Nutritional support in acute intestinal failure

Nutritional

support in acute intestinal failure

VIDYA P. PREM CHANDRAN ANDREW J. W. SIM

Acute gastrointestinal failure occurs as a secondary phenomenon in a variety of conditions caused by a number of different pathological processes (Table 1). One immediate result of acute gastrointestinal failure is starvation due to a partial or complete inability to digest and absorb nutrients. The starvation that occurs is often complicated by additional ongoing, metabolically disruptive processes such as sepsis, trauma or malignancy. Other aspects of gut function, including hormone production and the infection barrier, can be affected and will add to the effects of starvation. The body has a limited ability to adapt to starvation by means of altered metabolic responses. These are described teleologically as having been evolved to enhance survival when external support is not available. In the non-traumatized, non-septic patient without malignant disease the response Table 1. Classification of conditions when nutritional support may be necessary in acute gastrointestinal failure. After Pettigrew and Hill (1984). When the gastrointestinal tract Obstruction of gastrointestinal Paralytic ileus Pseudo-obstruction When the gastrointestinal Massive small bowel Intestinal fistulae

is ‘blocked’: tract

tract is too short: resection

When the gastrointestinal tract Inflammatory bowel disease Crohn’s disease Ulcerative colitis Severe infective diarrhoea Radiotherapy Chemotherapy (high dose)

is ‘inflamed’:

When the gastrointestinal tract cannot Intra-abdominal abscess or sepsis Acute pancreatitis Pancreatic pseudocyst

BailliLre’s Clinical GastroenterologyVol. 5, No. 4, December ISBN @702@1544-X

1991

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841 Copyright 0 1991, by Bailliere Tindall All rights of reproduction in any form reserved

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to starvation as described by Cahill et al (1966) takes on an adaptive form to reduce the consumption of body reserves. After trauma there is mobilization and utilization of body fuels as part of what Cuthbertson (1942) described as the ‘flow’ phase of the metabolic response. In short self-limiting acute gastrointestinal failure the mobilization and utilization of endogenous body fuels (carbohydrate, fat and protein) may be sufficient to permit complete recovery without additional supplementation or support. If the magnitude of nutritional demand and the duration of enforced starvation is great, nutritionally related complications, including failure of wound healing, decreased ability to combat sepsis and its effects, impaired respiratory muscle function, and apathy may develop, and lead to a poor outcome. In severe nutritional depletion associated with sepsis the body changes from being the protein donor to healing wounds to being the protein acceptor from healing wounds, with the disastrous consequences that skin wounds, abdominal wounds and anastomoses break down. The length of convalescence and the time taken to return to normal activity will in part be determined by the degree of nutritional depletion which occurs during the period of acute gastrointestinal failure. The nutritional status prior to the onset of acute gastrointestinal failure will in part dictate the reserves available. Pettigrew (1988) has suggested that nutritionally depleted patients are unable to withstand stress as well as their well-nourished counterparts and are therefore more prone to complications. The timing of commencement of active interventional nutritional support is important but difficult to define. If the following tenets are followed few patients will suffer because of a failure to attempt to provide nutritional support. Active interventional nutritional support should be considered in all patients when: 1. Starvation for longer than 5 days is expected. 2. Starvation for longer than 5 days has occurred. 3. The disease process is known to increase nutritional 4. Recognizable nutritional depletion or undernutrition to the onset of acute gastrointestinal failure.

requirements. was present prior

Effective techniques of nutritional support are well worked out and there are no rational reasons why a patient should be subjected to a period of starvation without specific reason. The decision to starve a patient should always be active and not by default. Wherever possible the gastrointestinal tract should be used to provide nutrition. Intravenous feeding is the only method of nutritional support available for those patients who have complete acute intestinal failure, either because of failure to digest and absorb nutrients, or because access to the gastrointestinal tract is interfered with. In incomplete intestinal failure it may still be necessary to provide intravenous nutritional support’ but if the gastrointestinal tract is accessible as much use as possible should be made of it. This chapter will discuss use of intravenous feeding, via either a central or peripheral vein catheter, and feeding into the stomach or jejunum.

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NUTRITION

Intravenous nutrition is a highly effective method of introducing nutrients into the body, but it is unphysiological-the materials bypass the control mechanisms associated with digestion and absorption in the gastrointestinal tract. The nutrient materials are in what is thought to be a readily usable form but instead of passing through the liver via the portal venous circulation they enter the systemic circulation directly. Despite these seemingly unnatural aspects of intravenous feeding, effective nutrition can be supplied via the intravenous route for both short and long periods of time. Early attempts to provide nutritional support through cannulae inserted into relatively small calibre, low blood flow, peripheral veins met with limited success (Lee, 1969), p rimarily because of the high incidence of thrombophlebitis. The introduction in the late 1960s (Dudrick et al, 1968) of ‘hyperalimentation’ via a catheter whose tip lay in a large calibre, high blood flow central vein made effective long-term intravenous feeding possible in both adults and children (Dudrick et al, 1969). Improvements in cannula construction and material, methods of insertion, procedures for catheter care, nutrient materials and mixtures have permitted the development of effective and reliable intravenous feeding systems. Now, as in the early days, intravenous feeding can be by peripheral or central venous routes. At first glance it may seem that this is simply a matter of a difference in where the intravenous catheter is inserted. However, more careful consideration demonstrates differences in the circumstances when a particular form of intravenous feeding is appropriate. The care of the catheter or cannula, the expertise necessary to provide an effective service, the nature of complications and the composition of nutrient materials used are different in the two feeding methods. The medical practitioner involved in the nutritional management of acute intestinal failure should make judicious use of both methods of intravenous feeding. Central vein intravenous

feeding

Indications

Central vein feeding is indicated: 1. 2. 3. 4.

In all circumstances where prolonged (greater than 7-10 days) intravenous feeding is either predicted or known to be necessary. When the predicted nutritional requirements are great and large quantities of nutrients need to be supplied. When a highly concentrated nutrient mixture needs to be administered in a small volume to prevent fluid overload. When good peripheral venous access is not available.

Venous access

All central venous catheterization should be carried out in an area of the hospital in which it is possible to guarantee full aseptic conditions, where all

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the necessary instruments are readily available and where the atmosphere is appropriate for the performance of a proper surgical procedure. In most institutions this means the operating theatre. The fundamental principle is that the tip of the catheter lies in either the superior vena cava, the right atrium or (rarely) the inferior vena cava; these sites permit rapid and effective dilution of infused nutrient materials, thus reducing the problems of chemically induced phlebitis. Direct access to these vessels is difficult and should only be used in exceptional circumstances. Indirect access is possible by one of three routes: 1. Direct cannulation of a major vein-subclavian or internal jugular. 2. Cannulation of a tributary vein-cephalic, external jugular or (uncommonly) the saphenous vein. 3. Cannulation of a peripheral vein with the ‘threading up’ of a long cannula. In general, veins can be cannulated by either a blind percutaneous or a direct exposure technique. Access via routes 1 and 3, and sometimes 2, can be by blind percutaneous cannulation, which in experienced hands can be reliable and safe (Bernard and Stahl, 1971). The majority of the severe complications of cannula insertion can be avoided by using a direct exposure technique, which, although more time consuming and perhaps requiring of more ‘surgical’ expertise, does permit positive confirmation of the precise position of the vein and allows controlled insertion of a cannula under direct vision. Many different techniques for catheter insertion have been described (Rosen et al, 1981); detailed descriptions of these are beyond the remit of this chapter. Once inserted it is essential to ensure that the catheter tip lies in the correct position before nutrient materials are infused. This can be done by X-ray screening during insertion, the taking of an X-ray film on completion of insertion, or using an ‘indirect’ technique such as recording the electrical activity from the tip of the catheter along a column of saline (Hoffman et al, 1989). Whatever technique is used, the patient should remain in the operating theatre until the correct position of the catheter is confirmed. The catheter should be made of a material which has low thrombogenicity and adequate strength and flexibility. Since the late 1970s catheters used for central vein intravenous feeding have commonly been made of silicone rubber. More recently polyurethane catheters have been available. Polyurethane is stronger and allows thinner walled, wider bore catheters to be manufactured. Catheters with Teflon cuffs which can be placed in the subcutaneous tissue adjacent to the skin exit site do not require to be fixed in position by suture of the hub to the skin. Multiple (double and triple) lumen catheters have been used with encouraging results (Paterson Brown et al, 1987; Payne-James et al, 1989) and may be of particular use when additional fluids need to be infused to replace the large losses associated with high output gastrointestinal fistulas or severe diarrhoea. Catheter care Prevention of catheter infection. Infection

of a foreign material inside the

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body is usually difficult to eradicate and once established may continue to act as a source of infection, leading to bacteraemia or septicaemia. An intravenous feeding catheter is the conduit for nutrient materials which might serve as effective culture media. This is particularly true if catheters have internal ‘cul de sacs’ where stasis can occur. Some organisms, such as Staphylococcus epidermidis, are ideally suited to infect intravenous feeding catheters; they produce a slime substance which sticks them to the catheter (Christensen et al, 1982) and they can etch holes in the luminal surface of silicone catheters (Peters et al, 1982). Organisms which infect catheters can be derived from either endogenous or exogenous sources. The former occurs when a patient has an abscess or other source of sepsis producing septicaemia. The infecting organisms are often gram negative, and if the primary source is removed catheter sepsis usually resolves, indicating the catheter was colonized rather than infected. Exogenous infection can come from the patient’s own skin flora, from another individual who is caring for the patient, from infected infusate or from other environmental sources. The catheter skin exit wound can get infected; potentially this can lead to the intraluminal surface being contaminated. However, the most important source of intraluminal catheter sepsis is infection of the catheter hub (SitgesSerra et al, 1984) or connection site. Linares et al (1988) reported that of 28 instances of catheter-related sepsis, 19 were hub related, three skin related, three infusate related and three were from haematogenous seeding. Available evidence indicates that hubs can get infected at the time of intravenous giving set manipulation or change. It would seem that a single breach of strict aseptic technique can be sufficient to establish infection and thus aseptic procedures used for catheter manipulation must be strictly adhered to. In a study of 43 infected intravenous feeding catheters from a general surgical ward (Sim, 1988b), staphylococci were cultured from 36 catheters. Only two of these were pure cultures of Staphylococcus aureus; of the remaining 34, 31 were pure cultures of Staphylococcus epidermidis, implicating it as the single most common catheter-infecting organism. Catheter careprotocol. In order to ensure that a catheter has the least chance of becoming infected, a well-defined catheter care protocol needs to be designed and put into effect. The lack of uniformity in such protocols and the fact that there are various aspects, such as hair removal, skin defatting, topical antibiotics, special dressings and in-line filters, which have strong proponents, attest to the fact that there is no single effective method of caring for catheters. Murphy and Lipman (1987) have drawn attention to the fact that controlled trials often fail to demonstrate that a single aspect of catheter care is significantly better than another. It is important that a protocol which has been shown to work is adhered to and that, if nothing else, strict asepsis is maintained during all catheter manipulations. Complications

other than sepsis

The complications

of central venous catheterization

fall into five categories

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related to catheter insertion, central vein thrombosis, embolism, mechanical problems and catheter removal. Catheter insertion. One complication of catheter insertion is damage to the surrounding structures. The most direct route to the superior vena cava is via one of the great veins (internal jugular or subclavian) in the upper part of the chest and neck. These veins lie in close proximity to other major structures, damage to which can lead to dire consequences. Blind percutaneous puncture of either the subclavian or the internal jugular is the commonest technique employed for the insertion of catheters. In expert hands this can be safe, but in the hands of the inexperienced, inexpert or those learning the technique, pneumothorax, laceration of a major artery, vein or thoracic duct, and nerve injury can occur (Bernard and Stahl, 1971). The use of fine needles followed by insertion of a ‘Seldinger’ type guide-wire before insertion of the catheter can minimize vascular damage. Correct positioning of the patient, particularly for subclavian puncture, can reduce the incidence of pneumothorax. After blind percutaneous catheter insertion, a chest X-ray must be taken to exclude a pneumothorax. It is essential, although time consuming, to exclude a pneumothorax following a failed attempt at catheter insertion before a further attempt is made on the other side, so that the potential disaster of bilateral pneumothorax is avoided. Direct exposure of the vein to be cannulated by careful dissection will not only avoid damage to surrounding structures but will also identify any abnormal venous anatomy. The internal jugular, subclavian, external jugular and cephalic veins can be readily exposed and safe cannulation performed. Care must be taken to ensure that the incision used for the cut down heals with the minimum of scarring. Before a catheter can be used to infuse hypertonic intravenous nutrient solutions the catheter tip must be known to be in the desired position. Depending on the route of insertion, the tip can lie in a contralateral subclavian vein, the internal jugular vein, it may go the wrong way into the brachial vein, it may not have reached the superior vena cava or it can even be in the internal mammary vein. Catheters can lie outside a vein and if solutions are then infused a ‘hydrothorax’ will occur. All catheters should be inserted in a suitable place where immediate X-ray facilities, preferably with image intensification, are available. Identification of a malpositioned catheter after the patient has returned to the ward will lead to delay in commencing nutritional support and to the added and unnecessary inconvenience of having to return to the operating theatre for catheter repositioning. Failure to cannulate a vein is particularly likely to happen with a blind percutaneous technique and occurs because of abnormal venous anatomy or thrombosed or collapsed veins (which may be present in the fluid-depleted patient). A direct exposure technique will go part way to solving this problem. In the patient who is known to be fluid depleted, intravenous infusion of a suitable intravascular expanding fluid should be considered. Central vein thrombosis.

Studies of the incidence of thrombosis in central

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veins which have been cannulated for the purpose of intravenous feeding indicate that there are a large number which contain intraluminal thrombi (Valerio et al, 1981). The majority of central vein thromboses are silent, but on occasions there can be a full-blown central vein thrombosis which if infected can be disastrous. If long-term parenteral nutrition is necessary then thrombosis of central veins can compromise the ability to provide intravenous nutrients. Infusion of heparin as part of the nutritional mixture has been suggested as a method for reducing venous thrombosis, but there is little real evidence to support this practice. Silastic and polyurethane catheters are generally accepted as being less thrombogenic than those made of polyvinyl chloride. Embolism. Air embolism is uncommon but can be life threatening. The tip of the catheter lies in an intrathoracic part of the venous system, and on inspiration negative venous pressures are created which, if exposed to the atmosphere, will permit the ‘sucking’ of air into the catheter and then the right heart, so all systems must be effectively ‘closed’ to the atmosphere. As little as 50 ml of air can be fatal. It is therefore important to ensure that all procedures which involve catheter disconnection are carried out in a fashion which does not allow negative pressures to occur: Valsalva manoeuvres, Trendelenberg positioning of the patient and clamping the catheter are all techniques which can be employed. Catheters must be protected to avoid rupture which could also lead to an opening of the system to the atmosphere. Catheter embolism occurs when the catheter or a portion of it becomes detached from its skin entry site and lies free in the venous system. A catheter embolism can lead to ‘pulmonary embolism’ or can become infected, and it is therefore important to attempt removal. Although this can usually be done by percutaneous ‘angiographic’ techniques, open surgery may on occasion be necessary. Mechanical problems. The two principal causes of catheter blockage are clot, associated with retrograde flow of blood into the catheter, and the accumulation of solid material which is a complex mixture of some of the components of the intravenous feeding mixture. Continuous infusion pumps or careful flow control mechanisms can decrease the incidence of clot formation. There is evidence that occlusion of catheters with complex mixtures occurs in patients on long-term intravenous feeding with ‘three in one’ mixtures containing fat (Main and Pennington, 1984). When a catheter becomes blocked, attempts to unblock it should be made prior to removing and replacing it; urokinase and tissue plasminogen activator have been shown to be of value (Atkinson et al, 1990). Rough or careless handling of catheters can cause damage leading to catheter breakage. This will allow intravenous nutrients to leak and also produce the potential for air or catheter embolus. Silastic is a relatively weak material and therefore clamping it with metal-jawed clamps during giving set change or other catheter manipulations should be avoided. Polyurethane catheters are stronger, but care should still be exercised

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during catheter handling. Repair kits are available and can be useful in catheters required for long-term use. Catheter removal. This can either be accidental, when the catheter is inadvertently pulled out by the patient or medical attendant, or elective. Accidental removal can be avoided by secure suturing of the catheter to the skin or by use of a catheter with an integral Dacron cuff which, when implanted under the skin entry site, prevents it being pulled out. Elective removal of catheters rarely causes problems, although occasionally bleeding may be encountered, in which case simple pressure over the vein entry site for a few minutes is usually sufficient. Catheters with integral cuffs are best removed by initial freeing of the cuff by dissection under local anaesthesia. Nutrient materials

The basic nutrients required in acute intestinal carbohydrate and fat.

failure are amino acids,

Amino acids. These are supplied in solutions of crystalline amino acids; such solutions should contain a balanced mix of both essential and non-essential amino acids. In most circumstances a regimen supplying 14 g of nitrogen/day will be adequate. Sometimes it may be appropriate to ‘tailor’-make the intake using a value such as 0.2 g of nitrogen/kg body weight/day (Larsson et al, 1990); in other instances matching the nitrogen intake to the nitrogen excretion based on daily measurements of the total nitrogen excretion may be used as a guideline for calculating the optimum intake. In addition to the standard crystalline amino acid solutions, others have been considered. There is some evidence that the branched chain amino acids (BCAAs) (leucine, isoleucine and valine), when given in high doses, can exert an anticatabolic effect in the stressed or septic patient (Cerra et al, 1982). BCAAs may reduce the energy intake required to produce positive nitrogen balance (Grimble et al, 1989) or may sensitize the muscle protein to the anabolic effects of insulin (Garlick et al, 1988). BCAAs have been reported to have a significant beneficial effect in maintaining nitrogen balance in patients with hepatic failure (O’Keefe et al, 1987). In addition to these ‘protein sparing’ effects, a BCAA infusion may to a variable extent reverse hepatic encephalopathy (Fischer et al, 1976). Recently, the amino acid glutamine has received a lot of attention. In the free amino acid pool of muscle it is present in higher concentrations than any other amino acid, and there appears to be a relationship between muscle concentrations and rates of protein synthesis-higher concentrations being associated with greater rates of synthesis. Over and above this, glutamine is a specific energy source for the gut (Windmueller, 1982) and for cells of the immune system (Schauder, 1990). Along with other amino acids such as cysteine and tyrosine which have limited solubility, glutamine, which is unstable in simple solution, is not found in sufficient quantities in a number of crystalline amino acid solutions. Adequate glutamine provision will be

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possible in the future as a number of studies have now demonstrated that peptides such as L-alanyl-L-glutamine can be used to good effect (Wilmore et al, 1988; Stehle et al, 1989). However, a study infusing large quantities of alanyl-glutamine to patients with acute pancreatitis failed, as have other studies in septic patients, to restore the depleted levels of muscle glutamine (Karner and Roth, 1990). The whole topic of the use of peptides for intravenous feeding (Furst et al, 1990) is one which will continue to attract attention. Use of dipeptide solutions will permit the infusion of otherwise difficult to supply amino acids, these solutions are of lower osmolality than those containing similar quantities of amino acids in the crystalline form. It should therefore be possible to infuse larger quantities in smaller volumes, and more dilute solutions may find a place in peripheral vein nutrition. Carbohydrate. The principal source of carbohydrate calories is glucose; not only is this the physiological fuel for most of the carbohydrate-using tissues but is convenient and cheap. Provision of 1000 kcaliday as glucose is not unusual; this is contained in 11 of 25% dextrose or 500ml of 50% dextrose. Its use is not without problems, the most important of which is hyperglycaemia. Those who use intravenous feeding regularly should have a standard method of dealing with the relatively frequent problem of hyperglycaemia; once recognized it can usually be dealt with in a relatively straightforward fashion. Control of blood glucose levels can at times pose problems; because of insulin resistance at these times (Heath, 1985) some flexibility of approach in terms of both substrate supply and insulin administration may be necessary. When patients become anabolic the combined effects of both glucose and insulin can lead to hypophosphataemia and hypokalaemia. The problem of hyperglycaemia in conjunction with the high osmolarity of concentrated glucose solutions has led to other carbohydrate materials being tried. These include fructose, sorbitol and xylitol. In some parts of the world they have met with some popularity but this is far from uniform. Fut. The use of fat as an energy source in addition to carbohydrate

is now commonplace. Much heated debate about the utilization of intravenous fat emulsions has occurred in the past, but it is now well established that modern fat emulsions (e.g. Intralipid), which are composed of a fat source, such as soy bean oil, and glycerol along with an emulsifying agent, are safe and effective. Fat has the advantage over glucose of not being osmotically active and having a higher calorie : weight ratio (1 g fat produces 9 kcal on complete combustion compared with 4 kcal for glucose). Not all calories should be provided as fat and thus it is not unusual to provide 1000 kcal as fat; this is contained in 500 ml of 20% or 11 of 10% Intralipid. In addition to fat being an energy source, there is a necessity to supply the essential fatty acids linoleic and linolenic acids. There is some evidence that in long-term intravenous feeding the addition of medium chain triglycerides (MCTs) to the lipid emulsion reduces

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metabolic complications such as liver function disturbance and the abnormal fatty acid pattern in red blood cell phospholipids (Carpentier et al, 1990). Whether MCTs can be of value in shorter term intravenous feeding has to be determined, but the fact that MCT emulsions are hydrolysed faster than the standard long chain triglyceride (LCT) emulsions and that there are higher increases in the non-esterified fatty acid levels (Carpentier et al, 1990) suggest that a combined MCT/LCT emulsion may find a place in routine intravenous feeding. Another substrate which has been suggested, over the years but has attracted more attention recently is the ketone bodies (beta-hydroxybutyrate and acetoacetate). Many tissues can be identified as predominantly glucose oxidizing (brain) or predominantly free fatty acid (FFA) oxidizing (muscle); others (liver, lung, heart and kidney) can oxidize either glucose or FFA. With the exception of the liver, all these tissues are capable of using ketone bodies as a substitute for either glucose or fat and thus ketone bodies seem an attractive energy source. In an extensive review Rich (1990) suggests that ketone bodies might be useful as part of a nutrient mixture. Other nutrient materials which have to be supplied are the trace minerals, fat- and water-soluble vitamins, minerals, electrolytes and water. If the acute intestinal failure is associated with substantial losses of gastrointestinal fluids, as with fistulae, and particularly if these contain large quantities of bile, careful monitoring of magnesium and zinc status (which are found in relatively high concentrations in bile) will be necessary to ensure adequate supplementation. Complete nutritive mixtures. Provision of intravenous nutrients has been substantially simplified by the advent of complete nutritive mixtures. Socalled ‘three in one’ mixtures of amino acids, fat, carbohydrate and all other essential nutrients (Jeppsson and Sjoberg, 1984) have been extensively used (Sim, 1986) and found to be safe and stable as long as well-defined recipes are adhered to. In the case of high fluid losses, such as fistulae, where there is a requirement for large quantities of electrolytes and minerals, it may be necessary to infuse these separately and not risk disturbing the nutrient mixture. Expertise required to manage intravenous feeding

Nursing staff, and not doctors, are responsible for the day-to-day in-hospital care of central venous feeding catheters. In some hospitals, specifically employed nursing teams are responsible for all catheter care (Hamoui, 1987), in others special units exist for intravenous feeding, and others may have an individual who oversees catheter care; commonly, though, it is the nurses who staff a particular ward that carry out the day-to-day care of central venous catheters (Sim et al, 1984). However, there is little doubt that the lowest catheter sepsis rates are achieved where specialist nurses are employed (Keohane et al, 1983; Haddock et al, 1985; Faubion et al, 1986).

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Peripheral vein intravenous feeding Peripheral vein feeding can be used as an effective means of nutritional support, but it must not be seen as an easy option to be used by inexpert individuals. If it is to be used as a therapeutic option then it must be done with great care and attention to detail. Indications Short-term nutritional support. A rational argument can be made for its use in those patients in whom it is not clear whether prolonged intravenous feeding will be required. If a policy of starting intravenous feeding after 5 days of starvation is employed then a substantial number of patients will be fed for periods of a week or less; these individuals could probably be fed via a peripheral vein for this relatively short period of time. If feeding is still required after a week then a central venous catheter can be inserted and intravenous feeding continued. Problems with central vein access. In the situation where it may be difficult to cannulate a central vein because of trauma or burns to the area of access or if there is central vein thrombosis, the peripheral veins may be the only route for intravenous infusion. Recent or recurrent catheter sepsis. In order effective eradication of an infecting organism peripheral vein cannula in order to avoid the central venous catheter, which would either source of infection.

to allow a period of time for it may be appropriate to use a possibility of infecting another require removal or persist as a

Venous access

The best vein is a straight large-calibre vein lying on the dorsum of the forearm. Once inserted the cannula should be fixed securely to prevent unnecessary movement of the tip which can cause mechanical damage by abrasion of the endothelium of the vein. The cannula should be resited, preferably in the other arm every 24 to 48 h. Catheter care

Unlike central venous catheters, where the principal management problem is catheter-related sepsis, the principal problem associated with peripheral venous cannulae is thrombophlebitis. In addition to being painful and distressing for the patient, thrombophlebitis damages the vein involved and because of the surrounding oedema and inflammation makes cannulation of veins in the proximity difficult if not impossible. Adequate catheter fixation, use of small cannulae and regular resiting of cannulae can reduce thrombophlebitis; Tanner et al (1980) and Isaacs et al (1977) have reported that use of heparin and steroids can also be of benefit.

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materials

In order to minimize the possibility of chemically induced thrombophlebitis the nutrient solutions used must be as nearly isotonic as possible. There is some evidence that the addition of fat emulsions may ‘protect’ the venous endothelium. Various regimens have been described and commercial nutritive mixtures specially designed for peripheral vein feeding are available. It should be possible to supply at least 9 g of nitrogen and 2000 kcal/day along with a reasonable supply of electrolytes, minerals and vitamins. The use of adjunctive measures, such as growth hormone, to increase the utilization of nutrient materials may be worth considering (Ponting et al, 1988).

ENTERAL

FEEDING

Enteral nutrition can be used in certain well-defined circumstances when acute gastrointestinal failure has occurred. However, if there is any doubt about whether the nutrient materials are either being utilized or provided in sufficient quantities intravenous feeding should be employed. The specific conditions where enteral nutrition can be used are: 1. High intestinal obstruction. 2. Well-established high enterocutaneous fistulae. 3. Well-established low enterocutaneous fistulae. Access to the gastrointestinal

tract

1. Fine bore nasogastric or nasoenteric tube. These can be inserted readily, are usually comfortable and remain patent if properly cared for. 2. Tubepharyngostomy. Thismethodhasnotgainedwidespreadpopularity but in situations when it is inappropriate to use the nasogastric or orogastric route it is a useful alternative (Graham and Royster, 1967). Recent improvements in technique have simplified the procedure of tube insertion (Gaggiotti et al, 1989). 3. Gastrostomy. This can be inserted at open surgery using the Stamm technique described by Farris and Smith (1956) or it can be placed percutaneously with endoscopic control (Gauderer et al, 1980). 4. Jejunostomy. This can only be inserted during open surgery. The tube can either be a fairly wide (14 gauge) Foley or T-tube catheter inserted as a Witzel jejunostomy (Williamson, 1987) or a fine needle jejunostomy (Yeung et al, 1979), both of which should be ‘tunnelled’ and the jejunum firmly anchored to the anterior abdominal wall. Nutrient

materials

Although a few proponents may still exist, nowadays there is no need to either use blenderized ward diets or to manufacture specific tube feeds in

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hospital kitchens. A wide variety of specifically designed and formulated liquid diets are available and should be used. In most situations diets containing whole proteins or peptides are well utilized. The absorption of ‘protein’ in the form of amino acids and/or peptides seems to be as, if not more, efficient with whole protein diets than with the elemental diets containing pure amino acids (Silk, 1986). The whole protein diets are, generally speaking, of lower osmolality than the elemental diets and are thus easier to use. Calorie sources can contain mixtures of fat and carbohydrate. The calorie density of liquid feeds varies, but a lot of formulated liquid diets contain 1 kcal/ml, making calculation of quantities to be administered straightforward. A number of manufactured feeds are lactose free. The rationale for this relates to two facts: 1. 2.

Lactase deficiency is fairly common in the general population, the incidence ranging from 5 to 10% in English people to almost 100% in some Asian populations. In starvation the brush border lactase rapidly decreases.

In reality, adverse effects due to lactose ingestion are uncommon and it is hard to implicate lactose as a cause of diarrhoea during enteral feeding. The carbohydrate energy source is often in the form of a complex carbohydrate; high molecular weight glucose polymers have been shown to be well absorbed even in the absence of amylase activity in the lumen of the small intestine (Jones, 1984). As long as there is adequate lipase and bile acid, fat can be digested and absorbed and triglyceride-containing feeds can be used as an energy source. In patients with severe pancreatic or biliary disease or a substantial loss of mucosal absorptive capacity, fat may not be well absorbed and a carbohydrate energy source may have to be used instead. There are claims that MCTs are better absorbed than LCTs in the compromised gastrointestinal tract; however, there seems to be little real evidence to support this. Administration

of enteral feeds

Nutrient materials can be given continuously or as a bolus. Continuous feeding has the advantage that a constant supply of nutrients is delivered to the gastrointestinal tract and regular and continuous digestion can take place. Continuous delivery can be by constant gravity drip, via a reservoir or burette system, or the use of a continuous infusion enteral feeding pump. Bolus feeding can be carried out at intervals varying from hourly (which in reality closely approximates to continuous feeding) to longer periods which might approximate to ‘normal’ meal times. Bolus feeding is generally more appropriate for patients who are well established on enteral feeding and are either feeding themselves or are being fed by a friend or relative rather than one of the nursing staff. Debate exists as to how enteral feeding should commence. There are some who believe that enteral feeding should be introduced gradually, giving the gastrointestinal tract time to adapt, and there are those who

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believe that a period of adaptation is unnecessary and that full feeding can be instituted straight away. After a period of starvation there is atrophy of the intestinal mucosa (Stanfield et al, 1965) and some of the brush border enzymes are either absent or are present in low concentrations. It therefore seems prudent to introduce nutrients to the starved gastrointestinal tract with some caution. In using regimens for the introduction of enteral feeding it should be borne in mind that in general the stomach is capable of handling high concentrations of nutrients whereas the jejunum is not. Feeding regimens for gastrostomy (or intragastric) and jejunostomy feeding are shown in Tables 2 and 3. Table

Day 1 2 3 4

2.

Regimen for gastrostomy feeding.

Rate (ml/h)

Feed strength

Calorie intake*/day

50 15 100 125

Full Full Full Fllll

1200 1800 2400 3000

* For feeds which contain 1 kcal/ml. Table

3.

Regimen for jejunostomy feeding.

Day

Rate (ml/h)

1

25 50 75 100 100 100 100 125

2 3 4 i 7 8

Feed strength

Calorie intake*/day 150 300 450 600 1200 1800 2400 3000

* For feeds which contain 1 kcal/ml.

Complications The principal complication is diarrhoea. The exact aetiology of enteral feed associated diarrhoea can, in an individual patient, be difficult to determine. Antibiotic administration at the time of enteral feeding can be a major factor in causing diarrhoea (Keohane et al, 1984). The use of starter regimens may not prevent diarrhoea occurring (Rees et al, 1986). Once diarrhoea is established it may be necessary to stop the enteral feeding in order to control it; attempts to reduce diarrhoea by giving codeine phosphate every time diarrhoea occurs can be successful. Other complications of enteral nutrition are well described by Silk (1983) and include: 1.

Those related to tube insertion-in

the case of nasoenteric tubes these

NUTRITIONAL

2. 3. 4. 5. 6. 7.

SUPPORT

IN

ACUTE

INTESTINAL

FAILURE

855

are oesophagitis, oesophageal erosions and oesophageal stricture. All tubes may be malpositioned and accidental withdrawal can occur. Metabolic-hyperglycaemia, hypokalaemia, hypomagnesaemia, hypocalcaemia, hypophosphataemia and low levels of zinc and red blood cell folate. Regurgitation and aspiration. Gastrointestinal side-effects-abdominal pain and distension. Abnormalities of liver function. Problems associated with administration of infected feeds (Anderson et al, 1984). Inadvertent intravenous infusion of enteral feeding materials.

RESULTS OF NUTRITIONAL SUPPORT IN ACUTE GASTROINTESTINAL FAILURE In as much as there are no diseases in which starvation as a mode of treatment has been demonstrated to produce a better outcome than feeding (ASPEN Board of Directors, 1986), it is self evident that patients with acute gastrointestinal failure will benefit from safe, active, interventional nutritional therapy by the intravenous or enteral route during the period when nutrient intake by the normal route is not possible. The effects of preserving body cell mass and fat stores will allow ‘natural’ healing processes to proceed and avoid the development of nutrition-related complications. In addition to these generalities, there are three disease processes in which nutritional support has a specific role: inflammatory bowel disease, acute pancreatitis and enterocutaneous fistulae. Inflammatory

bowel disease

Crohn’s disease in both its acute and chronic form can give rise to starvation and subsequent malnutrition. Following the observation by Steiger et al (1969) that a proportion of malnourished patients with Crohn’s disease being prepared for surgery with intravenous nutrition underwent remission, the possibility of intravenous nutrition as a specific therapy has been pursued. A number of studies (Greenberg and Jeejeebhoy, 1981; Muller et al, 1983; Ostro et al, 1985) have demonstrated that in approximately 60% of patients remission can be induced by intravenous feeding alone; unfortunately there is a high relapse rate of between 16 and 67% (Greenberg, 1988). The management of enterocutaneous fistulae in Crohn’s disease is considered in a later section. The concept of bowel rest as a specific therapy has also been suggested for the management of ulcerative colitis. In two prospective studies (Dickinson et al, 1980; McIntyre et al, 1986) no benefit seemed to accrue from the addition of intravenous nutrition to other standard treatments. In the severely ill patient with ulcerative colitis there is the suggestion that delaying effective surgery because of attempts to improve nutritional status may be harmful (Elson et al, 1980).

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SIM

Acute pancreatitis

Although there are some proponents of enteral nutrition, intravenous nutrition is the preferred method of support for moderate and severe attacks of acute pancreatitis (Sim, 1988a). The Board of Directors of the American Society of Parenteral and Enteral Nutrition has recommended that moderate to severe acute pancreatitis is a clinical setting where intravenous feeding should be part of routine care (ASPEN Board of Directors, 1986). Although there is some evidence that intravenous feeding might reduce mortality (Grant et al, 1984), its principal role is in supporting the patient while other therapies are being used (Goodgame and Fischer, 1977). Enterocutaneous

fistulae

Before the advent of antibiotics, effective fluid and electrolyte replacement, appropriate surgical management and active nutritional support, the mortality from enterocutaneous fistulae could be as high as 45% (60% if the patient was malnourished), with spontaneous fistula closure rates as low as 10% (Edmunds et al, 1960). It is claimed that the advent of intravenous feeding has dramatically improved the mortality of patients with enterocutaneous fistulae, but there are no prospective studies comparing intravenous feeding with starvation. It is, however, unlikely that nutrition alone is responsible for the improved figures. At the same time as intravenous nutrition was introduced, advances in the management of the severe sepsis that can accompany fistulae occurred. Soeters et al (1979) studied the outcome of fistula management during different periods of time and concluded that the most important determinant of outcome was uncontrolled sepsis; he failed to demonstrate that the mortality from small bowel fistulae was any better during the period of time when intravenous nutrition was introduced (1970-1975) than during the period of time before it was introduced (1960-1970). A number of papers demonstrate that spontaneous fistula closure rates are higher in patients receiving intravenous nutrition than in those who are not; for example, Kaminsky and Deitel (1975) reported an improvement in closure rate from 34% to 80%. Enteral nutrition using defined formula liquid diets can be used effectively in the management of fistulae. Voitk et al (1973) report that 100% of oesophageal and gastric fistulae, 59% of small intestinal, 83% of colonic and 85% of pancreaticobiliary fistulae heal spontaneously with enteral nutrition. However, it would seem that the principal use of enteral nutrition will be in one of three situations: 1. 2. 3.

Fistulae in the distal part of the bowel, terminal ileum or large bowel (Bury et al, 1971). Low output or almost healed fistulae. Fistulae in the upper gastrointestinal tract in which a feeding tube can be passed distal to the fistula. Patients with oesophagogastric, duodenal and high jejunal fistulae can often be fed through a feeding jejunostomy or more appropriately through a nasoenteric tube introduced with

NUTRITIONAL

SUPPORT

IN

ACUTE

INTESTINAL

FAILURE

X-ray screening so that the tip is positioned opening.

857

distal to the fistulous

CONCLUSIONS

All physicians and surgeons involved in the management of acute gastrointestinal failure need to be able to provide appropriate and effective nutritional support during the period that the patient is starving. Proper consideration of the route of administration and the techniques involved are necessary if the best use of this therapeutic modality is to be made. All nutritional support should be an active therapy instituted at the appropriate time with the appropriate objectives. The provision of adequate nutrients which can be effectively used will prevent further erosion of lean body mass and fat reserves; it should be remembered that it is unlikely that depleted stores will be built up in the acute stage of illness. Once established, nutritional support should be continued until the patient is able to take adequate nutrients by the oral route. Finally, active efforts should be made to ensure that adequate food is eaten during the period of convalescence when the patient is undergoing the final ‘stages of recovery outside of hospital.

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