Read Core Topics in General & Emergency Surgery: Companion to Specialist Surgical Practice Online
Authors: Simon Paterson-Brown MBBS MPhil MS FRCS
Route of nutritional support
The preferred route of administration of nutritional support is through the gastrointestinal tract (enteral), with intravenous (parenteral) nutrient delivery reserved for patients with intestinal failure.
If there is an intact and functioning gastrointestinal tract, enteral feeding should be used if oral intake is insufficient. Enteral feeding is contraindicated to various degrees in patients with intestinal obstruction, paralytic ileus, vomiting and diarrhoea, high-output intestinal fistulas or in the presence of major intra-abdominal sepsis.
Studies in animals have shown that in the absence of nutrients into the intestinal lumen, changes occur in the intestinal mucosa. There is loss of height of villi, reduction in cellular proliferation and the mucosa becomes atrophic.
25,
26
Activities of enzymes found in association with the mucosa are reduced and permeability of the mucosa to macromolecules increased.
27
Stimulation of the intestinal tract by nutrients is important for release of many gut- related hormones, including those responsible for gut motility and stimulation of secretions necessary for normal maintenance of the mucosa. The gut acts as a barrier to bacteria, both physically and by release of chemical and immunological substances. There is evidence to suggest that atrophy of the intestinal mucosa is associated with loss of intercellular adhesion and opening of intercellular channels. This predisposes to increased translocation of bacteria and endotoxin from the gut lumen into portal venous and lymphatic systems.
28
Loss of gut integrity may account for a substantial proportion of septicaemic events in severely ill patients. However, the extent to which it contributes to sepsis in patients is not fully understood.
Nasoenteric tubes:
Nasogastric feeding via fine-bore tubes (polyvinyl chloride or polyurethane) may be used in patients who require nutritional support for a short period of time. There has been considerable debate as to whether positioning the feeding tube beyond the pylorus into the duodenum will result in reduction in the risks of regurgitation of gastric contents and pulmonary aspiration (occurs in up to 30% of patients fed this way). This is most likely in patients with impaired gastric motility. In the latter patients, the fine-bore tube can be manipulated through the pylorus into the duodenum, reducing the risk of gastric aspiration. Other complications associated with the use of nasoenteric tubes include:
More recently, double-lumen tubes have been used – one lumen resides in the stomach and is used to aspirate gastric contents, while the distal lumen is placed in the jejunum for feeding, thus reducing risks of aspiration. This can be successful even in patients with relatively high gastric aspirates, previously thought to be a contraindication for feeding via the enteral route.
Gastrostomy tubes:
A gastrostomy tube can be placed into the stomach at laparotomy, although percutaneous endoscopic or percutaneous fluoroscopic techniques are preferred. Details of how these are performed can be found in standard texts.
The establishment and use of a gastrostomy has certain disadvantages and there is a recognised morbidity:
The overall mortality rate for a gastrostomy is 1–2%, with major and minor complications occurring in up to 15% of patients. Mechanical complications associated with the tube include blockage, fracture and displacement. Furthermore, ‘dumping’ and diarrhoea are more common when the tip of the tube lies in the duodenum or jejunum.
29
Jejunostomy tubes:
A feeding jejunostomy is usually carried out at the time of laparotomy if it is envisaged that a patient will need nutritional support for a longer period. Details of the operative technique are also in standard operative texts and the smaller needle-catheter tubes are to be preferred. Advantages of a feeding jejunostomy compared with a gastrostomy are:
A range of nutrient solutions are available for use in enteral nutritional support and examples can be found in specialised texts. However, there are four main categories of enteral diet.
Polymeric diets:
Polymeric diets are ‘nutritionally complete’ diets and provided to patients with inadequate oral intake, but whose intestinal function is good. They contain whole protein as the source of nitrogen, and energy is provided as complex carbohydrates and fat. They also contain vitamins, trace elements and electrolytes in standard amounts.
Elemental diets:
Elemental diets are required if the patient is unable to produce an adequate amount of digestive enzymes or has a reduced area for absorption (e.g. severe pancreatic insufficiency or short-bowel syndrome). Elemental diets contain nitrogen as oligopeptides (free amino acids are not as easily absorbed as dipeptide and tripeptide mixtures). The energy source is provided as glucose polymers and medium-chain triacylglycerols. Each oligopeptide molecule contributes as much to the osmolarity of the solution as one molecule of intact protein, and it can be difficult to provide complete requirements without producing side-effects associated with an osmotic load, e.g. ‘dumping’ and diarrhoea.
Special formulations:
Special formulations have been developed for patients with particular diseases. Examples of such diets include: (i) those with increased concentrations of branched-chain amino acids and low in aromatic amino acids for patients with hepatic encephalopathy; (ii) those with a higher fat but lower glucose energy content for patients who are artificially ventilated; and (iii) diets containing key nutrients that modulate the immune response (see later).
Modular diets:
Modular diets are not commonly used but allow provision of a diet rich in a particular nutrient for specific patients. For example, the diet may be enriched in protein if the patient is protein deficient or in sodium if sodium deficient. These modular diets can be used to supplement other enteral regimens or oral intake.
Previously, when starting an enteral nutrition feeding regimen, patients received either a reduced rate of infusion or a lower strength formula for the first 2 or 3 days to reduce gastrointestinal complications. Recent studies have demonstrated this is not required and nutritional support can commence using full-strength feeds at the desired rate in those not at risk of developing ‘re-feeding syndrome’. Cyclical feeding (e.g. 16 hours feeding with a post-absorptive period of 8 hours) is optimal and more closely mimics the natural feeding cycle than other types of feeding regimens.
30
Enteral nutrition should be administered through a volumetric pump. If not available, then it is possible to use a gravity drip flow but care should be taken to reduce the risk of a large bolus being administered. In patients whose conscious level is impaired or confined to bed, the head of the bed should be elevated by 25° to reduce risks of pulmonary aspiration. Some clinicians prefer patients to be sitting upright when receiving enteral nutrition. The stomach contents should be aspirated every 4 hours during feeding and if a residual volume of more than 100 mL is found, enteral nutrition is temporarily discontinued.
The aspirate is checked again after 2 hours, and when satisfactory volumes are aspirated (< 100 mL) feeding is re-instituted. If more than 400 mL per 24 hours is aspirated, then feeding is discontinued. Gastric emptying may be improved by the administration of cisapride or erythromycin, which may allow feeding to be continued.
Metabolic disturbances are less likely with enteral feeding. The other complications of enteral nutrition are those associated with the route of access to the gastrointestinal tract (
Box 17.4
).
Box 17.4
Complications of enteral nutrition
Gastrointestinal
Diarrhoea, nausea, vomiting, abdominal discomfort and bloating, regurgitation and aspiration of feed/stomach contents
Mechanical
Dislodgement of the feeding tube, blockage of the tube, leakage of stomach/small intestine contents onto the skin with the use of jejunostomies or gastrostomies
Metabolic
Excess or deficiency of glucose, electrolytes, minerals or trace elements. Some of these will be noted through routine testing protocols, e.g hyperkalaemia, but others such as hypophosphataemia may be missed if not specifically anticipated
Infective
Local effects (e.g. diarrhoea, vomiting) or systemic effects (e.g. pyrexia, malaise)
Patients who require nutritional support but with enteral feeding contraindicated will require parenteral nutrition. These include:
Detailed guidance for parenteral nutrition (PN) in patients has been published by the American Society for Parenteral and Enteral Nutrition (ASPEN).
31
Current ASPEN guidelines are available on their website (
www.nutritioncare.org
), as are those of the European Society for Clinical Nutrition and Metabolism (
www.espen.org/
).
Central venous access:
Central venous access is obtained by positioning a catheter into the superior vena cava through subclavian or internal jugular veins. The catheter either emerges through the skin (usually after being tunnelled in the subcutaneous fat) or is connected to a port placed in the subcutaneous fat of the anterior chest wall. A variety of techniques for insertion of central venous lines are used. For example, catheters may be introduced into the internal jugular or subclavian vein directly by ‘blind’ percutaneous puncture, using small hand-held ultrasound imaging, by ‘cut-down’ techniques utilising the cephalic vein to access the subclavian vein, or under fluoroscopic control. Details of these techniques, their advantages and disadvantages can be found elsewhere.
32
–
34
However, it is important that whoever inserts a central venous line is expert, well practised and carries out the procedure under full aseptic techniques.
Technical aspects of feeding lines:
Central lines are manufactured from polyurethane or silicone. Both of these materials are tolerated well with low thrombogenic potential. However, polyurethane does have advantages:
Catheter manufacturers have attempted to reduce risks of bacterial colonisation of the line by bonding antiseptics (e.g. chlorhexidene) and antibiotics (e.g. silver sulphadiazine) into the catheter's fabric. Some catheters have an antimicrobial cuff, usually made of Dacron, around their external surface. This acts as a barrier to micro-organisms, which may migrate from subcutaneous tissues along the external aspect of the catheter to its tip. Although studies have suggested that risks of septicaemia are reduced by using a cuff around the catheter, this makes positioning of the catheter more difficult technically. Complications of central venous catheters are shown in
Box 17.5
.
Box 17.5
Complications of central venous catheter placement and incidence of occurrence
Catheter-related sepsis: variable, but reported in up to 40% of catheters
Thrombosis of central vein: variable, but reported in up to 20% of catheters
Pleural space damage: pneumothorax (5–10%), haemothorax (2%)
Major arterial damage: subclavian artery (1–2%)
Catheter problems: thrombosis (1–2%), embolism (< 1%), air embolism (< 1%)
Miscellaneous problems: brachial plexus (< 1%), thoracic duct damage (< 1%)
Catheter care:
Appropriate dressings of the catheter are essential. The dressing should be changed weekly with strict aseptic technique, and the skin exit site cleaned with chlorhexidene. A variety of dressings have been used at the skin exit, but a transparent adherent type of dressing has the advantage of allowing a visible check on the puncture site for inflammation or pus.
Infection of the catheter tip is the most serious type of infection. The patient usually is pyrexial and may have systemic signs of sepsis. This may be diagnosed by blood (at least three cultures 1 hour apart) and catheter cultures.
35
Antibiotic therapy may result in recovery, but in some the feeding line has to be removed to eradicate the infection. However, less serious infection may occur in the skin at the exit site of the catheter. This is recognised by skin erythema, possibly associated with fluid exudate and pus.
Peripheral venous access:
Peripheral venous cannulation, using a sterile technique, may be used to supply nutrients intravenously, avoiding complications associated with central venous catheters. Peripheral intravenous nutrition is likely to be used in patients who do not require nutritional support for long enough to justify risks of central vein cannulation or in whom central vein cannulation is contraindicated (e.g. central line insertion sites are traumatised, increased risks of infective complications, thrombosis of the central veins or significant clotting defects).
Problems associated with the delivery of intravenous nutrition using the peripheral route include:
The lifespan of a peripheral intravenous cannula can be prolonged by treating it as if it is a central line with regard to aseptic care, and by using a narrow-gauge cannula giving better mixing and flow characteristics of the nutrient solution. Risks of phlebitis can be reduced by frequent changes of infusion site, ultrafine-bore catheters or using a vasodilator patch over the cannulation site (e.g. transdermal glyceryl trinitrate). Furthermore, peripheral intravenous nutrition can only be used where fat emulsion is part of the single-phase administration of nutrients to avoid thrombophlebitis.
Various nutrient solutions (amino acids, glucose and fat) are available and a complete list is given in the
British National Formulary
(
www.bnf.org/bnf/
). There are also available a variety of pre-mixed bags containing various concentrations of amino acids and glucose, with or without fat, which are suitable for different clinical situations. These mixtures do not usually contain vitamins or trace elements, which must be given in addition to avoid development of metabolic complications. Care should be taken that patients receive sufficient electrolytes and minerals to satisfy requirements.
Nitrogen sources:
Nitrogen sources are solutions of crystalline
L
-amino acids containing all essential and a balanced mixture of the non-essential amino acids required. Amino acids that are relatively insoluble (e.g.
L
-glutamine,
L
-arginine,
L
-taurine,
L
-tyrosine,
L
-methionine) may be absent or present in inadequate amounts.
Attention has focused on the provision of
L
-glutamine because of its key roles in metabolism. Despite being one of the most abundant amino acids, its use in PN fluids has been limited by instability. It can, however, be supplied as
N
-acetylglutamine (hydrolysed in the renal tubule to free
L
-glutamine) or as
L
-glutamine dipeptides such as alanylglutamine (broken down to release free
L
-glutamine). Recent evidence, however, questions the need for enrichment of PN with glutamine.
36
Energy sources:
Energy is supplied as a balanced combination of dextrose and fat. Glucose is the primary carbohydrate source and the main form of energy supply to the majority of tissues. During critical illness the body's preferred calorie source is fat (fasted or fed states).
37,
38
There are controversies as to the utilisation of fat in sepsis because of defects in energy substrate metabolism at the oxidative level.
Glucose utilisation may be impaired in certain patients and glucose is then metabolised through other pathways. This results in increased production and oxidation of fatty acids, resulting in increased carbon dioxide (excreted through the lungs). In addition, if glucose is the only energy source, patients may develop essential fatty acid (linolenic, linoleic) deficiency.
Fat (e.g. soyabean oil emulsions) provides a more concentrated energy source. Usually, approximately 30–50% of the total calories are given as fat, with non-protein calorie to nitrogen ratio varying from 150:1 to 200:1 (lower in hypercatabolic conditions). The provision of exogenous lipids has also been associated with problems. Intravenous fat emulsions can impair lung function, inhibit the reticuloendothelial system and modulate neutrophil function; recent interest has also focused on the use of fish oils as a source of fat rich in omega-3 polyunsaturated fatty acids, as this appears to be associated with reduced incidence of hepatic dysfunction.
39,
40
Other nutrients:
Commercially available preparations of trace elements (e.g. Additrace®) and vitamins, water soluble (e.g. Solivito®) and fat soluble (e.g. Vitlipid®), supply daily requirements. Larger amounts, particularly of the water-soluble vitamins, may be required initially if recent nutritional intake has been inadequate. Additionally, total fluid volume and amounts of electrolytes can be modified daily to meet particular requirements.
In practice, commercially available solutions for parenteral infusion are mixed under sterile conditions in laminar flow facilities. The feeding regimen is made up in an inert 3- to 4-litre bag (ethyl vinyl acetate), comprising all nutrients and stored for up to 1 week, although compatibility between different constituents must be ensured. No additions of drugs should be made as this could make the emulsion unstable, affect the bioavailability of the drug or compromise sterility. Advantages of pre-mixed bags include:
Pre-prepared bags are available where the fat emulsion is stored separately from the aqueous solution and is mixed by bag rupture immediately prior to administration, conferring the advantage of a longer shelf life.
Instant availability of nutrients provided by the intravenous route can lead to metabolic complications if the composition or flow rate is inappropriate. Rapid infusion of high concentrations of glucose can precipitate hyperglycaemia, which may be further complicated by lactic acidosis. Electrolyte disturbances may present problems, not least because the intravenous feeding regimen is usually prescribed in advance for 24 hours. Prediction of the patient's nutrient requirements must be complemented by frequent monitoring. The provision of nutrients may lead to further electrolyte abnormalities when potassium, magnesium and phosphate enter the intracellular compartment. This is particularly noticeable in patients whose previous nutrient intake was especially poor, as highlighted previously. Others complications of PN are shown in
Box 17.6
.
Box 17.6
Metabolic complications of parenteral nutrition
Glucose disturbances
Hyperglycaemia: excessive administration of glucose inadequate insulin, sepsis
Hypoglycaemia: rebound hypoglycaemia occurs if glucose is stopped abruptly but insulin levels remain high
Lipid disturbances
Hyperlipidaemia: directly through excess administration of lipid, or indirectly through excess calories that will be converted to fat or reduced metabolism (e.g. renal failure, liver failure)
Fatty acid deficiency: essential fatty acid deficiency leads to hair loss, dry skin, impaired wound healing
Nitrogen disturbances
Hyperammonaemia: occurs if deficiency of
L
-arginine,
L
-ornithine,
L
-aspartate or
L
-glutamate in infusion. Also occurs in liver diseases
Metabolic acidosis: caused by excessive amounts of chloride and monochloride amino acids
Electrolyte disturbances
Hyperkalaemia: excessive potassium administration or reduced losses
Hypokalaemia: inadequate potassium administration or excessive loss
Hypocalcaemia: inadequate calcium replacement, losses in pancreatitis, hypoalbuminaemia
Hypophosphataemia: inadequate phosphorus supplementation, also tissue compartment fluxes
Liver disturbances
Elevations in aspartate aminotransferase, alkaline phosphatase and γ-glutamyltransferase may occur because of enzyme induction secondary to amino acid imbalances or deposition of fat and/or glycogen in liver
Ventilatory problems
If excessive amounts of glucose are given, the increased production of CO
2
may precipitate ventilatory failure in non-ventilated patients