risk is approximately £5 billion in the United Kingdom (2005 figures)—around 6% of the entire health care budget. Oral nutrition support has been shown to reduce mortality by upto 24% compared to unsupplemented patients in certain hospital and community settings. In addition, the reduced complications (odds ratio 0.29—confidence intervals 0.18–0.47) and lengths of hospital inpatient stay result in significant cost savings with oral nutrition support. Perhaps unsurprisingly (given that comparator groups are likely to be significantly undernourished), studies have demonstrated even greater outcome benefits with the use of enteral nutrition support where indicated.
Most importantly, an increased awareness of the critical importance of nutrition in clinical care is likely to improve the recognition of malnutrition and lead to the institution of appropriate preventive measures—with significant benefits in all areas of clinical medicine.
Few innovative nutritional interventions (including novel nutrient substrates that modulate disease processes and disease-specific feeds—Table 5) are yet in routine clinical use despite considerable theoretical promise, due to the lack of adequately powered trials. Much potential still remains to be unlocked in the field of therapeutic nutrition.