enteral nutrition andthe criticallyenteral nutrition to the critically ill, the difficulties...

Postgrad Med J' 1996; 72: 395 -402 (© The Fellowship of Postgraduate Medicine, 1996

Management options

Enteral nutrition and the critically ill

Scott A Shikora, Angela M Ogawa

SummaryCritically ill patients invariablyrequire nutritional intervention.Traditionally, enteral nutritionhas not been widely employed inthis patient population. This isdue in part to the success ofpresent-day parenteral nutrition,and to difficulties encounteredwith enteral feeding. Recent evi-dence has demonstrated that ent-eral is preferable to parenteralnutrition in terms of cost, compli-cations, gut mucosal mainte-nance, and metabolic andimmune function. Enterally ad-ministered nutritional supportcan and should be utilised as thepreferred route of nourishmentfor the critically ill. The appro-priate choice of access and for-mula, as well as a rational strategyfor implementation, should im-prove the likelihood of success.This article describes the uniquefeatures of critical illness as theypertain to nutritional support, thebenefits of enteral nutrition, andthe obstacles to success, and offerssuggestions which may improvethe ability to provide nutrientsadequately via the intestinal tract.

Keywords: malnutrition, nutrition sup-port, critical illness, enteral nutrition

Nutrition Support Services, WilfordHall USAF Medical Center, LacklandAFB, Texas, USASA ShikoraAM Ogawa

Correspondence to Scott A Shikora, MD, FACS,Director, Nutrition Support Service, Departmentof Surgery, Faulkner Hospital, Boston, MA02130, USA

Accepted 13 November 1995

The opinions expressed herein are those of theauthor and do not necessarily reflect the opinions ofthe United States Air Force or the Department ofDefense.

Critical illness is characterized by significant morbidity and mortality. Diseaseprocesses evolve quickly and patient status may repeatedly fluctuate. Often,multiple organ systems are affected. Overall, these patients are among the mostchallenging for the clinician. Physiologically, critically ill patients exhibit thestress response, which is characterised by hypermetabolism and hypercatabo-lism. Storage nutrients in the form of fat, carbohydrates and protein areliberated and utilised to fuel the engine of metabolism and provide substratesfor tissue repair. Successful recovery is often dependent upon the ability tocomplete the healing process prior to the exhaustion of fuel. Without the properadministration of nutrients to offset lean body wasting, recovery is rare.Our expanding ability to administer nutritional support has greatly improved

the outcome for patients in the intensive care unit. Unlike the typicalhospitalised patient, the critically ill are more difficult to nourish adequately.They tend to have greater requirements for protein and calories, yetcharacteristics such as fluid overload, hyperglycaemia, and pre-existing medicalconditions often complicate the ability to provide sufficient nutrients. Ironically,it appears that the patients who require the most nutritional intervention, areoften those least likely to be adequately fed.

Traditionally, enteral nutrition has not been widely employed for this patientpopulation. This is due in part to the success and ease of present-day parenteralnutrition, and to difficulties encountered with enteral feedings. Feeding thecritically ill can be challenging, no matter which route of administration ischosen, due to problems with fluid restrictions, metabolic derangements andhyperglycaemia. Clinicians attempting to utilise enteral feeding are furtherfrustrated by patient conditions such as gastric dysmotility, diarrhoea, formulaintolerance, and occasionally, by intestinal ileus. Appropriate gastrointestinalaccess can also be a problem and may require surgical placement.Over the last few years, the value of gastrointestinal feeding has been

redefined. Numerous benefits have been identified and myths concerning itsinappropriateness for patients in intensive care units debunked. Additionally,with the proper understanding of the unique environment encountered in theintensive care unit, enteral nutrition can be utilised successfully and its benefitsattained. This review discusses the rationale behind the impetus to administerenteral nutrition to the critically ill, the difficulties encountered, and somepoints to optimise the potential for success.

Metabolic characteristics of critical illness

The critically ill form a unique subset of hospitalised patients. Many of thesepatients have pre-existing medical conditions that significantly influence theiroutcome, including heart disease, diabetes, chronic obstructive pulmonarydisease, renal insufficiency, and cancer. In many cases, the nutritional status ofthese patients prior to their admission to the intensive care unit is alreadyseverely compromised. In addition, many will go on to develop organdysfunction as a consequence of sepsis or the inflammatory response. Boththe pre-existing illnesses and the acquired conditions will significantly alter theability to nourish.A common characteristic of critical illness is the stress response. This process

is a cytokine- and hormone-mediated mobilisation of endogenous substrateswhich are utilised for the stabilisation of organ function, maintenance ofimmunocompetency and recovery from injury."2 It is known that the stressresponse is responsible for many of the metabolic consequences of criticalillness, namely fluid overload, hypercatabolism, hypermetabolism, and glucoseintolerance.More than 50 years ago, Cuthbertson and Tilson3 described this

phenomenon as a two-phase process. The ebb phase occurs immediately afterinjury and lasts approximately 24-48 hours. During this short-lived period,there is an increase in sympathetic activity and a stimulation of thehypothalamic-pituitary axis.4 It is characterised by marked hypometabolismand decreased oxygen consumption.4 It is now recognised that these findings

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Metabolic characteristics ofcritical illness

* hypermetabolism: increased energyexpenditure

* hypercatabolism: increased proteinbreakdown

* hyperglycemia: secondary to insulinresistance, glycogenolysis, and/orgluconeogenesis

Benefits of enteral nutrition

* prevents intestinal mucosal atrophy* supports the intestinal immunologic

shield to invasion by pathogens* attenuates the hypermetabolic

response to injury* less costly than parenteral nutrition* may improve outcome for critically

ill or traumatized patients

are primarily the result of hypovolaemia leading to decreased cardiac outputand inadequate oxygen transport to the tissues. In contrast to the ebb phase,the second, acute or flow, phase is one of hypermetabolism, catabolism, andincreased oxygen consumption.6 These mechanisms are thought to be mediatedby cytokine release and afferent nerve signals from the injured tissues.7 Duringthis period, there is an active liberation of endogenous substrates such asglycogen-derived glucose, skeletal muscle-derived and labile amino acids, andadipose tissue fatty acids. 1'2'8'9 Increased sympathetic and hypothalamic-pituitary activity stimulate the release of the catecholamines and the counter-regulatory hormones, namely, the glucocorticoids, glucagon, growth hormone,prolactin and aldosterone. These hormones act synergistically to promotelipolysis, muscle protein breakdown, insulin resistance and glycogenolysis.2,4,10,11 Since the glycogen stores are limited, this source of glucose is quicklyexhausted.1 The need for readily available glucose will then depend onenhanced muscle protein breakdown to provide amino acids for hepaticgluconeogenesis. 12'4 In response to the rising plasma glucose levels, insulinsecretion is increased. However, the hormone's actions on glucose metabolismare greatly restricted by the profound insulin resistance. 14" 0The net effect of these metabolic pathways is the liberation of peripherally

stored substrates to meet the energy requirements of the major organ systems.Each substrate plays an important physiologic role in the stress response.Glucose is an important fuel for the central nervous system, the wound, and theimmune system, all ofwhich are metabolically active during stress.1'2'6 The fattyacids function to provide energy for cardiac and skeletal muscle, the liver, andmany other tissues. 1,2,6 Although some liberated amino acids are utilised forgluconeogenesis, the majority are required for the synthesis of the acute phaseproteins, for thermogenesis, and as precursors for tissue repair.'2'6'9. In statesof semistarvation, the ongoing demand for amino acids can lead to markedwasting of lean body tissue. The healthy human body stores approximately100 g of labile protein nitrogen and is designed to withstand about one week ofstress without feeding.'2 In the critically ill, where catabolism is more intenseand nutrient stores are likely to be inadequate, storage fuels are more rapidlyexhausted. Further protein wasting without supplementation can lead todecreased protein synthesis, organ dysfunction, immunodeficiency, sepsis, andultimately, death.2'4'

Recovery, should it occur, is marked by a decrease in metabolic rate, arestoration of appetite, a replenishing of the body energy stores, and a markedrebuilding of the lost lean body mass. The cytokine, catecholamine, andcounter-regulatory hormone influences subside, and insulin again becomes theprimary nutrient regulatory hormone. There is also a significant uptake ofamino acids in the muscle for synthesis and glucose for the production ofglycogen and triglycerides.

Benefits of enteral nutrition for the critically ill

In the intensive care unit, parenteral and enteral nutrition should not bemutually exclusive, but rather, complementary. Both modalities offer uniquebenefits and have inherent limitations. For many reasons, total parenteralnutrition (TPN) is still considered the gold standard for the nutritional supportof the critically ill. It offers the best means of insuring both macro- andmicronutrient delivery and is an excellent modality for correcting metabolicderangements. For the fluid-overloaded patient, it can be utilised as a vehicle todeliver intravenous medications without increasing the volume load and can beconcentrated significantly, while still providing adequate nutrition. Since mostpatients in the intensive care unit already have an indwelling central venouscatheter and many hospitals provide TPN as stock solutions, prescribing TPNcan be quite simple. Occasionally, it also represents the only nutritional optionavailable for patients with severe gastrointestinal dysfunction.

Unfortunately, TPN is significantly more expensive then enteral nutritionand requires a dedicated central venous catheter or a dedicated lumen of anindwelling multilumen catheter. It also has a higher incidence of seriouscomplications, not exclusively related to the central venous catheter.'3"4The reliance on TPN often coincides with gastrointestinal deprivation which

can lead to a breakdown of the gut barrier to bacterial invasion, and possibly,bacterial translocation.'5"6 To prevent the invasion of microbes into thesystemic circulation, the small intestine relies on both a physical baffler and animmunologic shield. The physical barrier is created by the tight junctionsbetween intact epithelial cells, gastric acid, digestive enzymes, mucusproduction, intestinal motility and a normal bacterial flora. The intestinalimmune system, often referred to as the Gut-Associated Lymphoid Tissue


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Enteral nutnition and the critically ill 397

(GALT), consists of cells such as lymphocytes and macrophages situatedthroughout the intestinal wall and the production of the antibody IgA which issecreted into the lumen and prevents the adherence of microbes to the mucosa,a step necessary for invasion.17 Conditions in the intensive care unit maypredispose patients to translocation. Gastric acid is commonly neutralised toprevent gastritis and ulceration. With the use of sedation and narcotics, there isa tendency toward decreased intestinal motility leading to luminal stasis.Antibiotic usage, commonplace in the intensive care unit, leads to the bacterialovergrowth of pathogens. Without enteral nutrient stimulation, the mucosaatrophies,'5'18 causing increased permeability.'9 The GALT system alsoatrophies.20 The combined effect of these changes is a weakening of the gutdefence to invasion. The resultant translocation is believed to be associated withand maybe even the underlying cause of the nosocomial sepsis and themultisystem organ dysfunction seen with critical illness.'6'2' However, theactual relationship between translocation and nosocomial sepsis remainscontroversial.While present-day parenteral nutrition can substitute nutritionally for the

interruption of oral nutrition, gut mucosal atrophy and immune dysfunction arenot prevented.'5'22'23 A stream of luminal nutrients seems to be essential. It hasalso become apparent that certain nutrients are indispensable for maintainingthe intestinal barrier to microbes. Both the epithelial cells of the mucosa as wellas the lymphoid cells of the GALT system require specific nutrients for growthand normal function. These nutrients (glutamine, arginine, nucleotides, andshort chain fatty acids) are not found in standard parenteral solutions or even inmost enteral formulations.

Enteral nutrition has recently gained new popularity. A large body ofliterature describes benefits in terms of cost, lower complication rates, andfavourable effects on metabolic and immune function. The infusion ofnutrientsintraluminally has been shown to be important for maintaining gut mucosalintegrity, a key factor for organism homeostasis and immunologic compe-tence.2 25 The provision of nutrients intraluminally has also been shown toattenuate the stress response. The acute phase reactive protein secretion isblunted and higher levels of synthetic proteins are seen.26 Lowry demonstratedlower counter-regulatory hormone and C-reactive protein levels in subjects fedonly enterally after exposure to endotoxin versus those fed parenterally.24 Thenet effect is a lower rate of catabolism and energy expenditure.

Improvements in outcome have also been reported. Studies including thoseby Moore and co-workers have demonstrated in trauma patients improvednitrogen balance, lower infection rates, and improved wound healing with earlyenteral nutrition.'3'27 In similar work, Kudsk et al demonstrated a significantlylower infection rate in critically ill trauma patients who were provided nutritionenterally."4 A recent meta-analysis of eight published studies by Moore's groupalso concluded that high risk surgical patients fed enterally had reduced septiccomplications compared with patients given parenteral nutrition.28 Otherbenefits seen with enterally administered nutrition include improved gallblad-der contraction leading to a reduction in the likelihood of gallstone formationand acalculous cholecystitis, increased pancreatic stimulation with a reductionin sluggish secretion and functional insufficiency, and improved gut healingafter surgical anastomosis.29Most intensive care physicians support the early institution of enteral

nutrition for critically ill patients. In general, it is believed that the earlyinitiation of intestinal feeding attenuates the stress response, decreases theloss of lean body tissue from catabolism and improves patient outcome.Unfortunately, these theories have never been conclusively proven to betrue. While a number of investigational studies have demonstratedimproved metabolic parameters and patient outcome when comparingearly enteral nutrition to early parenteral feeding, there are few publishedreports that evaluate the differences between early and delayed enteralnutrition.Grahm et al compared early jejunal feeding (within 36 hours of injury) to

late gastric feeding in head-injured patients and demonstrated a reducedincidence of bacterial infections and hospital stay in the early fed group.30 Incontrast, Eyer and co-workers evaluated the effects of early enteral feeding(within 24 hours of injury) versus initiating feeding after 72 hours and foundthat early' feeding did not blunt the stress response or alter patientoutcome.

Despite the lack of strong clinical evidence to support early gut feeding, mostintensive care physicians would support initiating enteral nutrition within thefirst 48 hours of injury or surgery in a stable patient since it is usually well-tolerated and may improve outcome.32


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Obstacles to providingenteral nutrition for thecritically ill

* fluid restriction* acid-base disorders* electrolyte abnormalities* access difficulties* formula intolerance

Obstacles to providing enteral nutrition for the critically ill

Unfortunately, administering enteral nutrition to the critically ill can bedifficult. It is far easier to prescribe TPN through an indwelling catheter than tocontend with the problems associated with enteral feeding. Most of thesedifficulties fall into two main categories, access problems and feedingintolerance. In addition, enteral feeds are often withheld for diagnostic testingor surgery so that patients commonly receive only a fraction of the requiredfeeding. It is therefore no surprise that TPN-fed patients tend to receive morenutrients per kilogram of body weight than those given enteral nutrition.14While these concerns frustrate clinicians, many have reported good success inproviding enteral nutrition in the intensive care unit.

ACCESS PROBLEMSMany critically ill patients will manifest some degree of gastric dysmotility.Potential aetiologies include sepsis, use of hyperosmolar feeds, electrolyteabnormalities, gastritis, peptic ulcer disease, chemotherapy, medications andcomorbidity such as diabetes mellitus.33 Interleukin-l, a cytokine releasedduring stressed states, has been shown to delay gastric emptying whenadministered to rats fed a liquid diet.34 Feeding into the stomach in thesecircumstances was believed to increase the risk of regurgitation and aspiration.However, recent studies have failed to support this notion.35'36 Patients withnormal gastric emptying but diminished ability to protect their airway, such asthose with neurologic disorders may also require postpyloric tube placement.The appropriate gastrointestinal access can also be challenging to obtain and

maintain. Placement may require endoscopic, fluoroscopic or even surgicalassistance. Often, after successful access has been obtained, feeding tubesocclude, dislodge or are inadvertently removed. Tubes commonly occlude,particularly ifused to deliver crushed medications or when not carefully flushedclear with water after the feeding has been discontinued.

FEEDING INTOLERANCEIntolerance may present as vomiting, abdominal pain and/or bloating, paralyticileus or diarrhoea. While postpyloric tube placement alleviates gastric emptyingproblems, the other manifestations ofintolerance are more difficult. Diarrhoea, acommon problem for the critically ill, has a number of potential causes. Theseinclude medications, such as antibiotics, antacids, and sorbitol, infections such asClostridium difficile and other enteric pathogens, formula osmolality and fatcontent, infusion rate, malabsorption, lactose intolerance, and hypoalbuminae-mia.37-4 Many studies have evaluated the contribution of some or all of thesefactors. There seems to be no true consensus concerning the relative importanceof each. In all likelihood the cause of diarrhoea is usually multifactorial. If theaetiology can be elucidated, the offending agent can then be addressed. Forinstance, C difficile colitis can be treated, sorbitol-based medications may beeliminated, and the choice of enteral formula being used can be reconsidered.The contribution of formula osmolality in feeding intolerance and diarrhoea

is also controversial. Traditionally, hyperosmolar feed has been thought to bedifficult to tolerate. However, Borlase et al have demonstrated that evenformulas with an osmolalit of 630 mOsm, about twice that of serum, can besuccessfully administered. Presently most commercial products are isosmolaror slightly hyperosmolar relative to serum.

Formula options

Currently there is no consensus in the literature regarding the optimal choice ofenteral product for the critically ill. As patients and illnesses vary widely, itcould be said that the formula of choice is that which the patient best tolerates.Fortunately, there are many commercial enteral products available which offer avast array of options to fit the needs of most critically ill patients. Theseproducts differ in protein source and form, fat content and source, caloricdensity, and osmolarity. Carbohydrate source is less important since mostcommercial formulas are lactose free and most other types of carbohydrate aregenerally well tolerated.

Formulas are usually categorised based on their contents and applications(table). These include polymeric (encompasses standard, high calorie/highnitrogen, fibre enriched, and disease specific), peptide, special nutrient, andmodular. For the critically ill, the choice is usually between a low fat, peptideformula or a standard formula that contains intact protein and providesapproximately 30% of its calories as fat. Some studies have demonstratedimproved tolerance with peptide (+/- low fat) formulas.38'42 Meredith and co-


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Enteral nutrition and the critically ill 399

Manifestations of formulaintolerance

* abdominal bloating and distention* abdominal pain* diarrhoea* high gastric residuals* paralytic ileus

Table 1 Selected enteral formulas for critically ill patients

Vol to meetFormula Calciumlml Protein (gll) Fat (%) mOsm US RDA

Peptide formulas: partially hydrolysed protein source, may be better absorbed and utilizedduring critical illness, the early postoperative period and with malabsorptive conditionsVital HN1 1.0 42 10 500 1500Reabilan HN2 1.3 58 35 490 1875Peptamen VHP3 1.0 62.4 35 430 1000

Standardformulas: intact protein with moderate fat contentOsmolyte HN1 1.06 44.4 30 300 1321Promotel 1.0 62.5 21 300 1250Sustacal4 1.01 61 21 650 1060

High nitrogenlhigh calorie formulas: hyperosmolar, high fat content formulas useful for fluidrestricted and/or hypermetabolic patientsEnsure Plus HN' 1.5 63 30 650 947Two Cal HN1 2.0 84 41 690 947Isocal HCN4 2.0 75 46 690 1000

Fibre-enriched formulas: polymeric formulas with intact protein and added fibreJevityl 1.06 44 30 310 1321Compleat5 1.07 43 31 300 1500Ultracal4 1.06 44 37 310 1250

Special nutrientformulas: standard or peptide formulas containing specific nutrients thought tobe conditionally essential during critical illnessAlitraql 1.0 53 14 575 1500Impact5 1.0 56 25 375 1500Perative' 1.3 67 25 385 1155

Disease-specific formulas: modified substrate form and contents to meet restrictions of specificorgan dysfunctionNeprol 2.0 70 43 635 947Hepatic Aid II6 1.2 44 28 560 *Pulmocarel 1.5 62.5 92 520 1420

This list represents only a sample of the many commercial products on the market. A numberof equally useful formulas are also available. l=Ross, 2=Elan Pharma, 3=Clintec, 4=MeadJohnson, 5=Sandoz, and 6=Kendall McGaw. RDA: recommended daily allowance; *, notnutritionally complete

workers demonstrated better hepatic protein responses in trauma patients whenfed a peptide formulation.42 In contrast, other studies have had similar successwith standard whole protein, high fat formulas.4345 While small peptides havebeen shown to be better absorbed and utilised by the intestinal mucosa, itwould seem that whole protein can be well tolerated in most cases in which theintestine is normal. The type and quantity of fat may also play a role indetermining success. Long chain triglycerides (LCTs) such as those commonlyseen in most commercially available enteral products require significantdigestive effort as well as sufficient mixing with bile and pancreatic lipase toget absorbed into the intestinal lymphatics. Formulations high in LCTs maycause diarrhoea.46 On the other hand, medium chain triglycerides (MCTs)require less digestive effort and can be absorbed directly into the portalcirculation.47 Therefore, formulas containing small amounts of LCTs and/orutilising MCTs as the predominant fat source, may be better choices forpatients with gastrointestinal dysfunction.

For patients requiring extended enteral feeding, it is wise to choose aneconomical formula suitable for extended use. Excellent choices includestandard, fibre-enriched formulas and high calorie/high nitrogen products. Forpatients with potential malabsorption secondary to the prolonged interruptionof enteral nutrition, it may be best to introduce these formulas after tolerancehas been established to peptide or standard isotonic feeds. The high calorie/highnitrogen formulas do require significant digestion but may be useful for thefluid-restricted patient. In these cases, postpyloric administration is stronglyencouraged since the high fat content and hyperosmolality may contribute togastric retention. Fibre-containing products may also be introduced in theintensive care unit setting; tolerance needs to be established gradually to avoidthe associated side-effects including gas production and abdominal bloating.Two recommended strategies are offered. Either begin with a formulacontaining a lower fibre content or use a mix of a high-fibre formulation anda standard fibre-free feed. When tolerance is established, the patient can beplaced on a high-fibre formula.


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Figure 1 Algorithm for determining appro-priate enteral access for the critically ill

In the past few years, disease-specific products have been introduced. Theseare predominantly polymeric formulas in which the macronutrients, free water,and electrolytes have been modified to accommodate the specific requirementsof certain disease states such as liver failure, renal insufficiency, intestinalmalabsorption, diabetes and respiratory failure. Renal failure formulas areuseful as they do not significantly increase the need for haemodialysis and arerelatively concentrated. Hepatic failure formulas contain di- and tripeptides aswell as higher concentrations of branched chain amino acids and lowerconcentrations of aromatic amino acids. Both of these types of formula arerelatively low in protein. Unfortunately there is little evidence demonstratingimproved outcome with the use of these formulations. In addition, for thecritically ill where higher nitrogen requirements exist, standard, nondisease-specific products may be necessary.

Respiratory compromise may be complicated by excess carbohydrateadministration. Formulas with less carbohydrate and greater fat content maybe useful for decreasing carbon dioxide production thus decreasing the work ofbreathing. However, for most patients, the avoidance of overfeeding with astandard product may be sufficient.Modular enteral products can be used to augment specific macronutrient

requirements at a sensible cost. Specific products exist to provide additionalprotein, carbohydrate and fat to enteral formulas. The use of modular productsgreatly expands the flexibility of standard feeds to better support a wide varietyof patients.The newest enteral products have been supplemented with nutrients such as

glutamine, arginine, nucleotides, fish oil and MCTs for their theoreticalbenefits. These nutrients have been shown to be required in greater quantitiesduring critical illness. Preliminary studies have demonstrated a decreasedincidence of sepsis and improved outcome for the critically ill with the use ofthese formulations.48'49 Two studies have reported reduced septic complica-tions and hospital length of stay in critically ill cancer patients after majorsurgery when given a formula which contained arginine, fish oil andnucleotides.49'50 A recent multicentre trial in critically ill patients by Bowerand colleagues also demonstrated a decreased incidence of acquired infectionsand shortened hospital stay with the same enteral formula.5' In the near future,these formulations may become the standard of care in intensive care units.

Keys to success

With so many obstacles to overcome, it is paramount to have a good game planto maximise the potential for successful utilisation of enteral nutrition in theintensive care unit. While certain principles may hold true in most cases,following a rigid protocol is undesirable. A good game plan should allow forflexibility and creativity. Not all critically ill patients will respond in a similarfashion. What might succeed for the majority may fail miserably for theminority. Equally important is persistence. A setback should be viewed only as atemporary situation requiring reassessment of the patient's status and possiblereconsideration of the present formula, rate, or access.Upon entry into the intensive care unit, all patients should be evaluated

for placement of enteral access. The choice of access must be based upon

NUTRITION SUPPORTINDICATED

+ NO IPAENERALGUT CAN BE USED NUTRITION

+YESENTERALNUTRITION

POOR GASTRIC EMPTYING ORINCREASED RISK FOR ASPIRATIONNO YES

SHORT-TERM INTERMEDIATE LONG-TERM SHOR-TERM INTERMEDIATE LONG-TERM

|NASOGASTRIC ||PERCUTAN>EOUS| SURGICAL [| NASONTRIC | PERCUTANEOUS| SURGICAL|I UE | ATRSOIY||GASTROSTOMY | ~TUE JEJUNOSTOMY||JUOTM|Blind passage Endoscopic Open BSlnd passg EndoscoplcOpon

Radiographic Lenaroacopec Fluoroacopic Rad1oQgrpIhk LaeoecCEndoacopic


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Enteral nutrition and the critically ill 401

Figure 2 Nasoenteric feeding tube

Enteral feeding in thecritically ill: keys to success

* carefully select the most appropriateenteral access (usually postpyloric)

* initiate enteral feeding early (usuallywithin 48 h)

* start formula at a low rate (10-25 ml/h)

* increase formula rate based on thepatient's condition and the durationof time that oral nutrition has beeninterrupted

the particular needs of the patient (figure 1). In most cases, postpyloricplacement is desirable. The majority of patients requiring a laparotomyshould have a jejunostomy tube placed at that time. While needle catheterjejunostomies have been successful for elemental feeds,27'52 placement oflarge bore rubber catheters such as Red Robinson and T-tubes may be morereliable.43,53 These are usually 'witzeled' or 'stammed' in place and securedto the abdominal wall. For patients who are not scheduled for abdominalsurgery, consideration should be given to determine whether the feedingtube will be temporary, of long duration but possibly not permanent, orneeded permanently. Those patients who are deemed likely to depend upontube feeding for an extended period of time should be considered forpercutaneous or operative jejunal access. A limited laparotomy can beperformed solely for placement of the jejunostomy tube. This can be donequickly, through a small incision and is relatively well tolerated. Currently,techniques even exist for laparoscopic jejunal tube placement. If surgery iscontraindicated, or for those patients who are considered likely to recover inthe near future to the point of nutritional self-sufficiency, a thin, flexiblenaso-jejunal tube can be placed (figure 2). A number of techniques havebeen described to improve passage into the duodenum. If migration throughthe pylorus is unsuccessful, endoscopic or fluoroscopic guidance may benecessary. In some cases, the use of metoclopramide or erythromycin whichstimulates gastric motility can aid in the successful migration of the tubepostpylorically.54'55 If access to the jejunum proves impossible in a patientwho is not a candidate for surgical placement, every attempt must be madeto establish gastric feeding. This may require a low fat (LCT) formula, aslow increase in infusion rate and even the use of motility-stimulating agentssuch as metoclopramide, cisapride or erythromycin.Once reliable access has been established, enteral feeding should be initiated

in a timely fashion. There is good evidence to suggest that the intestinal mucosabegins to atrophy within 24 hours of nutrient deprivation. The longer the delay,the greater the risk of translocation and formula intolerance. While it would beoptimal to commence feeding within hours of admission to the critical care unit,this may not always be practical or desirable. Patients should never receive tubefeeding if they are haemodynamically unstable or require inotropic support tomaintain blood pressure. Should intestinal hypoperfusion exist, enteral feedingcould lead to pneumatosis intestinalis or bowel infarction.32 In addition, thefirst few days of intensive care unit admission are often interrupted by tests,procedures, and other activities. The initiation of enteral nutrition can alwaysbe delayed until the dust settles. As briefly discussed above, the selection of theenteral formula which will maximise the potential for success has not beendefinitively agreed upon in the literature. The choice is generally between apeptide formula with low fat or supplemented with MCT versus one with intactprotein which provides approximately 30% of its calories as LCT. Oneacceptable strategy is to begin all patients on the peptide formula and after goodtolerance is established, consider switching to the intact protein mix. A secondoption would be to attempt to use the intact protein formula first and substitutethe peptide formulation if intolerance presents.

Formula infusion rate can also influence ultimate success. While there aremany recommendations in the literature concerning how rapidly to increase therate of infusion, one simple principle should be mentioned. The initial rateshould be low, such as 10-25 ml/h and the rate of increase should be inverselyproportional to the duration of nutrient deprivation and the degree of intestinaldysfunction. In nearly all cases, formulas do not need to be diluted unless thereis also a need to administer supplemental free water. Most formulas are iso- ormildly hypertonic relative to serum. As previously stated, even formulas ashyperosmolar as 630 mOsmnl have been shown to be well tolerated whenproperly administered.37One final issue to discuss is how to treat intolerance when it develops. In

most cases, intolerance can be overcome. It should not necessarily lead toabandonment of enteral nutrition. If the problem is due to high gastricresiduals a few simple maneuvers can be attempted. First, reassess tubeposition with an X-ray. It may be coiled in the oesophagus or, if it wasinitially positioned postpyloric, it may have pulled back into the stomach.Consider switching the formula to one that is lower in fat. One might alsotry improving gastric emptying with medications such as erythromycin,cisapride, or metoclopramide. In most cases, stopping the infusion for a fewhours then resuming at a lower rate and increasing slowly will be effective. Ifintolerance manifests as diarrhoea, one must first rule out treatableaetiologies such as those related to infections or medications. Stool outputcan be decreased by adding fibre to the feed or slowing transit time with


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Summary points

* nutrition support is an importantadjunct to critical care

* early enteral nutrition is thepreferred route for feeding criticallyill patients with functionalgastrointestinal tracts but may bedifficult to provide

* postpyloric tube placement may benecessary due to poor gastricemptying

* with careful formula selection,enteral feeding can usually succeed,even in critically ill patients

opiates or codeine. If patients develop abdominal pain, bloating, or dilatedbowel on X-ray it is probably best to hold tube feeding until the conditionresolves. With all cases of intolerance, one must reassess the patient's clinicalcondition. In many circumstances, the sudden development of intoleranceafter a period of successful enteral feeding is probably due to a change inclinical status such as a new episode of sepsis, etc.

Conclusion

There is little debate that enteral nutrition is difficult to institute in mostcritically ill patients. Many obstacles have to be overcome. Yet the manybenefits offered to the patient who is fed enterally more than compensatesfor the difficulties in delivery. Can enteral nutrition be successfully utilisedin the critically ill? From the published reports in the literature andpersonal experience, the conclusion is an unconditional yes. All that isnecessary is an understanding of the potential problems to be encounteredand the many treatment options in the nutritional armamentarium tocombat these issues.

1 Blackburn GL. Nutrition in surgical patients. In:Hardy JD, Kukora JS, Pass HI, eds. Hardy'stextbook of surgery, 2nd edn. Philadelphia: JBLippincott, 1988; pp 86- 104.

2 Hensle T`W, Askanazi J. Metabolism and nutri-tion in the perioperative period. Jf Urol 1988;139: 229-39.

3 Cuthbertson DP, Tilstone WJ. Metabolismduring the post-injury period. Adv Clin Chem1969; 12: 1-55.

4 Douglas RG, Shaw JHF. Metabolic response tosepsis and trauma. BrJ Surg 1989; 76: 115 -22.

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